ML20155H190
| ML20155H190 | |
| Person / Time | |
|---|---|
| Site: | Three Mile Island  |
| Issue date: | 10/11/1988 |
| From: | Auxier J, Fabrikant J GENERAL PUBLIC UTILITIES CORP., INTERNATIONAL TECHNOLOGY CORP. |
| To: | |
| Shared Package | |
| ML20155H117 | List: |
| References | |
| OLA, NUDOCS 8810180351 | |
| Download: ML20155H190 (197) | |
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{{#Wiki_filter:_ _ _ _ _ - _ _ _ _ _ _ _ . October 11, 1988 i UNITED STATES OF AMERICA NUCLEAR REGULATORY COMMISSION - J BEFORE THE ATOMIC SAFETY AND LICENSING BOARD In the Matter of )
)
GPU NUCLEAR CORPORATION ) Docket No. 50-320-OLA
) (Disposal of Accident-(Three Mile Island Nucloar ) Generated Water)
Station, Unit 2) ) L 3 i 4 j LICENSEE'S TESTIMotiY OF i DR. JOHN A. AUXIER AND DR. JACOB I. FABRI) WIT ' 4 ON THE HEALTH EFFECTS OF _ TRITIUM (CONTENTION." 3 and Sd) l i J i ) i
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,l e , l Q.l. Pletse state your names. A.l. (JAA) My name is Dr. John A. Auxier. (JIF) My name is Dr. Jacob !. Fabrikant.
- Q.2. Dr. Auxier, by whom are yeu employed and what is your I position?
A.2. (JAA) I am the Director of Radiological Sciences for i International Technology, Inc. Q 3. Please summarize your professional qualifications and 1 experience relevant to this testimony, l 1 A.3. (JAA) I have a Bachelor of Science degree in Physics i from Berea College (1951); a Master of Science Degree in Physics from Vanderbilt University (1952); and a Ph.D. in Nuclear Engi-neering from the Georgia Institute of Technology (1972). I have l been certified by the American Board of Heelth Physics since 1960
- and have 35 years of professional experience in health physics l And radiation dosimetry. Prior to my affiliation with Interna-tional Technologies, I was President of Apolied Science Laborato-ry, Inc., and before that I was Director of the Industrial Safety S
l and Applied Health Physics Division of the oak Ridge National j Laboratory. I have served on numerous special task forces and l Advisory Committees concerned with radiation issues, and was Chairman of the Task Group on Health Physics and Dosimetry of the President's Commission on the Accident at Three Mile Island. ! was until recently a consultant to the Radiation Effects Research l 2-l } r J
[ Foundation, Japan, which is the organization reassessing the j dosimetry from Nagasaki and Hiroshima. I am also a mcmber of the i National Council on Radiation Protection and Measurements. In addition, I serve on the Safety Advisory Board for TMI-2. A more I complete statement of my professional qualifications and experi-ence is appended as Attachment 1 to this testimony. i Q.4. Dr. Auxier, what is Health Physics? l A.4. (JAA) Health Physics is a professional scientific discipline devoted to the radiological protection of humans and our environment. It is an interdisciplinary science that com- j t bines several interrelated areas of study, including but not limited to physics, chemistry, biology, ecology, and radiological ! medicine. The health physicist is a scientist engaged in the study of problems and practices of providing radiation protec-tion. He is concerned with the understanding of the mechanisms ! of radiation damage, with the development and implementation of , i methods and procedures necessary to evaluate radiation ha:ards, i and with providing protection to humans and our environment from , I unnecessary exposure. Q.5. What is the significance of being a "Certified Health j Physicist?" A.5. (JAA) The purpose of professional certification by the American Board of Health Physics is to ensure that practi- , I tieners of this scientific profession have a comprehensive l I
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understanding of these diverse elements as applied to
) radiological protection in their area of expertise and that they have demonstrated an adequate level of professional competence, r J
- As a Certified Health Physicist, I am committed to maintaining i
1 technical competence, reflecting the highest standards of profes-4 ! l sional ethics and integrity, and limiting my professional prac- } - l 1 tice to those areas where I have demonstrated competence. : i Q.6. Dr. Auxier, you stated that you are a member of the Na-tional Council on Radiation Protection and Measurements. What is j this organisation? . A.6. (JAA) The National Council on Radiation Protection [ i and Measurements (NCRP) was originally founded in 1929 as the U.S. Committee on X-Ray and Radium Protection. It later became j the NCRP as it is known today. It is a nonprofit corporation
.;hartered by Congress in 1964 toi (1) collect, analyze, develop, (
l and disseminate in the public interest information and l 1 recommendations about (a) protection against radiation and (b) i radiation measurements, quantities, and units, particularly those i concerned with radiation protection; (2) provide a means by which organizations concerned with the scientific and related aspects j l of radiation protection and of radiation quantities, units, and i measurements may cooperate for effective utilization of their j combined resources, and to stimulate the work of such organi:a- l L tions; (3) develop basic concepts about radiation quantities, ; I
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t I units, and measurements, about the application of these concepts, i j and about radiation protection, and (4) cooperate with the Inter- , 4 national Commission on Radiological Protection, the International , i Commission on Radiation Units and Measurements, ar.1 other nation-f 1 al and international organizations, governmental and private, t
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concerned with radiation quantities, units, and measurements, and l I with radiation protection. The Council is made up of experts who serve on the sixty-one Scientific Committees of the council, f
, l l Q.7. Has the NCRP evaluated tritium? >
4 A.7. (JAA) Tritium has been extensively assessed by the NCRP. NCRP Scientific Committee 38 evaluated the physical prop- i
- I e arties of tritium, physical transport of tritium, the biology of I i
! tritium exposures, and long-term dosimetric considerations. The j Committee's evaluation was published in 1979 as NCRP Report No.
- 62. In addition, NCRP Scientific Committee 24 examined whether l l
f any special hazards might arise from the incorporation of ; I radionuclides such as tritium into the genetic material of the { ceil. This evaluation was also published in 1979, as NCRP Report : l No. 63. These evaluations were extensive, encompassing an effort , to review and assess the world's literature on tritium, NCRP Re-I ports No. 62 and 63 represent the foremost and most authoritative , i evaluation of the dosimetry of tritium. i l 5-I I l
1 J l Q.8. Dr. Fabrikant, by whom are you employeJ and what is your position? A.8. (JIF) I am presently Professor of Radiology at the University of California School of Medicine at San Francisco; Se-nior Scientist at Lawrence Berkeley Laboratory, University of I California, Berkeley; Physician-in-Charge of the Donner Pavilion, ' r q Cowell Memorial Hospital, University of California, Berkeley: and Professor and Member of the Graduate Physics Group, Department of ) Biophysics and Medical Physics, University of California, I herkeley. My professorial and academic activities are devoted to . I l ~ 4 patient care, primarily diagnostic and therapeutic radiology and J nuclear medicin=; to research in radiology and biophysics, pri- ; { marily in the radiological sciences in the medical school and in j i the graduate school at the University of California. I have I l practiced radiological medicine for 30 years and continue to be ; l actively engaged in patient care in the ut.tversity hospital and . clinic. ; I i 1 i Q.9. Please summarize your professional qualifications and j I experience relevant to this testimony. j A.9. (JIF) I have a Bachelor of Science degree in chemis- , i I try and mathematics from McGill University (1952), a Doctor of l ) Medicine degree and a Master of Surgery degree (1956), both from ] I McGill Univereity; and a Doctor of Philosophy degree in i j i j biophysics, University of London (1964). I did post-doctoral j i f I t i ! l , i
training in surgery and pathology at Duke University Hospital. I trained in radiology at Th9 Johns Hopkins Hospital, and was ap-pointed to the faculty of The John Hopkins University School of Medicine and School of Hygien6 ond Public Health. I am certified by the American teard of Radiology in diagnostic radiology, therapeutic radiology and nuclear medicine. I am a Fellow of the American College of Radiology, and a Member of the Royal Society of Medicine of Great Britain. Prior to my affiliation with the University of California, I was Professor and Head of the Depart-ment of Radiology of the University of Connecticut School of Med-icine, and Professor and Chairman, Department of Diagnostic Radiology at McGill University Faculty of Medicine. I currently serve or have served on eleven committees and boards of the National Academy of Sciences-Mational Research Council, including its committees en the Biological Effects of Ioni:ing Radiation (BEIR). I served on the 1972 BEIR I Committee and its Subcommittee on Somatic Effects and the Subcormittee on Teratogenic Effsets. I was Vice-Chairman of the 1977 BEIR !! Committee. ! vas a member of the 1980 BEIR !!! Committee, served on the Subcommittee on Somatic Effects, and was Chr.: man of the Ad Hoc Committee for Estimating the Total Cancer Risk or Low-Dose, Low-LET, Whole-Body Radiation. I was Chairman of the 1988 BEIR IV Committee. I am presently a member of the current BEIR V Committee. 7-
1 t ) ; I i In addition, I am a member of 'she Board of Radiation i i Effects Research of the National Academy of Sciences-National Rs-- 1 I search Council, and I am a consultant to the National Academy ot' ! I l Sciences Board of Radioactive Waste Management. I am a'.so a mem- l
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l : ber of the International Commission of Radiological Protection l I snd the NCRP, and like Dr. Auxier, I too serva on the Safety Ad-I visory Board for TMI-2. I have previously served on advisory i committees of the President's Commission, The National Academ'f of ! P Sciences, USPHS, NIH, NCI, USAEC, USDOE, BRH, NASA, American Col- i i
- lege of Radiology, the National Radiological Protection Board of
i l Canada and the United Kingdom, and other scientific bodies deal-F l ing with radiation and health and cancer research. 1 t i A fuller statement of my professional qualifications 1 l and experience is appended as Attachment 2 to this tes*,imony. This attachment also lists the over 300 scientific articles, re- ) { ports, books, chapters and reviews that I have published in the f I open literature. These are all in the fields of radiological 4 sciences, medicine and surgery, radiobiology, radiation sciences 1 and radiological health, cancer biology, cancer research, and re-f t lated disciplines. J Q.10. You stated that you are a member of the International Commission on Radiological Protection. What is this organiza- ) i tion? I i , 8 s
s A.10. (JIF) The International Commission on Radiological Protection (ICRP) is the oldest and most respected scientific ad-visory body on radiation and health; it dates to 1928. The ICRP is represented by some 75 internationally recognized scientists from some 15-20 countries throughout the world with responsibil-ities to evaluate the health risks of radiation, particularly concerning radioisotopes, occupational exposure, and medical ap-plications, to estimate the extent of these risks, and to provide guidance and recommend limits on radiation exposures to worker populations and the general public. Q.11. Has the ICRP evaluated exposure to tritium? A.11. (JIF) Yes. The ICRP's findings are published at pages 65-67 of ICRP Publication 30, Part I, adopted in July 1978. Q.12. Please describe the National Academy of Sciences' BEIR Committees and their work. A.12. (JIF) The BEIR Committees are the expert scientific advisory committees on radiation and health effects of the Na-tional Academy of Sciences-National Research Council. In 1970, the first of the BEIR Committees (BEIR I) undertook a complete review and evaluation of existing scientific knowledge concerning radiation exposure and the health effects on human populations.
- Emphasis was placed on the health effects of exposure to low-1 level, low-LET radiations. The BEIR I Committee produced its report in November 1972. In 1973, the BEIR II Committee
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undertook an evaluation of the benefits as well as the risks of radiation. The BEIR II Report was completed in 1976. In September 1976, the NAS-NRC directed the BEIR Committee to update the 1972 BEIR report on the health effects of exposure to radia-tion on the basis of newly developed information. The EEIR III Committee was formed and produced its report in July 1980. In 1984, the BEIR IV Committee, which I chaired, undertook a de-tailed scientific study of the health effects of radon and other internally deposited alpha emitters. Q.13. Please describe the selection of the members of the BEIR Committees. A.13. (JIF) Each BEIR Committee has been comprised of a designated number of nationally and internationally recognized scientists, assisted by additional scientific consultants. The members are selected fer their contribution to scholarship and expert knowledge in science and public policy. For example, the BEIR III Committee was comprised of 22 scientists who specialized in the broadest spectrum of scientific disciplines, including medicine, public health and hygiene, epidemiology, biostatistics, genetics, medical genetics, population genetics, health physics, nuclear physics, radiology, endocrinology, nuclear medicine, mam-malian radiobiology, experimental radiobiology, cell biology, I physical biology, biophysics, pediatrics, reproductive biology, i cancer biology, radiological sciences, and occupational health, i l l l l l l
The criterion for membership has been a record of sci-entific achievement and scholarly contribution to the member's scientific discipline and recommendation by his scientific peers in the relevant discipline. Each BEIR Committee and its consul-tants are among America's most outstanding radiation scientists Q.14. Dr. Fabrikant, are you the only scientist to have served on all five of the BEIR Committees? A.14. (JIF) Yes. Q.15. What is the significance of the BEIR III Committee's Report? A.15. (JIF) The BEIR III Report (1980) is the consensus of the BEIR III Committee regarding the scientific basis for evaluating the health effects in human populations exposed to low levels of ionizing radiation. The report broadly encompasses two areas: (1) it reviews the current scientific knowledge -- epidemiologic surveys and laboratory animal experiments -- rele-vant to late effects of low-level radiation exposure of human populations, and (2) it evaluates and analyzes these late health effects -- both somatic and genetic effects -- as risks from ex-posure to low-level radiation. In its review and estimates, the EEIR III Committee took into account all known potential factors, to the extent pos-sible, influencing estimation of risks -- carcinogenic, genetic, and teratogenic -- from exposure to low level radiation. For
. . l example, for cancer risks and genetic risk estimations, observa-tions are based on epidemiological surveys of exposed human popu-lations exposed primarily to high-dose radiation and examined statistical techniques and procedures for extrapolating the data obtained from high doses to low doses; extensive research on lab-oratory animals and extrapolations from animal data to man; anal-ysis of dose-response relationships, both from experimental and epidemiological data, and from mathematical and theoretical mod-els of carcinogenesis and genetic and other effects; from known mechanisms of cell injury, transformation, repair, and recovery; in vivo and in vitro experiments; biological factors thac modify radiation risks in mammals and in human beings, such as age and sex; physical factors and types of radiation, such as linear en-ergy transfer and relative biological effectiveness. All these are detailed in the various sections of the BEIR III Report. The current BEIR V Committee is charged with building on the BEIR III process and new scientific knowledge, and with greater apprecia-tion of computational mathematics and statistical methods, to issue a further report by 1989.
Q.16. How do the BEIR reports compare with the findings of
- other national and international organizations such as NCRP and l
l ICRP? A.16. (JIF) The approaches, assessments, and evaluations ! of potential health effects from low-level ionizing radiation in l l I
the BEIR reports are consistent with and confirmed by the obser-vations and published reports of all leading national and inter-national scientific advisory committees and commissions concerned with radiation protections, standards, and health. These in-clude, for example, the ICRP (Report No. 26, 1977), the NCRP (Report No. 43, 1975; Report No. 64, 1980), and the United Na-tion: Scientific Committee on the Effects of Atomic Radiation ("UNSCEAR" Reports, 1977, 1982). Q.17. Dr. Auxier and Dr. Fabrikant, what is the purpose of your testimony? A.17. (JAA, JIF) The purpose of our testimony is to address the issues raised by Joint Intervenors' Contention 5d and by Joint Intervenors' Statement of Material Fact number 13 on Contention 3. In particular, our testimony responds to the issues raised by the prior statements of Dr. Charles Huver and Dr. K. Z. Morgan, concerning the dose and risk estimates associ-ated with the evaporation of accident generated water (AGW) at TMI-2. Our testimony explains the concepts of dosimetry, de-scribes the dosimetry of tritium, assesses the validity of GPU Nuclear Corporation's dose modeling, and provides an estimate of the potential radiation risks to the public associated with the evaporation of the AGW. Q.18. Would you please summarize your conclusions. men
A.18. (JAA, JIF) The radiation dosimetry of tritium is well studied and well understood, and it is properly considered in GPUN's dose modeling. The radiation doses to the members of the public from the evaporation of AGW are de minimis -- orders of magnitude below the doses received from natural background and other sources routinely encountered in every day life. The risk of even a single fatal cancer, genetic disorder, or teratogenic effect in the potentially exposed population and all their future progeny from the tritium release during evaporation of AGW is vanishingly small, and probably zero. II. Desimetry Q.19. Dr. Auxier, please define the terms "radiation" and "activity" for the record. A.19. (JAA) The nuclei of certain isotopes are unstable and undergo radioactive decay, disintegrating and emitting ener-getic particles or photons. The emitted particles or photons constitute radiation. The three principal forms of emission from radioactive isotopes are alpha radiation (the emission of the nuclei of helium atoms), beta radiation (the emission of elec-trons), and gamma radiation (the emission of photons). The activity of a radioactive material is a measure of the number of atoms that disintegrate in a given period of time. 10 One unit of activity is the curie (C1), which equals 3.7 x 10 disintergrations per second. Q.20. What is dosimetry? A.20. (JAA) Literally, the term refers to the measurement of dose. However, in the application of the term, many more fac-tors other than dose are considered. When a person is exposed to radiation, the moving alpha or beta particles or photons will transfer kinetic energy to the cells and tissues of the body. The amount of energy absorbed per gram of absorbing tissue is termed the "dose." The unit of ab-sorbed dose normally used is the rad, which is defined as 100 ergs per gram. When radiation delivers kinetic energy to an absorbing medium or tissue, it has an ionizing effect -- i.e., the energy transferred may rupture the atoms and molecules of the cellular constituents and produce electrically charged fragments or spe-cies. Different types of radiation, however, deliver their ener-gy at different rates per unit of length of the path traveled in tissue. The rate at which a particular radiation transfers its energy per unit length traveled in a tissue is called the linear energy transfer (LET). Alpha particles have a very high LET and are more damaging biologically per rad than gamma and beta radia-tion. Because different types of radiation may produce dif-forent amounta of damage to exposed tissue, many studies have been undertaken to compare the extent of damage by a particular type of radiation against the degree of damage from a reference
radiation (usually 200 kev X rays) This comparison is expressed as the relative biological effectiveness (RBE) of a particular type of radiation, which is an experimentally derived ratio of the dose of the reference radiation to the dose of the investi-gated type of radiation that produces the same biological effect. Note, however, that an RBE for a particular type of radiation depends not only on the LET of the radiation but also on the par-ticular biological system (e.g., different tissues) and biologi-cal endpoint (e.g., cell death, biochemical alteration, genetic alteration, etc.) being examined. Because different types of radiation can produce dif-
'ering degrees of damage in exposed tissues, absorbed dose in rads is not by itself a sufficient measure for radiation protec-tion purposes. In order to account for the overall difference in the degree of damage caused by the different types of radiation, dose is multiplied by a quality factor (Q), derived in part from experimental RBE values, to arrive at a dose equivalent. The quality factor represents the best scientific judgment based upon consideration of the studies' biological systems, effects, and experimental RBE values. ICRP recommends a factor of 20 for alpha particles, and a factor of 1 for gamma and beta radiation.
Dose equivalents (rads x Q) are measured in rem. Radiation doses from radionuclides may be caused by ei-ther external or internal exposures. External exposures are caused by radioactive materials outside the body, such as radioactive material in the air. Most external exposure is attributable to gamma radiation. Beta particles are far less , penetrating, and when emitted from an external source will gener-ally deliver only a small dose to or immediatel* Selow the skin. Alpha particles have very short ranges in tissues and therefore will not penetrate the skin and usually do not contribute to ex-ternal dose. External dose depends on the energy and intensity I of the radiation and the duration of exposure. Internal exposures are caused by radioactive material that has been absorbed, inhaled or ingested. Internal dose depends on the radionuclide inhaled and ingested and the effec-tive half-life of the radionuclide. The effective half life is 1
! the time required to eliminate half the amount of radioactivity that has been incorporated into the body, and is affected by the rate of radioactive decay of the radionuclide as well as the rate of the biological elimination of the chemical form from the body.
Q 21. How are doses due to environmental releases calculat-i ed? A.21. (JAA) Calculation of dose due to environ *;sental re-leases requires the application of models that are derived from biological and physical experimental and clinical evidence, insofar as possible. When a dose attributabic to the release of radioactive material into the environment is involved, the first step is the calculation of the transportation and distribution of l 1
the material through the environment that would affect humans. Environmental transport models such as those described in the NRC's Regulatory Guide 1.109 evaluate the known exposure pathways and derive the concentrations of each radionuclide to which "av-erage" and "maximally exposed" members of the public may or will be exposed. The next step is the calculation of the radiation doses in living systems, including humans, rasulting from each exposure pathway. For internal exposures, dose conversion factors (DCF) are applied to translate an inhaled or ingested quantity of a ra-dioisotope into a dose. The DCF's are established values that have previously been determined by models that consider how par-ticular inhaled or ingested radioactive materials are metabolized, and the effective half life of the radionuclides. Q.22. How is tritium transported thvough the environment? A.22. (JAA) The movement of tritium through the environ-ment has been well studied and is addressed in detail by NCRP Report No. 62. Tritium is an isotope of hydrogen, and its chemi-cal properties and distribution in nature are essentially the same as hydrogen. A tritium atom may combine with hydrogen and oxygen to form tritiated water (HTO). All water in the environ-ment has some tritium in it. The tritium in the AGW at TMI-2 is in the form of tritiated water and would be released in that fore by evaporation. The dispersal of tritiated water from the evaporation of AGW will follow the same pathways of natural water in the environment. When tritiated water is released to the environment, some of it will eventually become part of other molecules, including organic molecules in plants and animals. Tritium which becomes incorporated into such molecules is referred to as organ-ically bound. There are several ways by which tritium can become part of an organic molecule. The simplest and most prevalent way is through the natural exchange of hydrogen ie,ns conded to oxy-gen, nitrogen, sulfur, or phosphorous. In living tissues, about 80 percent of organically bound hydrogen exists as exchangeable hydrogen which readily assumes equilibrium with tritium. The remaining 20 percent of organically bound hydrogen is non-exchangeable. Non-exchangeable hydrogen is primarily bound to carbon. Tritium can become incorporated into an organic molecule as non-exchangeable hydrogen by the photosynthetic con-version by plants of carbon dioxide and HTO to form hexose, and the ingestion of plants and subsequent cellular synthesis can in-troduce this non-exchangeable tritium into animal and human tis-sues. As the organic molecules containing non-exchangeable tritium undergo biological turnover, these molecules and the tritium are degraded and eliminated as metabolic waste. Q.23. Will tritiated water accumulate in the biological systems of plants or animals? A.23. (JAA) Yes, but the evidence shows that there is no significant concentration of' tritium in either plants or animals. In transpiring plants with leaves having large surface areas, tritium levels may exceed environmental levels through preferen-tial transpiration of non-tritiated water from the surface of leaves to the atmosphere. This preferential transpiration is attributable to the difference in mass between H C2 and HTO (18 vs. 20) which reduces the vapor pressure of tritiated water to 90-92 percent of that of normal water. Under extreme condi-tions of low atmospheric humidity (such as in deserts), the tritium content in plants may be increased by as much as a factor of three over the specific activity of the environmental soil water. This phenomenon is insignificant in temperate climates. After considering thir phenomenon and the pertinent literature, NCRP Report No. 62 concluded: There is no evidence for a significant con-
- entration process for tritium in either plants or animals. . . . However, there may be an apparent discrimination factor when measurements are made under non-equilibrium conditions.
Q.24. What does NCRP 62 mean when it states that there may be a discrimination factor under non-equilibrium conditions? A.24. (JAA) When plants or animals are exposed to tritiated water, som3 of the tritiated water will become organ-ically bound. Under equilibrium conditions, the percentage of ' tritium in organically bound pools in the tissues of the body l l \ l {
will be equal to the percentage of tritium in freely a~ tilable body water. If the amount of tritium in the environment is then reduced or eliminated, the tritium in freely available body water will be eliminated and the percentage lowered at a faster rate than tritium that is organically bound. Therefore, during the transition period, there may be a higher concentration of tritium in organically bound pools than in the body water. Eventually, however, the tritium in organically bound pools will also be eliminated, and the organically bound and freely available tritium will equalize. Q.25. Dr. Huver refers to Koranda and Martin (1969), Ko-randa and Martin (1973), and Kirchmann (1971) on pages 2-4 of his affidavit. Did NCRP 62 consider these studies? A.25. (JAA) Yes, each of these articles was considered. After specific discussion of the data in the reports referenced by Dr. Huver, NCRP 62 concludes: No apparent enrichment or concentration effect for tritium has been found in aquatic or terrestial food chains. In fact, dilution in larger hydrogen or organic pools is the general rule, as tritium moves *.o consumer
- populations.
Q.26. What is the significance of Koranda and Martin (1969) to the evaporation of AGW? ! A.26. (JAA) Koranda and Martin (1969) is not relevant to I the exposure of humans to atmospheric releases of tritiated water i j
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for several reasone. 71rst, the "small mammals" examined in this study are Kangaroo Rats, which are extremely unusual and cannot be considered to represent a human model. The Kangaroo Rat is an animal highly adapted to a desert environment, and one of its primary adaptions is its ability to derive all of its water from the moistura content of vegetation and from water of combustion from the metabolic processes on food solids. Therefore, the uptake and retention of tritium in the Kangaroo Rat cannot be considered applicable to humans. Second, the study site was a desert nuclear weapon test site (with unique climatic conditions) in which the tritium concentration in the environment was slowly decreasing. The ratio of organically bound tritium to body water tritium in excess of one (it was measured at 1.2) may simply re-flect the discrimination phenomena in non-equilibrium conditions. NCRP 62 at p. 57-58 concludes that this assumption appears valid. Q.27 What is the significance of Koranda and Martin (1973)? A.27. (JAA) The information in Koranda and Martin (1973) is completely consistent with the current methods used for dose modeling (e.g., Regulatory Guide 1.109 and CPUN's MIDAS code). Koranda and Martin obtained access to a small plot of irrigated farmland in California, which included established young corn plants. Tritiated water was applied directly to the soil in the plot, and the movement of the tritium through the soil and the plants during the growing season was observed. The experiment involved the application of 0.0225 , curies per square meter to a growing patch of established young corn plants. This amount of activity corresponds to a concentra-tion of about 50,000 pCi per gram in the soil plowed layer (as-suming a 30 cm plowed layer). The data in Koranda and Martin (approximately 40,000 pCi/g in the leaf on day 1) suggest a soil to vegetation transfer factor (Biv) of about 0.8. The calcula-tions perfcrmed by GPUN use a Biv of 4.8 pCi/g in vegetation per pCi/g in the soil plow layer for tritium. The calculations per-formed by the GPUN computer code therefore assume r. ore tranfer to the vegetation than demonstrated by Koranda and Martin. It also appears from the Koranda and Martin data that the fixation of tritium in the corn ear is actually about one tenth of that in the leaf. The Koranda and Martin data do indicate that tritium was incorporated into the organically bound pool of hydrogen in corn. However, the quotation of the data has been used incor-rectly by Dr. Huver. He states, at page 3 of his affidavit, that corn ears which had not been formed at the time of tritium appli-cation showed levels of 500 pCi/g. The value of 500 pCi/g of tritium in the organic fraction must be represented as per gram of the organic matter, and not as per gram of the total mass of the corn ear, as Dr. Huver implies. The paper clearly indicates that the organically bound portion was analyzed by combustion of the dried vegetation. The value as quoved should be 500 pCi/g of tissue solids, or about 50 pC1/g of total mass, when adjusted for the approximately 1 to 9 ratio of solids to ' tater in typical veg-etation. The approximately 1,000 curies of tritium to be re-leased from the AGW represents about 0.00000005 curies per square meter average in the ingestion pathway zone normally considered for dose calculations. Since all of the activity will not be de-posited, this value represents an upper bound. Since the 0.0225 curies per square meter experiment resulted in about 50 pCi/g of plant tissue, 0.00000005 curies per square meter from the AGW could be expected to result in 0.0001 pCi/g of plant tissue. In contrast, the background tritium activity in surface waters and foods in the TMI region as a result of netural production and re-sidual fallout from nuclear weapons tests is on the order of 0.1 p01/g -- 1,000 times greater. The studies conducted by Koranda and Martin provide much useful information. It is likely, however, that the incor-poration of tritium into the organically bound pool by food crops 1 ! in the eastern U.S. will be lower than that observed in these studies for California. There is little rain in the summer growing season in the area of California where Koranda and Martin carried out these studies. Irrigation provides the required i water for farming the area af the test. According to Koranda and Martin, "The irrigation rate was just slightly above that esti-mated to be needed for growth and evapo-transpirational l l l
requirements and, thus, there was only a small amount of excess water to move the tritium pulse deeper. . . . It is possible that the high water requirements of the corn effectively held the tritium pulse in the surface. . . . The lower evaporation losses and presence of repeated rainfall events in the TMI area suggest that the displacement of tritiated water in the soil would be higher than that observed by Koranda and Martin. Higher displacement rates in the soil would, according to Koranda, re-duce the incorporation of tritium into the organically bound pool. Kirchmann (1982) also reports that climatic conditions in central Pennsylvania (humid temperature) will result in incorpo-ration of tritium of from one-half to one-third that of the dry climate of California (dry mediterranean). Dr. Huver's discussion of these studies might suggest that the dominant route of exposure will be from soi'. to the plant, but such is not the case. While some transfer of tritiated water from the vapor in a plume to the soil surface certainly does occur, the majority of the tritium uptake by plants will be through the direct absorption of tritiated water vapor into the above surface plant structures. Table 1 of Ko-randa and Martin shows that the transfer coefficient between at-mospheric water vapor and the water in eight species of plants range from about 0.17 to 0.49, depending on the species. The calculational model used by GPUN uses an even more conservative value of 0.5 for the transfer coefficient.
Q.28. Please comment on Kirchmann et al. (1971), discussed i by Dr. Huver on pages 3 and 4 of his affidavit. I i A.28. (JAA) Kirchmann et al. (1971) provided data on the , uptake of tritium into the organically bound hydrogen pool in cows. The Kirchmann data does show higher uptake with tritium I e labeled forage than with tritiated water, but the uptake from f i l vegetation is actually consistent with the relative masses of the two components (water and milk solids). In the case of ingestion of tritium as water, from 3% to 4% of the tritium activity in the milk was found to be in the milk solids, largely in milk fat. For tritiated vegetation ingestion, from 10% to 16% of the tritium in the milk was found to be in the milk solids. Since the actual solids content of milk is on the order of 10%, the re-sult for the vegetation ingestion is about as expected, while the result for tritium ingestion as water is lower than could be ex-pected from the simple ratios of the mass of the milk components. Q.29. If a human ingests tritiated water how is it distri-buted in the body? A.29. (JIF) Tritiated water can be absorbed through skin, the lungs, or the gut. The uptake from tritiated water in the air is about egaal for respiration and diffusion through the skin. In general, 98 to 99 percent of inhaled tritiated water is absorbed through the 'Aungs. In each case, the tritium is rapidly distributed throughout the body via the blood. When tritium
r enters through the lungs or gut, maximum blood concentrations are reached within a few minutes. When absorption is through the skin, maximum blood concentrations are reached within two hours. i. Tritiated water in blood equilibrates with extracellular fluid (lymph, interstitial and intestinal fluids, or cerobrospinal fluid) in about 12 minutes, j If a human ingeets tritiated water, can some of the f Q.30. i tritium become organically bound? l l A.30. (JIF) Yes. Tritium may enter organic compounds by [ exchanging with hydrogen at any of the labile sites in the mole- ! cule. In addition, tritium may be incorporated into stable mo- ; locular configurations. Thore are extensive stud.ies on animals that show that between 1 and 3 percent of a single administration of tritium in water is incorporated into organic constituents of l the body. The rate at which those turn over is dependant upon the half-life of the molecules into which they are incorporated. In a general sense, the more rapidly a molecule is turning over, i the more tritium will be incorporated into it per unit of tima j and the more rapidly will the label be removed from this molecu- } lar species. Long-lived molecules will incorporate smaller , amounts of tritium per unit time, but will turn over much more j slowly, and will thus retain the radionuclide longer if the f I tri. tium is in a stable position within the moleculte. [ I i i t
y . . _ _ . ._ __ l i Q.31. Is there a specific situation by which tritium may be incorporated into organic molecules as non-exchangeable hydrogen? A.31. (JIF) Hydrogen bonded to carbon is usually not ex- - changeable except during some enzyme-mediated reactions. The ! only mechanism by which tritium can bond to carbon is apparently by de novo biosynthesis. Thus, tritium will generally not become incorporated into molecules as non-exchangeable hydrogen, except i to a very limited extent during enzyme-mediated reactions. l Q.32. How is tritiated water eliminated from the body? ( t A.32. (JIF) Tritiated water is excreted in the urine, j l r sweat, breath, and s*. col. It has been shown that tritiated water in urine has the same specific activity as that of blood i f f (Feinendegen, 1967; Seelentag, 1973; Pinson and Langham, 1957), i i Q.33. What is the effective half-life of tritiated water in f .i the body following ingestion of tritiated water? I I A.33. (JAA/JIF) Reasonably detailed studies have been made ; on 300 individuals who have been accidentally contaminated with critiated water (Wylie et al., 1963; Butler and LeRoy, 1965). 1 The range in the biological half- life has been between 2.4 and 18 [ ! days. Exchangeable organically bound tritium has a half-life of 21-30 days, and non-exchangeable organically bound tritium has a f t l half-life of 250-550 days. , l I i r When warranted a raultiple compartment model may be used j to account for incorporation of the tritium into organically I f 3 1 i f
- i i !
i t 4 ! l ;
- . - = . - - . ._ _ . _ _ ~ ~
bound pools, and the elimination of tritium can be determined by I the combined elimination rate of the three compartments t (tritiated water, exchangeable organically bound tritium, and ; I non-exchangeable organically bound tritium). However, the cells l or molecules with long tetention of tritium because of their bio- [ t . logical turnover rates also are slow to incorporate tritium; and j at any time only a small portion of these cells are in a biologi-l cal development stage that permits them to react with the tritium j t in the body. Therefore, the body eliminates most of the tritium before these pools can respond to its presence. Accordingly, for t
- practical purposes, the tritium in organically-bound compartments j i !
usually may be neglected. Inclusion of these compartments com- ; l j plicates calculations and results in a minor change to the com-1 ! mitted dose equivalent 1/ to body tissues (ICRP 30, Part 1). In ( f i essence, biological elimination of all but a small portion from i i ! the body of an average man occurs at a rate of 50 percent every f 10 days. ] Q.34. Compared to the existing tritium in the environment, [ i 4 l what will the impact be to the exposure of the public from the tritium in the AGW once evaporated? l l i l 1/ Committed dose equivalent refers to the total radiation dose 4 from exposure to any fraction of the radionuclide intake remain- ! ing in the body any time within fifty years after its intake. I 1 1 ! 29-l I i l i
A.34. (JAA) In the long term, the amount of tritium in the body depends on its equilibrium levels in the environment. Since evaporation of the AGW from TMI-2 will be expected to add only slightly more than 1,000 curies to the existing environment pool of 70,000,000 to 140,000,000 curies (Jacobs, 1968) and a natural generation rate into the environment of about 4,000,000 curies per year, the contribution of the AGW to public dose will be neg-ligible. Constant dilution within the hydrosphere continually reduces tritium concentrations to the equilibrium levels of the general environment. Q.35. What will be the overall effect of the tritium in AGW if the tritium is incorporated directly into the biologically-active macromolecules of the cells of the body? A.35. Negligible. Tritium-labeled compounds that are spe-cificaly incorporated into the biologically-active macro mole-cules of the cells and tissues of the body are produced only in minute amounts in the body following ingestion or inhalation of tritiated water into the body. Thus, this, together with the di-lution and dispersion factors, will have an extremely small, if any, effect on the total activity or exposure, and thus radiation dose, in the body. If the tritium is ingested or inhaled as tritium-labeled organ't molecules, particularly biologically-active nucleosides, the dose, and hence the potential health effect, could be greater than from the inhalation or ingestion of i
an equal amount of tritiated water of equal activity. However, these tritiated organic compounds rarely, if ever, occur natural-ly in nature. They are not produced in nuclear power generating plants and will not exist in the AGW. It is only tritiated water that will enter the environment through evaporation of the AGW, and thus it is tritiated water that wculd be of consideration. Q.36. Would biologically-active, tritium-labeled nucleosides be produced in plants and transferred to humans through the food chain? A.36. (JIF) The presence of tritium in the organically bound pool of hydroq9n in plants does not indicate any modifica-tion to the dosimotry of the tritium in humans is required. In an actively photosynthesi-ing plant, the vast majority (ap-proaching 100%) of the organically bound tritium will exist as tritium associated with the sugar monomers and polymecs (i.e., starch), the lipids, and the proteins in the plant. If these plants are ingested by humans, the sugars and proteins would be largely catabolized and little will be incorporated in the human organic pool. Lipids are primarily membrane structural materials and as such are no*. intimately associated with the DNA. Lipid incorporation of tritium would therefore be equivalent to irradiation by water. Since any small deviation from the tritium dosimetry based on water could only be dependent on the incorpo-ration of the tritium in the DNA, the presence of the tritium in
l
. . l the organically bound pool is relatively unimportant to the dosimetry model of the human cell nucleus. The cell nucleus dose is mainly dependent on the tritium in the water.
Q.37. Dr. Morgan states that a reason for concern is that a tritiated water is considered to be about 100 times more hazard-ous than tritium gas. Please comment on this statement. A.37. (JAA) Tritium released as tritiated hydrogen gas ' rather than as tritiated water vapor yields lower doses because i it disperses more in the environment and is not readily taken up in plants or animals. However, the initial release of AGW from l the evaporator during the evaporation process involves HTO, and therefore, it is treated entirely as tritiated water in CPUN's modeling and dose estimates. Furthermore, the discussion of tritium dosimetry in this testimony relates specifically to tritiated water, not tritium gas. Dr. Morgan's observation is' irrelevant. Q.38. How does tritium deliver dose when metabolized in the body? A.38. (JAA) Tritium decays to helium by emitting a very low energy beta particle which has an average energy of 5.7 kev and a maximum entegy of 18.6 kev. In water or tissue, this beta particle has a very limited range. The mean range of a 5.7 kev electron in water is 0.68 micrometer (um) and opproaches 6.0 um for maximum energy beta particles. :n comparision, the average t cell diameter is about 15 um and its nucleus has a diaineter of about 8 vm. For a chronic exposure to tritiated water, tritium will be in equilibrium with hydrogen in body water and organically bound pools. Ur. der this condition, the dose rate for a given specific activity within the tissue is essentially constant. A specific activity of one microcurie (uci) of tritium distributed uniformly in one gram of tissue delivers a dose rate of 12.14 millirad per hour. Q.39. What biological effects mights occur from exposure to tritiated water? A.39. (JIF) If large amounts of tritiated water are ingested or inhaled, and the specific activity is high (e.g., curies), then the dose to the tissues will be high--on the order of hundreds of rads. The biological effect at the cellular level would be expected to be profound. However, wha" the dose is low and it is delivt 2 at a low dose '. ate, the biological effect would be expected to be minimal, or even not measurable. The primary concern for exposure at low doses and low dose rates is that the beta radiation might damage the DNA in the cell nucleus. If the cell is killed, the effect would 'se no dif- . forent than natural cell death which occurs in large numbers daily throughout the body tissues. If, however, a cell is in-jured and repairs aberrantly, then initiation of a cancer process l
might occur. If the cell is a germ cell of the testes or ovary, then a mutagenic process could result. Both these processes are dose-dependent and dose-rate-dependent. , i Since it is the DNA together with its related molecular coraplex that is regarded as the target molecule in which poten-tial radiation injury may result from los-level exposure, it is l largely the dose absorbed in the DNA of the cell nuclous that is biologically significant. However, since tritiated water is dis-tributed uniformly throughout the body water and thus randomly throughout the cells and tissues, the dose rate to the nucleus and its biological constituents is on the average the same as the dose rate delivered everywhere else in the cell. The occurrenec of interactions between emitted beta particles anc the DNA in cell nuclei is random. Therefore, the , i probability of the occurrence leading to injury would be low if l the dose is low, and it would further diminish by the fact that the low dose-rate would introduce a dose-reduction effectiveness factor, permitting tome repair of any DNA damage incurred. The < probability of a cancer or mutagenic effect, although extremely low, is nevertheless greater at high doses delivered at high dose on the other hand, the probability of their occurrence at f rates, i' very low doses, of the order we are discussing here, while still extremely low, is nevertheless very much decreased if delivered , at low dose rates. In this specific situation, the dose to any tissue or cell of an exposed person is vanishingly small, and ! l i !
hence the probability of the occurrence of a carcinogenic or mutagenic event approaches zero. Q.40. Dr. Morgan in his affidavit states that tritium in-corporated into DNA will be transmuted to a helium atom when it decays. What is the significance of this transmutation effect? A.40. (JIF) The genetic hazards of transmutation have been studied in detail. Depending on its chemical position in the DNA, transmutation of tritium to helium can break molecular bonds i and cause single-strand and double-strand breaks in the DNA. However, the frequency is extremely low, and single-strand breaks , are repaired efficiently. The DNA double-strand breaks from tritium transmutation add only insignificantly to the radiation effects of the tritium beta particle. The contribution of such events to the total genetic effect of decay of tritium in the cell nucleus is expected to be negligible in relation to the ef-fects induced by ionizations from the beta particles. Q.41. Will the recoil energy of tritium incorporated into DNA break or rearrange chromosomes as Dr. Morgan suggests? l A.41. (JAA) The effect of recoil should be insignificant. The maximum nuclear recoil energy from tritium decay is 3 eV and j I is too low to produce secondary ionization or breaking of carbon-hydrogen or carbon-carbon bonds. 1 1
Q.42. In what experir .tal organisms has a transmutation effect of tritium been observed? A.42. (JIF) Drosophila (the fruit fly), and in prokaryotes (single-cell organisms, such as bacteria and algae, lacking a nuclear membrane). There is evidence of a transmutation effect in prokaryotes of a transmutation effect for cytosine in the 5-position incorporated into DNA, as well as suggestive evidence 3 for such an effect in Drosophila; the decay of H in the 5-position of cytosine appears to cause a specific coding change 3 from cytosine to thymidine with high efficiency, and the H cytosine was more effect've than other tritiated DNA precursors 3 by a factor of 6 or 7. In prokaryotes, decays in H-6-thymidine and in 3 H-2-adenine also produce transmutation effects, although 3 with lower efficisney than in the case of H-5-cytosine. Q.43. Has a transmutation effect of tritium ever been found 1 at other DNA or P.NA sites, or in any other organisms more closely related to humans? , i A.43. (JIF) No. No transmutation effect has been detected : for decays in any of the other stable hydrogsn positions in DNA (the 6-position of cytosine, the motbel group of thymidire, and the 8-positions of adenine and guanine), or for decays ori- l qinating in RNA or protein. None have been observed in mammals in vivo.
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Q.44. On the bases of these observations, should there be any added effect of transmutation taken into account when consid-ering the biological e"fe:tiveness of tritium incorporated in the DNA molecule in the cell nucleus? A.44. (JIF) Since the relative abundance of hydrogen atoms attached to the three DNA positions for which transmutation ef-facts have been demonstrated among all DNA hydrogens is very low tiess than 0.0005 percent of the hydrogen in cell nuclei is in these positions), it appears reasonably conservative to assume, for the purpose of practical hasards considerations, that there is no cignificant transmutation effect for tritium incorporated in DNA, and that one may estimate hasards solely on the basis of absorbed beta dose. This is the conclusion of the NCRP. (NCRP Report No. 63 at 101.) Similarly, the ICRP Publication 30 con-siders the formation of tritiated organic compounds following, inhalation or ingestion of tritiated water and concludes that the formation of such compounds in the body is too small to have any effect on the total dose. ICRP Publication 30, Part I, at 65-67. Q.45. Dr. Huver cites a number of studies concerning the effects observed in the animals injected with or exposed to tritiated thymidine. Are these studies consistent with the find-ings of the NCRP and ICRP? A.45. (JIF) Yes. Thymidine is a specific DNA precursor, and is selectively incorporated into the DNA during synthesis of nucleic acids in the nucleus in preparation for cell division. The experiments cited by Dr. Huver selected tritiated thymidine because thymidine will become incorporated into one of the three key positions in the DNA molecule of the nucleus of mitotically active cells. Some studies suggest that when tritium-labelled thymidine is incorporated into the key positions in DNA, it can cause biological effects in excess of those that would be expect-ed on the basis of absorbed dose alone. Clearly, the incorpora-tion of nucleic acid precursors labeled by short range beta emit-ting tritium leads to a microscopic heterogeneous dose distribution where cell nuclei are exposed to much higher doses of radiation than adjacent cytoplasm. In the case of single tritium decays et infrequent intervals, however, critical volumes of DNA leading to carcinogenesis or genetic mutation may not be involved or repair may take place. Exposure to tritiated water is a very different circum-stance. Other than the negligible amount of tritium that might be incorporated into DNA by de novo biosynthesis following inges-tion or inhalation of tritiated water, only tritium that has been incorporated into organic molecules by photosynthesis, passed through the food chain, is subsequently syntherized into a DNA precursor in the body, and is taken up in a mitotically active cell undergoing cell prol;feration can end up in one of the key positions in DNA. The relative abundance of tritium in such po-sitions will be extremely small, and the biological effect is expected to be negligible. Q.46. Please desribe generally the radiobiological studies of tritiated thymidine and its effect on spermatogonia and cancer induction in mice that have been referred to by Dr. Huver. A.46. (JIF) In experiments on germinal cells of the mouse testis, and on tumor-induction in mice, it has been demonstrated that dosages of tritiated thymidine much greater than 1 microcurie per gram body weight are necessary to cause observable effects, such as spermatoginial cell death or tumor induction. The activity of tritium-labeled thymidine injected per gram body weight have produced decreases in germinal cell count in the mouse testis or induced tumors equivalent to about four times the activity of tritiated water injected per gram of body weight. I r. other words, the tritiated water is at least four times weaker in its ability to cause the cellular damage. It must be recognized, however, that direct quantita-tive extrapolation of such results as these i Y ce directly to humans is not possible because of (1) the diff nt mechanisms of germinal cell production and radiosensitivity in the two species, mouse and human, and (2) the fact that the mouse is a poor animal model for cancer-induction experiments for direct application to humans. And most important, the health effect in the intact or-ganism, mouse or human, will depend to a very large extent on the number of cells damaged and the relative importance of these cells. i ! l Q.47. Which are the reliable animal studies of radiation- l 1 a associated neoplasms due to tritiated thymidine, and what were j the findings of these studies? f A.47. (JIF) Only a few large-scale studies of the late J carcinogenic effects of tritiated thymidine have been reported j s ! thus fari (1) Baserga et al. (1965) reported an increased inci- l 1 dence of tumors of various kinds in CAF 1 mice injected with 1 9Ci of tritiated thymidine per gram of body weight at the ages of 2, ) 6, and 12 months; (2) Cottier et al. (1963) fcund no increase in , t { lymphomas in C57B mice injected with 10 vCi/g cf tritiated l J thymidine at the age of 6 weeks; (3) Johnson and Cronkite (1967) $ found no increase in tumors in Swiss albino mice injected with l j 5 uCi/g at 6-12 weeks of age; (4) Mewissen and Rust (1973) ob- l served an increase in the incidence of tumors after 0.3-1.5 uCi i j per g of body weight of tritiated thymidine when given to newborn j I I male and female mice. i ! i I Q.48. What do these studies suggest? A.48. (JIF) If these data are valid and if the differences { in results are due to differences in strain susceptibility, then f tumor incidence for the dose range of 1 to 10 uCi per g of body [ i weight is detectable in mouse experiments. It is to be expected f i i that tritiated thymidine in sufficiently large doses will cause { measurable increase in the nur.ber of neoplasms in an animal popu- . 4 ! ! lation. The important question is whether this compound, because j I l ! i i i I ! l l l ; l i i [ I
of its incorporation into DNA, has a unique encogenic potential i l beyond that which would be expected according to the dosimetric considerations that are usually applied to other internal emitters. Q.49. How do ths fin. dings of these studies relate to the potential dose-effect relationships for cancer induction? A.49. (JIF) It is of interest to compar[ the effects with those expected based upon radiation dosimetra . The injected
- amount of tritiated thymidine can be related approximately to the absorbed radiation dase. In nuclei primarily labeled after an injection of 1 pCi/g body weight, the absorbed dose rate is esti-mated to be about 4 rad per day in mice. This agrees well with observations on dose-effects in mouse spermatogonia (Johnson and l
Cronkite, 1959) and other systems (Bond and Feinendegen, 1966). . Q.50. Are these radiation doses and dose-rates high? A.50. (JIF) Yes. Considering the occupational guidelines t established for radiological protection (5 rads annual permis-I sible dose s ' low-LET radiation), they are extremely high. I Q.51. Would you expect these effects to occur in humans ex-l posed to the tritiated water from evaporation of the AGW? i A 51. (JIF) No. The amount of tritiated thymidine pro-duced would be negligible or none at all. Thus, the amount in-l ! corporated in the DNA of a proliferating stem cell in a human
f would be even less or more likely, none at all. Accordingly, the i potential radiation dose from the tritium in cells at risk would be negligible, or none, and there could be no radiation effect. Q.52. What studies are there that suggest that the incorpo-ration of tritiated thymidine in DNA of the reproductive germ cells can cause genetic injury? A.52. (JIF) Johnson and Cronkite (1959) and Lambert (1969) have reported direct observations on the effectiveness of tritiated thymidine for killing of mouse spermategonia compared with the effect of toth tritiated water and externally adminis-tered x-rays. The endpoint used was depletion of primary spermatocytes that presumably resulted from killing of type B spermategonia. Although it was difficult to estimate doses to the target cell nuclei aciurately, Lambert concluded that these results were compatible with RBE values (for tritiated thymidine) in the range of 1.3-2.4. 1 1
- Q.53. Does that mean the effectiveness of the tritium con-i I
, centrated in the DNA of the nucleus was less than twice that of i tritium dispersed uniformly in water throughout the cell for cell I killing of mouse apermatogonia? i A.53. (JIF) Yes. Moreover, this signifies that if the ra-e diation dose is extremely small, then even if the tritium were in ! large measure attached to thymidine, its potential genetic ef-fects wou.d be extremely small as well. 1 I
\
Q.54. Does this apply to the extremely lote doses expected from tritium in the tritiated water during evaporation of the AGW? A.54. (JIF) Yes. Q.55. How much tritiated water or tritiated thymidine would be required to deliver the ann'Jal permissible dose of low-LET ra-diation, that is, 5 rads, to the spermategonial stem cell nuclei, based on reference man? A.55. (JIF) If given in the form of tritiated water, 60 mci by intravenous injection or 60 mci by ingestion are the amounts that would deliver 5 rads per year to the spermategonial stem cell nuclei in reference man. If given in the form of tritiated thymidine, 1.4 mci by intravenous injection or 7.0 aCi by ingestion are the amounts that would deliver 5 rada per year to the spermatogonial stem cell nuclei in reference man. The bi-ological effects are expected to be the same. This means tritiated water is about 45 times less effect* than tritiated thymidine for spermatogonial cell killing in the t.couse if admin-istered as an intravenous injection to a dose of about 5 rads to the testes, and about 9 times less effect4ve than tritiated thymidine for spermatogonial cell killing in the mouse if admin-istered by ingestion to a dose of about 5 rads to the testes. Q.56. Do you expect such doses to the human testes to occur in humans as a result of evaporation of the AGW7 A.56. (JIF) No. The doses from evaporation of the AGW ; would be an extremely small fraction of the annual permissible dose, and in fact so small as to be negligible. Q.57. Are there experimental studies with animals given relatively large amounts of tritium with no deleterious health effects? A.57. (JIF) Yes. Many studies with animals tnat had been given tritiated water over long periods revealed no deleterious effects. When rats were given 86 ui/g body weight in a single injection, no harmful effects were observed during 9 months (Thompson and Ballou, 1954). With tritium given to young rats at a concentration of 4-5 uCi/mi in drinking water, beginning in early life and continuing for 6 months, no harmful effects were seen. No visible effects were produced in rats exposed to simi-lar levels from conception throughout life (Pinson, 1952; Thompson and Ballou, 1956). The concentration of tritium in body water was approximately 3 uC1/ml. Since 1 uCi/ml delivers 0.3 rad / day, this dosage delivered 0.9 rad / day plus the dose from the amount of tritium that was incorporated into the organic constit-uents of tissue. Baserga and Lisco (1966) followed mice for 2 years after giving newborn animals 15 uCi HTO/g body weight and observed no harmful effects. Q.58. Compared to experimental studies of tritiated thymidine, would you expect such high doses in humans as a result of evaporation of the AGW? A.58. (JIF) Again, the studies of the effects of tritium in mice have dealt mainly with the effects of tritium-labeled thymidine, and the levels of tritium activity that have been studied are far greater, by many orders of magnitude, than are to be expected frem tritium in the form of water in the environment occurring either naturally (natural background radiation) or in this case from the evaporation of AGW at TMI-2. Further, tritiated water, when taken into the body, is uniformly dispersed throughout the body and diluted by the cody water pool. Since the intracellular and extracellular water comprises about 70% of the body's tissues, any effects z.em the irradiation are simi-larly dispersed and diluted. For example 1 microcurie in 1 gram (ml) of water distributed throughout the body of the 70 kilogram man (normal weight) is diluted and dispersed throughout about I 50,000 grams of water in the body. Most of the tissues therefore will not be irradiated by the very short-range (less than 1/10,000th of a millimeter or 1/250,000th of an inch) of the beta particles. In sum, the tritium dosa from evaporation of the AGW will come from tritiated water, and any contribution from i tritiated thymidine will be negligibic. Accordingly, overall health effects are to be directly correlated with the absorbed dose from tritiated water, and no detactablo health effects are to be expected, f
Q.59. Dr. Huver refers to Lisco et al. (1961), Baserga et al. (1962), and Torok, Schmahl, Mayer and Kistner (1979) as indicating that tritiated thymidine and tritiated water may cause increased tumor formation. Please comment on these studies. A.59. (JIF) The studies cited by Dr. Huver illustrate the principles I just discussed. In Lisco, Baserga and Kisieleski (1961), mice were administered a single intraperitoneal injection of tritiated thymidine with a specific activity of 360 mci /mmole, producing an activity of 1,0 uCi/g of body weight. This injec-tion did result in some increase in the incidence of tumors, but the authors noted, "The mortality among the experimental animals has been remarkably low and the capacity of tritiated thymidine to induce tumors under these conditicas has not been spectacu-lar." Further, the dosage of 1 uCi/g of body weight was an acute uptake for the mouse. It corrgsponds to an uptake of 70,000 uCi (70 mci) for an adult human male. Since a single intake of 1 mci of tritiated water in reference man (60% water) results in a total body dose of 81 mrem (for Q=1), 70 mci in the human male would deliver approximately 6.0 rem whole body dose. This dose is many orders of magnitude greater that would ever be expected to result in any human from evaporation of t:iated water in the AGW. In Baserga, Lisco and Kisieleski (1965), the authora again reported an increase incidence of tumors from injection for 1 pCi/g of body weight of tritiated thymidine, but also reported that tritiated water at levels as high as 10-15 uci/g of body weight did not produce any tumors. One year later, the same , authorn reported observing no harmful effects after two years in mice given 15 uCi/g of body weight of tritiated water when they were newborn. (The equivalent dose to reference man would exceed 120 rads). See NCRP 63 at p. 65. Torok et al. (1979) examined organogenesis in developing mice, i.e., prenatal and postnatal development of mice i exposed in utero to different amounts of tritiated water (0.1-2 ) mci /ml). The doses of injected radioactivity of tritium during I the prenatal incorporation period ranged from a low of 54 rads to a high of well over 1,000 rads. At the upper end, the doses were sufficiently high to kill the mother. They correspond to dosages to reference man in the range of 4,900,000 uCi to 94,500,000 pCi. Effects on organogenesis were observed in the prenatal and 3 postnatal studies, but they relate solely to high dose effects 1 and are irrelevant to the AGW, The doses examined were many or-l ders of magnitude greater than the potential exposure to the pub-lic from evaporation of the AGW. l Q.60. Dr. Huver refers to Oakberg (1955), Johnson and Cronkite (1959), and Dobson and Cooper (1974) as evidence for the radiosensitivity of germ cells. Please comment on these studies. A.60. (JIF) Johnson and Cronkite (1959) involved in-l traperitoneal injection of tritiated thymidine producing activicy i l-
levels of 0.5 to 20 uCi/g of body weight. Again, these levels are relatively high, not "low" as Dr. Huver suggests. The doses would range up to 40 rem whole body dose (ani spermategonial stem cell dose) in reference man. The authors concluded that an in-i traperitoneal injection of 1 uCi/g of tritiated thymidine pro-duced an effect on mouse spermategonia comparable to 5 R of acute whole body radiation, and dose of 5 and 10 uCi/g are comparable J to about 10 rada and 20 rads of gamma irradiation respectively.
; It should be pointed out that the authors specifically chose mouse spermategonia for their experimental model because of the ,
great radiosensitivity of these cells. A dose of 5.0 pCi/gm body weight was required to reduce the number of surviving l spormatocytes by a statistically significant value, and this rep-1 resents a dose of about 10-15 rads. Oakberg (1955) was a study of the relative radiation
; sensitivity of spermatogonial cells of the mouse testis at dif-l forent stages of development, exposed to ./*,ernal irradiation from x-ray and Co-60 gamma sources. The stages of the mouse spermatogonial renewal differs from that of the human.
Dr. Oakberg only examined rodents; he never equated his observa-tions to the human situation, and he did not use tritiated water or tritiated thymidine as a source of radiation in these studies. In the study described in Dobson and Cooper (1974), fe- -{ male mice were continuously exposed to tritiated water from the , time of conception to 14 days of age. The three levels of I l i I
exposure corresponded to 8.5 pC1/ml, 0.85 uCi/ml, and 0,085 uCi/ml, resulting in dose rates of 2400, 240, and 24 mrads/ day, respectively. The percent reduction in primary oocytes for the three experimental groups were 93%, 44%, and 13% relative to the control animals. From the nearly linear dose-response curve, Dobson and Cooper estimated that a tritium tissue concentration of 2 uCi/ml, which corresponds to a dose rate of 560 mrad per day, would reduce the number of primary oocytes to the 50% level y of unirradiated controls. Since the mouse's gestational period is 19 days, the i total in utero does producing a 50% reduction in primary occytes j was 10,640 mrads (19 days x 560 mrad / day), or about 11 rads. This would be orders of magnitude greater than any potential ex-posure to an individual during evaporation of the AGW. Further-1 more, the biological stages of the mouse oovytes do not corre-spond to the human female, and this difference is a matter of considerable importance in estimating the genetic risk of radia-tion. The second and even more important factor that must be l considered in assessing the relevance of Dobson and Cooper's 1974 i study is the variation in species sensitivity to radiation. While animal models may parallel the human response, the sensi-tivity of their germ cells for certain agents may differ by sev-1 ! eral orders of magnitude. This is particularly the case for mice I and humans following exposure to ionizing radiation. The human i i { l l i l
germ cells are much more resistant to radiation injury than the mouse germ cells. Dobson, the very author of the article under review, states that: Great caution must be exercised in extrapolating from the results reported here on mice to possi-ble effecta on human beings. Available experi-mental evidence, though limited, suggests that occytes of primates are very much more resistant to radiation than are those of mice and rats In a more recent article (Dobson, et. al. 1982), Dobson further states that,
... human oocytes are probably not highly sensi-j tive to radiation...
l The National Academy of Sciencies (BEIR III, 1980) also has stat-ed that,
...the radiation doses required to kill a given fraction of primar'i follicles are also specie- ,
dependent in the mouse, a single acute dose of 10 R of x-rays reduecd the number of primary oocytes to half; in the rat, the comparable dose was 100 R; and in the monkey, perhaps as high as 900 R." (Note: a dose of 1 R of x-rays is ap-proximately equal to 1 rem or 1000 millirems). l Q.61. Dr. Huver refers to two studies -- Painter et al. (1958); Hori and Nakai (1978) -- which he asserts "reveal a simi-larity of types of effects with tritiated water showing rela-tively less damage than H - thymidine." Please comment on these studies. A.61. (JIF) The studies cited by Dr. Huver in fact indi-cate that acute doses of both tritiated water and tritiated
thymidine can produce observable cellular effects, but would sug-gest that tritiated thymidine is 100 to 1000 times more effective in producing such biological effects. The studies do not indi-cate that tritiated thymidine and tritiated water are comparable. For example, Painter et al. (1958) demonstrated that growth irthibition by HTO of Hela cells grown in tissue culture was accomplished only by concentration in the growth medium of 5 mci /mi -- on the order of 1,000 times that at which tritiated thymidine exhibited its effects.2/ Hori and Nakai (1978) exam-ined the capability of tritiated water and tritiated thymidine to produce chromosone aberrations in human lymphocytes in vitro. The exposure-effect curves for both tritiated water and tritiated thymidine were linear for the higher exposures but were less than linear for the lower exposure levels. (See NCRP 63 at p. 111). The yields of aberrations were very small at doses lower than 5 uCi/ml of tritiated water and below 0.05 uCi/mi of tritiated j thymidine. This study confirms a substantial difference in the i ability of tritiated thymidine and tritiated water to incorporate into cells and cause chromosone aberrations. Tritiated water re-quired 100 times the dosage to reach the same level of chromosome l damage. In other words, for efficiency in producing chromosome aberrations, tritiated thymidine appears to be about 100-fold more effective than tritiated water, i , 2/ Painter later reported that the inhibition of cell growth Drew and
; was really due to cell killing at the dose levels used.
l Painter (1959). ! l l 1 l l
- - - - - - - , -~ -_ . .__
Q.62. On pages 6 and 7 of his prior statement, Dr. Huver refers to several studies which he contends reflect genetic muta-tion. Please comment on these studies. A.62. (JIF) Kaplan and Sisken (1960) described the possi-ble intrachromosomal damage that may follow the incorporation of tritiated thymidine in the testes of the fruit fly, Drosophila melanogaster. Fruit flies were fed tritiated thymidine in food ; l and fruit fly medium. The amount of radioactive food ingested is not given, hence the doze is not known. No explanation is given for the mutagenic-effect observed. While it is recognized that drosophila has been used in the past for experiments in radiation genetics, it is not considered a surrogate for humans. Further-more, stages of biological hierarchy in the fruit fly testis are completely different than those in humans. The radiosensitivity of the germ cells of the fruit fly is f ar less than germ celfs in humans. Since no doses are given, a dose response relationship cannot be constructed. Nothing is stated about the effects of tritiated water. Stromnaes (1962) Ivestigated the mutagenic effect of tritium-labeled DNA precursors injected into Drosophila melanogaster. He compared the radioactive compounds, adenine-C-14, cytidine-H , and thymidine-H, to examine which would yield the highest induced mutation rate in the sperm of male fruit flies. It should be noted that the experiments were carried out in 1958, just over 30 years ago. In these i experiments, four groups of Drosophila melanogaster males were 14 3 injected it.trabdominally with C and H labeled precursors. The author found that dominant lethal mutations (measured by the fre-quency of non-hatched eggs) were not induced by the radioactivity used in the experiment, but that there was an increase in the frequency of sex-linked recessive lethals. The author concluded: 3 t (1) the amount of cytidine-H injected in males caused no de-
- tectable changes in the hatchability of eggs fertilized by sperm I from the males injected with radioactivity, and (2) dominant le-thal mutations were not induced on measurable amounts.
, t j This paper is dated and the data and findings are ir-1 relevant to the matter of the evaporation of the tritiated water i l in the AGd. First, the paper deals with genetic mutations in the fruit fly that are assumed to be radiation-induced. This is hardly applicable to humans since radiation-associated genotic l mutations have never been demonstrated in humans. Second, no doses are given, or even estimated; thus, no dose-response analy-sis is possible to assess the significance of the findings or , i their ralevance to radiation. Third, the study did not deal with ingestion of tritiated water, but rather tritiated DNA precutsors l
- l I injected directly into the abdomen of the fruit fly. Finally, the author refers to 700 r as a low dose (it in not), suggesting [
t
] that even greater doses were being administered.
1 Bateman and Chandley (1962) examined the genotic effect l i
; of trittated thymidine administered to mice. They administered ,
I j , l
d tritiated thymidine to 40-gram mice intraperitoneally in six 0.25 j mi fractions at a concentration of a 200 vC1/ml, for a total ac-tivity (or dosage) of 300 9C1 per mouse. They found that about ! 1% of the transmutations of tritium incorporated into the DNA thymidine produced a dominant lethal mutation (equivalent to a chromosone break). However, the authors concluded that "(T]he great majority of transmutations fail to produce a chromosone break at the site of the transmutation or in the track of the electron." This, they conclude, may be due to the absence of initial damage or the high rate of recovery. The authors further observed, "What is remarkable to us is the quantitative aspect: that it requires a concentration of tritium which gives 25 grains per sperm to produce one dominant iethal mutation per sperm."3/ contrary to Dr. Huver's statement, this study did not find a definite increase in abortions. It does not mention or imply anything relative to abortion. Contrary to Dr. Huver's statement, it did not estimate that 1% of tritium disin-tergrations produced a dominant lethal in the sperm. The article discusses the effects of transmutations of tritium within the sperm DNA, not the effects of tritium disintergrations. The num-ber of transmutations per sperm peaked at 100 in the fifth week 3/ "GrLins" is a term used in autoradiography to estimate gen-eral dose level. 25 grains corresponds to a spot on the film when 25 grains in the film's amulsion are exposed. According to send and Feinendegen (1965), about 16-17 intranuclear disintegra-
.avns are required per grain, so that 25 grains corresponds to about 400 intranuclear disintegrations.
4 after injection of tritiated thymidine. By then, 100% of sperm were labeled (i.a., had tritium-labeled thymidine in their Dl!A). i The number of tritium disintegrations from 300 uCi is over 11 million per second. Finally, Dr. Huver misses an important point. No doses are stated, and therefore, no dose-response can be estimated or determined from the data to begin to conclude that the findings 4.re radiation-associated. ] If one wished to draw an analogy between the two iaonth old mouse and the human funreaso', ably ignoring the greater ra-1 diosensitivity of the mouse), one could proceed to estimate dose in the following manner. Tt,e accumulated average dose to dit-i I ferentiating spermatocytes in the mammal is about 70 rems from a 1 single intravenous injection of 1 uCi of tritiated thymidine per gram of body weight. In the Bateman and Chandler study, the ] , tritium dosage of 300 uCi to a 40 gram mouse is 7.5 uC1/g. This l would yield a dose equivalent (of radiation) to the sperm of f about 525 rems (70 x 7.5) of low-LET radiation. This is not a low dose. A uniform whole body dose to man in this range (if de-livered acutely or over a short period of time) results in death from the acute radiation syndrome, usually within a month or so 1 after exposure. Tha intake would be equivalent to a total dosage j I of rodiactivity of over 500,000 uCi to a 70 kg human. To achieve ] a comparable intake from the AGW requires that an individual get all his normal daily intake of water diractly from TMI-2 ACW in-Ventory (at the measured concer.tration of 0.12 uci/ml) for over l 1
)
I l i I
2000 consecutive days (about 1100 gallons in all), assuming no
! biological elimination and no dilution from other sources of water. The experiment is clearly not relevant to tritiated water
. ingested following evaporation of the AGW. Moreover, drinking tritiated water is a much less effective method of incorporating tritium into DNA of maturing j sperm cells than intraperitoneal injection of tritiated thymidine. (ICRP 30, page 67 suggests that the annual limit on j intake might be as much as 50 times lower for tritiated thymidine j that for tritiated water.) Thus, in the human situation, the amount of tritium incorporated from water would produce a frac-i tien of the dose derived from thymidine. Greulich (1961) administered tritiated thymidine in aqueous solution orally to mice with an average weight of 28 l grams to achieve an activity level of 300 pCi over a period of 24-32 days. This is again an extremely high dosage. (To achieve the same dosage to a 70 kg man would require 750,000 uC1). Greulich found substantial fertility impairment by tritiated thymidine at those administered dosage levels, but did not dis- ] cuss or report data relative to dominant lethal mutuations. The j second generation progeny from the first mating also showed sub-stantial (a 70%) reduction in reproductivity, but this group was l irradiated in-utero. I Greulich's work took place in 1958-59, some 30 years j ago, and Gruelich is an anatomist, not a radiation scientist. I l 1
l Thus, some statements, in fashion at that time, should be consid-ered no more than observations and remarks, not scientific truths. For example, Greulich states (at 84) "Evidence is also presented which suggests the consequences of radiation injury after contamination by tritiated thymidine are not necessarily restricted to the individuals originally receiviaq this material, l but may also be transmitted to their progeny." The implication ' is that there is a teratogenic and/or mutagenic effect observed ; in his experiments that are radiation-associated. However, he fails to demonstrate any association -- e.g., (1) there are no f radiation dose estimates; (2) there are no dose-incidence rela- ; t tionships presented (dose-effect data are absent); (3) the "prog- ; eny" are restricted to immediate offspring only; (4) the off-spring with abnormal morphology amounted to three mice stillborn, from the mating of the same femalu and male; (5) tl.ese 3 still-born mice represented the only 3 out of 87 mice born in 1 mating experiment; (6) no other mice were born in the abnormal litter; (7) no other risk factors (other than radiation) were examined that may involve a casual-association; (8) there was no i autoradiographic evidence that the abnormalities were associated with incorporated radiactivity. In reality, Greulich's work at most suggests only that very large doses of tritiated thymidine ingested in drinking water could have adverse effects on subse-quent litter size. i I i r f I I
Q.63. What is the conclusion one should draw from these studies? A.63. (JIF) Perhaps the most important overall conclusion ; is that tritiated water and trititted thymidine, even in the ex- i perimental studies with relatively high doses, are not very effective as a carcinogen and mutagen. This conclusion is re-flected by the radiotoxicity ranking assigned t.' tritium by the , International Atomic Energy Agency (IAEA). The IAEA has invosti-gated and ranked the radiotoxicity of 235 radionuclides based i primarily on experimental evidence. The relative ranking incor-porates all variables with potential adverse human health ef-facts. Tritium is 225 on the list in order of descending ra-diotoxicity, which classifies it as having very low radiotoxicity. The low ranking reflects tritium's very weak en- ; ergy, its association with water, its distribution in body water l l after incorporation into the body, and its RBE/LET relationships. ; Q.64. Joint Intervenors state that in a study by Mewissen and Rust, it was found that incorporation of tritium into RNA was ! five-fold greater than in DNA. Please comment on this assertion. [ A 64. (JIF) As genetic material, RNA serves a secondary role to DNA. Among the principal functions of RNA is the j coordination of amino acid sequencing in polypeptide formation of l protein molecules. However, through enzymic action, a small per- ; centage of the nucleotides in RNA can be converted into DNA
-sa- l e
[ t i
i j l precursors and end up as molecular constituents in the DNA mole-cule, through metabolic interconversions in the nucleic acid ] precursor pool. Mewissen and Rust's 1973 study was considered in NCRP 62 and NCRP 63. NCRP concluded that the labeling of DNA from la-1 beled RNA breakdown products is not expected to exceed the label-ing intensity observed after application of the same amount of labeled thymidine. NCRP 63 states, "it appears justified to es-timate the long-term hazard from the labeled RNA precusors . . . ] l to be not larger than that from the same amount of equally la-i beled thymidine." NCRP 63 at p. 82. ] q Q.65. If beta radiation from tritium in the body damages i i the DNA in chromosomes in a cell, or if such damage were caused by the transmutation of tritium in these molecules, would a can- ) car or serious genetic abnormality necessarily occur? t ! A.65. (JIF) No. The probability of cancer or genetic ill j health occurring is vanishingly small, for a number of reasons. The initial event must be associated with too many biological l factors subsequently that select against the occurrence of J i neoplasia or mutation. For exa:ple, only the stem and germ cells i are at risk, and these constitute only a small fraction of the l cells in the body. Second, only sublethal damage to such cella I can lead to a can:er or, in the case of germ cells, a genetic l disorder. Chromosome aberrations such as breaks and deletions j -s9 i ?
i I are invariabl, ' ethal, precluding the probability of somatic or genetic mutativn Third, stem and germ cells can repair readily or are killed and are promptly eliminated from the body. Q.66. Dr. Huver refers to several studies an indicating ] that beta rsdiation from tritium is biologically more damaging per dose than gamma radiation. In particular, Dr. Huver refers j to Gray (1959), Furchner (1957), and Worman (1954). What Q value i should be assigned to the beta radiation from tritium? ) i
/. 66. (JAA/JIF) As previously mentioned, an RBE is an ex-
! perimental value calculated as the ratio of the doses of dif-4
- forent types of radiation that are required to produce the same t
j biological affect. In any particular experiment, a number of l variables may affect the measured RBE, including (1) the choice
- of a reference radiation, (2) the dose rate used, (3) the biolog-i ical system examined, and (4) the biologicial endpoint measured.
Therefore, the value of the FSE of a particular radiation can be cifferent from one experimental situation to another. ' The reference radiation for determining the RSE should i j have a confirmed RBE value of one. X-rays with as effective photon energy of 200 kev are the recommended reference radiation. $ Compared to x-rays, the RBE for tritium is about 1 tr most exper-
- iments. However, some investigators use Co-60 as the reference i
4 radiation. The RBE for Co-60 relative to 200 kVp x-rays has been
\
reported to range from 0.85 to 0.29 with decreasing dose rate. ) i l
b . , Thus, a measured RBE for beta radiation can be changed by as much as a factor of 2 depending upon whether gamma rays or x-rays are used as the reference radiation. The RBE value also depends on the biological system and i specific endpoint selected for investigation. The biological 4 systems vary, for example, from chromosomes within the cells,
' l cella cultured in vitro, cells in tissues, tissues, mammals, and 1
epidemiological studies. The biological endpoint, i.e. the par-i ticular effect being studied such as cell death or tumcr induc-4 l tion, is equally variable. I The variety of reported RBE values for tritium are due l mainly to the different measured biological endpoints and to the 1 l selection of a reference radiation. These considerations are re- ; 4 flected in the studies cited by Dr. Huver. 1 j Turchner (1957) used Co-60 gamma radiation as the ref-erance radiation. NCRP-63 examined Furchner's study and found that when the results are adjusted to take into account the dif- f i forent reference radiation and other factors, the RBE tends to- ! i. ! ward 1. NCRP 63, p. 62. ! Worman (1954) is not identified in Huver's list of ref- [ erences, but from Huver's description it appears that Worman was , examining a different biological endpoint (thymic and splenic at-i rophy). This is a relatively crude measure of RBE. It involves
- an acute effect caused by cell killing and is not relevant to late stochastic biological damage (vis., cancer and genetic risk) l at low doses.
l l 1
Dr. Huver cites Gray (1959) on page 4 of his affidavit. i A review of the literature has revealed no article authored by Gray in 1959. I presume that Dr. Huver intends to cite Gray i (1954), which is listed among the references to Huver's affida- l vit. This study, however, does not address tritium or beta radi-ation. ! I Q.67. What is the appropriate Q factor for tritium? t A.67. (JAA/JIF) There are numerous experiments in mammals, cells and tissues and measurable endpoints which establish the RBE of tritium in a particular experimental system The ranges , for the various experimental RBE values for tritium, even when uncorrected, are nevertheless low, only slightly above unity. ! When corrections are made for uncertainties introduced by the ra- 1 diation quality and dose rate of the reference radiation, and the i mean energy, effective half-life, and distribution of tritium in [ 1 the cells and tissues, there is ample evidence to ascribe to the tritium beta radiation an RBE of 1.0 provided the reference radi- [ ation is of the order of 60-80 kVp x-rays, f The Quality Factor Q is a universal value for the radiation { as defined by scientific consensus from the totality of all l available experimental data, existing scientific knowledge, and r L theoretical evidence, and is relative to overall health effects resulting from exposure of the general population to that radia- l tion. Based on extensive consideration of many studies and I t I l l t i f l
O 4 facters, including the reported RBEs, both ICRP (ICRP Pnolication
- 26) and NCRP (NCRP Report No. 91, 1987) have adopted a Q value of 1 for tritium radiation. This value represents the best scien-1 tific consensus, i
Q.68. What would happen if a Q value of 2 instead of 1 was used? A.68. (JAA) The dose eq ivalents calculated for a tritium j exposure using a Q value of 2 would be twice the dose equivalents calculated using a Q value of 1. The dose conversion factors used in GPUN's MIDAS model, however, are conservatively based on a Q value of 1.7. Further, the doses attributable to the evapo- i ration of AGW and the associated risks are so low that the selec-tion of a Q factor of 1, 1.7, or 2 is immaterial. > III. Health Effects and Risk Estimates I Q.69. Dr. Fabrikant, what are the potential health effects t in human beings that may be associated with the evaporation of I AGW at TMI-2? l A.69. (JIF) only three potential late health effects can i occur from exposure to low-dosa, low-LET ionizing radiation, j namely, cancer, genetically-related ill health, and developmental f abnormality of the newborn (teratogenesis). The probability of f i occurrence of cancer, genetic, or teratogenic effects from the evaporation of AGW at TMI-2 is extremely small, indeed i 4 h i t
i ! j d negligible. The risk estimates in the NRC's Programmatic Envi- ! ronmental Impact Statement support this conclusion, as I will ( demonstrate further in this testimony. l il There are other potentia.t health effects that could i l l occur from radiation exposure, such as cataracts, impaired fer-1 , I l! tility, and even heart disease, but the dose levels from the evaporation will be far too low for any of these diseases to be j t 1 considared as potential health risks. No other known health ef- [ t l facts are expected to occur following such low-level, low-LET ra- t diation exposure. I i ! Q.70. Have cancer induction, genetic ill health, or devel- ; 1 l l opmental abnorcality of the newborn ever been observed to occur [ 1 in humans or in human populations exposed to doses equivalent to I those that are estimated to result from the evaporation of the AGW? l A.70. (JIF) No, f i ! } Have such effects ever occurred after exposure to
; 7 71. }
f j dose levels higher than those calculhted for the evaporation of l I ] , ACW? l l A.71. (JIF) Cancer-induction has occurred in human popu-1 lations exposed to much htgher dose levels, but this has only j been demonstrated statistically at dose levels of about 25 rads ! i i ) or more. There are some reliable epidemiological data that indi- j cate a statistical excess of cancer after exposure down to 50 l 1 , f i i ! I i I i t _ _ _ - _ - - - _ - .
rads, and even 25 rads, but the numbers are small and the data in these low-dose regions are weak. There are a few epidemiological studies that suggest potential carcinogenic effects in the 10 rad range, but these are few and each relate to a special circum-stance with problems of analysis that remain unresolved. These dose levels are many orders of magnitude greate. than those which are expected to occur in association with the evaporation of AGW. Genetic health effects have never been demonstrated by direct measures to occur in the progeny of any human populations exposed to ionizing rt'" stion. Further, the most recent evalua-1 tion of genetic risks ir. the Japanese atomic bomb survivors sug-gest that human beings are less susceptible to genetic effects of ionizing radiation than people had feared in the past. (Neel et al, 1988). Q.72. Do teratogenic effects occur at very low doses? A 72. (JIF) BEIR III examined this issue and concluded that with respect to teratogenic effects, threshold doses proba-I bly exist below which such effects are not induced in man by ex-posures at sensitive stages in development. These thresholds may
- be higher for protracted or fractionated radiation than for acute single exposures, i
l l Q.73. Is it possible that no health effects may occur from the low-level radiation in the evaporator effluent? l l A.73. (JIF) Yes. With respect to the range of potential effects from the low-level radiation, BEIR III reaches the fol-lowing conclusion: Expectations based on linear ex-trapolation from the known effects in man of large doses delivered at high dose rates in the range of rising doss-incidence relatier.- ship may well overestimate the risks of low-LET radiation at low dose rates, and may, therefore, be regarded as upper limits of risk for low-level low-LET irradiation. The lower limit, depending on the shape of the dose-incidence curve for low-LET radiation and the efficiency of repair proresses in counteracting carcinogenic effects, could be appreciably smaller (tne peccioility of zero is not excluded by the data). (BEIR I, 1972, at 88; BEIR III, 1980, at 139) This conclusion applies to genetic and teratogenic effects as well, and is in accord with the findings and conclusions of the current 1988 BEIR V Committee. Q.74. What procedure did the BEIR Committees follow in estimating potential risks of radiation-induced cancer in human populations exposed to low-level low-LET radiation? A.74. (JIF) Risk estimates are based on the data derived from examination of epidemiological surveys of human populations, most frequently exposed to high-dose low-LET radiation, together with theoretical, mathematical, and statistical considerations and with extensive experimental cellular, tissue, and laboratory animal studies. The chief sources of epidemiological data cur-rently used for risk estimation are the Japanese atomic bomb survivors exposed to whole-body irradiation at Hiroshima and Nagasaki, the patients with ankylosing spondylitis and other pa-tients who were exposed to partial body irradiation therapeutically or to medical diagnostic radiography and fluoroscopy, and various occupationally-exposed populations such as uranium minero and radium dial pai- With the above tools, the BEIR reports define dose-response relationships be-tween radiation dose and observed cancer incidence, and thereby derive cancer risk coefficients in human populations exposed to lo'<-level radiation. The procedures are complex and require the talents of numerous scientific experts. Q.75. What are the various postulated dose-response curves for low-level, low-LET radiation doses? A.75. (JIF) Analysis of a number of dose-incidence curves for cancer-induction in irradiated populativns, both in humans and animals, has demonstrated that for different radiation-induced cancers, different forms of the same complex multicomponent dose-response curve can be defined. Simplifica-tions of the complex model can be achieved by reducing the number
- of components which have the least effect on the form of the dose-response relationship in the low-dose range. Such simpler models, with increasing complexity, include the linear, the pure quadratic, the quadratic (with a linear term in the low-dose re-1 i
gion), and finally, the multicomponent linear-quadratic
l dose-response form with a linear term and an exponential modifi-er. On tho basis of microdosimetric and biophysical theory, for low-LET radiation at low doses, the linear-quadratic relationship alters in the low dose range so that the quadratic term becomes progres:ively unimportant, and the linear term is expected to be more dominant. However, the slope of the linear section of the curve in the low dose range is less when derived from the linear-quadratic dose-response relationship than when extrapolated lin-early from high doses. Therefore, the risk indicated by the lin-ear portion of the linear-quadratic relationship would be less per unit dose at low dose than at high dose. A fourth model, one with a rapidly rising positive (convex upwards) curvilinear dose-response form and a decreasing J quadratic function (sometimes referred to as "supralinear" dose-response curve) has also been described for effects of low-LET radiation exposure. It is not used by any recognized national or international re.diological protection organization for risk esti-mation for low-dose, low-LET radiation exposure, since there is no experimental evidence or epidemiological evidence that this dose-response relationship is appropriate for risk estimation. l Q.76. Prior to 1980, what was the position of the BEIR Com-I mittee regarding the shape of the dose-response curve for l l low-level radiation doses? I l A.76. (JIF) The 1972 BEIR I Committee considered it sci-entifically appropriate to adopt a no-threshold linear hypothesis of the dose-response to estimate the cancer risk at very low-level, low-LET, whole-body radiation exposure. It was as-sumed the same proportional risks are present at low levels as at high levels of radiation. Q.77. Did the position of the 1980 BEIR III Committee change regarding the shape of the dose-response curve for cancer-induction? ., A.77. (JIF) Yes. The 1980 BEIR III Committee examined all possible dose-response relationships for estimation of carcinogenic risk in human populations exposed to low-level, low-LET radiation. The most compelling scientific and epidemiological evidence led the BEIR III Committee to select and apply the multicomponent linear-quadratic no-threshold dose-response form (with the linear term in the low-dose region). To estimate carcinogenic risk of low-dose, low-LET whole-body radia-tion, the linear-quadratic dose responsa relationship wes consid-ered the preferred model, that is, it would lead to the most appropriate central ris), estimate for the defined exposure condi-tions. The linear dose-response model was determined to be the most conservative and would lead to overestimates of risks. See BEIR III Report at 139. This change from the 1972 BEIR report was based upon the existing available experimental evidence, new J techniques of statistical analysis and certain epidemiological surveys (e.g., studies of leukemia), new experimental and cell culture evidence, and current microdosimetric theory. Q.78. Dio the scientific community accept the concept of a linear-quadratic dose-response relationship for human radiation-
- risk for cancer induction?
A.78. (JIF) In general, yes. The NCRP (1980) reviewed the l extensive experimental and epidemiological studies, and concluded that the linear quadratic model fit the radiation responses for l low-LET radiation exposure. The ICRP (1977) also concurs with this view. Q.79. Has any other scientific committee since the BEIR III Committee disagreed witn the BEIR III conclusions? A.79. (JIF) No. The 1985 NIH-NCI "Probability of Causa-2 tion" Committee used the linear-quadratic model for all cancer sites studied for its report, except for breast and thyroid, l where the Committee believed the epidemiological data tended to-l ward linearity (the statistical analysis of the data fit the lin-ear model slightly better than the linear quadratic model, but l did not exclude the linear-quadratic model). In general, the current BEIR V Committee, as it is developing its report, concurs with the BEIR III Report and the 1985 NIH/NCI Report. For example, breast and thyroid cancer fol-lows a linear model. Similarly, the UNSCEAR Cocmittee doec not 1
disagree with the application of the linear-quadratic model for whole-body low-dose, low-LET radiation and carcinogeneses. The UNSCEAR Committee, however, has specifically chosen to be as con-servative as possible, and has always chosen to project risk es-timates on the basis of linearity, recognizing that the model overestimates the risk of radiation carcinogenesis from low-LET radiation. Q.80. What dose-response curve is used in the PEIS for can-cer induction, and is this conservative? A.80. (JIF) The PEIS utilizes the linear dose-response model from BEIR I for estinating potential carcinogenic risks. See NUREG-0683, Supp. No. 7, at 5.4. This is a reasonable ap-proach, because the risks estimated will be conservative. Q.81. Why do you say the linear dose-7.esponse model is con-servative? A.81. (JIF) The best experimental and epidomiological ev-idence available to the scientific community indicates that the linear model probably tends to over_ estimate the risk of most radiation-induced cancers in man as a result of exposure to low- . dose, low-LET radiation. The consideration of the repair and recovery of radia-tion injury in the cells and tissues of the body and of dose-rate effectiveness factors (NCRF, 1980) strongly supports this conclu-sion. In experimental systems, the risk per unit dose of low-LET 1
3 I radiation for cell killing, for the induction of chromosome aber-rations, for genetic mutations, for cancer induction, and for other effects, consistently depends upon both the magnitude of l the dose and its temporal distribution. In general, the dose-response curves for low-LET radiation for late delayed health ef-fects (carcinocenesis and genetic effects) increase in slope with increasing dose And dose rate. Thus, linear interpolation be- ( tween the naturally-occurring or spontaneous incidence of effect and the incidence observed following exposure at intermediate-to-high doses and dose rates generally overestimates the risk of ! low-LET radiation at low doses and low-dose rates. In other words, the risk per unit dose of low-LET radiation is less at low doses than at high doses, and less when delivered at low dose rates than at high dose rates.
- Q.82. You have mentioned the dose-rate effectiveness fac-tor. What exactly is that?
A.82. (JtF) The existence of dose-rate effectiveness fac-tors (DREF) has long been recognized from clinical experience and from studies of both genetic and somatic effects in experimental l animals. From the studies on somatic effects in animals (NCRP, l 1980), the effectiveness per unit dose of low-LET radiation for cancer induction is lower at low doses and low-dose rates than at high doses and high-dose rates. The effectiveness per unit dose i ! of high- vs. low-dose and dose rate exposure ranges from a factor i I l f 4
I l of about 2 to ab'out 10. In other words, linear interpolation from high doses (say, 150 to 350 rads) may overestimate the ef-i facts of either low doses (say, 0-20 rads or less) or of any dose i r delivered at dose-rates of the order of 5 rad per year or less by a factor of 2 to 10. This factor is referred to as the Dose Rate Effectiveness Factor (DREF). (NCRP, 1980) Q.83. Are there convincing human epidemiological data to establish what the DREF may be for humans for cancer induction by low-LET radiation exposures? .i A.83. (JIF) Existing human epidemiologic data do not dem-
- onstrate conclusively that a dose rate effect does or does not exist in man. However, the experimental evidence from many dif-ferent biological effects, including carcinogenesis and genetic I effeccs, and for many species of animals in support of a dose rate effect is so extensive that it would be extraordinary if f such dependence did not apply to the came endpoints in the human ,
being as well. The NCRP (1980) concludes that the DREF range is ; 2 to 10 when the actual aosorbed dose la 20 rr.ds or les s or when the dose rate is 5 rads per year or less. The UNSCEAR (1977) Report uses a factor of 2. The ICRP (1977) reconmendations apply ;
- a factor of 2.5. The BEIR V Committee is currently considering a l
range from about 1 to 5 for cancer induction in human depending on the cancer si*.e and type and a number of other relevant fac-j tors. I l l t t l l I
Q.83. Is this dose-rate effectiveness factor recognized in human medicine? A.83. (JIF) Yes, very definitely. The concept is the basis for modern radiotherapy of cancer. It is also the basis for the management of persons involved in acute exposures in ra-diation accidents as opposed to those exposed chronically (as in the case of occupational exposure). Q.84. What are the estimated risks of radiation-induced cancers? A.84. (JIF) From analysis of the available epidemiological data, in the most recently published report (the 1985 NIH.NCI Report, Rall et al.) the total excess of radiation induced can-cers has been estimated to approximate 0.6 to 1.8 excess cases per 100,000 persens at risk per year per rem whole-body (low-LET) irradiation starting 5-10 years after irradiation and continuing for the romainder of life. The cumulative lifetime excess has thus been estimated to approximate roughly 30 to 100 additional cancers per 100,000 persono per rem, or an increase of about 0.1% to 0. 4*/, per rom in the lifetime risk of cancer (UNSCEAR, 1977; BEIR III, 1980). The important risk factors, among many, include the dose, age at exposure, cancer type or site, duration of expression of risk, and the dose-response model used in the estimation process. The most recent of these estimated risks of radiation-induced
cancers of different organs in relation to age of exposure and corresponding baseline incidence can be derived from the 1985 NIH-NCI (Rall et al.) Report, as follows: Spontaneous Age at Exposure Baseline Incidence 20-34 35-49 50+ (per million Cancer Type Excess Cancers Per Million persons per or Site Persons Per Year Per 100 Rems year) Leukemia Males 80 110 160 80 Females 50 70 100 60 Esophagu s Both sexes 5 8 22 35 Stomach Both sexes 300 50 130 95 Colon Both sexes 20 30 90 325 Liver Both sexes 3C 30 30 50 l Pancreas l Both sexes 20 30 80 95 Long Both sexes 60 90 1.20 500 Breast Females 490 310 80 900 Urinary Both sexes 20 40 60 220 i l Thyroid Males 50 50 50 20 Females 150 150 150 60 Q.86. Are these estimates based on established dose response models? 1 I
i i A.86. (JIF) Yes. All are based on the linear-quadratic dose-response models, except for breast and thyroid which are based on the linear model. Q.87. If these were based on the linear model solely, how i would the the total risk change? A.87. (JIF) It would increase, overall, depending on age. Roughly all risk estimates would double, except for breast anc . thyroid, which would remain the same since they are based on the linear model. Q.88. Are the risk values in the table, in general, in the san.e range as those estimated by the UNSCEAR, 1980 BEIR III and ICRP Committees? A.88. (JIF) Yes. Thef are all very close. Q.89. Dr. Morgan indicatas that new data regarding the
- hiroshima and Nagasaki bombings will change the cancer risk esti-mates. Please describe the data to which Morgan is referring and its significance.
A.89. (JAA/JIF) Until the mid-1950's, there appeared little hope that reasonable estimates of the radiation doseu re-ceived by the survivors of the nuclear bombings of Hiroshima and Nagasaki would ever be possible. However, in 1956, a project, designated Ichiban, was commenced at the Oak Ridge National Labo-ratory (ORNL) to attempt such estimates. After a decade of s
1 i 6 study, calculation, measurements in Japan, and weapons radiation measurements during tests at the Nevada Test Site (NTS), a system of dose estimation was developed. This dosimetry was designated T65D, since the estimates were Tentative (T) as of 1965 (65) f doses (D). (Auxier, 1977). In the late 1970's, computer calcu-lations at the Lawrence Livermore National Laboratory (LLNL) in-dicated that the T65D should be revised. Though the T65D calcu-
, lations showed the same values of the key parameters as the LLNL 1
calculations, the scientists who did T65D anchored their results in measurements made by Japanese scientists soon after the bombings. Commencing in 1981, an intensive multilaboratory, i multinational team effort was made to reevaluate the T6SD. The results, published in 1987, are designated DS86 for Dosimetry System as of 1986. (Radiation Effects Research Foundation, DS86, 4 Final Report, 1987.) Essentiaily all parameters varied to some l extent. At the large distances, low dose region, the major d'.f-ference was fer Hiroshima, where the new studies concluded that, though the total doses were essentially the same as T65D, they were composed almost entirely of gamma rays. In Nagasaki, the l doses were essentially unchanged. Although new studies of radia-tion associated carcinogenic, genetic, and teratogenic effects ! using the new doses are presently in progress (the first reports i i are currently being published), it is clear that there will be some upward revision in some of the radiation risk coefficients
based on these data, but not by a large amount and in many cases not at all. A few scientists believe that some of the risks may change by up to a factor of two, but the change could be in ei-ther direction. A conservative discussion of this is found in a recent report by the National Council on Radiation Protection and Measurements (NCRP). NCRP Report No. 91, at 23, Q.90. Are any scientific committees currently reviewing re-cent data on risks of carcinogenesis from exposure to radiation? A.90. (JIF) The UNSCEAR Committee and the National Academy of Sciences BEIR V Committee are reassessing estimates of the carcinogenic risks associated with exposure to ionizing radia-
'cion. The main sources of dats are the Japanese survivors of tne l stomic bombings at Hiroshima and Nagasaki and some groups of pa-tients who received therapeutic doses of radiation. The two com-mittees are taking into account the reassessment of the atomic bomb dosimetry at Hiroshima and Nagasaki. In general, maximum revision upward for most cancer sites excluding leukemia may be about a factor of 1.5 to 1.7. In most cases, the factor is ex- )
pected to be less; and for a few sites, the adjusted risk esti-mate may be less than was previously determined using the T65D dosimetry. Even if the cancer risks were revised upward by a fac-tor of two, and there is no evidence for this at this time, it would still not result in any additional ill-health from evaporation of the AGW, because the doses would be too low. Q.91. Briefly describe the BEIR Reports' treatment of potential genetic effects of low-level radiations in humans. A.91. (JIF) As indicated, genetic effects due to ionizing radiation have never been directly observed in man. However, they have been observed in laboratory animals. Estimations of the radiation risks of genetically related ill-health are based mainly on these laboratory animal observations -- primarily from laberatory mouse experiments. The genetic disorders that may result from radiation exposure ares (1) those which depend on changes in individual genes (gene mutation, or small deletions); and (2) those which depend on changes in chromosomes, either in total number or in gene krrangement (chromosomel a.borrations). Gene mutations are expected to have greater health consiquences than chromosomal ab-errations. At a low level of exposure, the effect of radiation in producing either kind of genetic change in experimental studies is proportional to the dose. The 1960 BEIR III Report's genetic health effects revies and estimates are describsd in Chapter IV of that report and are summarized in Table IV-2, at p.
- 85. The 1988 BEIR V Report, due to appear in the early part of 1989, reinforces the findings of BEIR III, and for all relevant purposes, is in complete accord with the BEIR III Committee find-ings.
J.t-Q.92. How does the 1980 BEIR III Committee's analysis of ! genetic risks in exposed human populations compare with the peer-reviewed scientific literature? A.92. (JIF) The BEIR III analysis of potential genetic disorders and genetic risks is in complete accord with the world's peer-reviewed scientific literature on radiation genetics, population genetics, cytogenetics, environmental mutagenesis, human genetics, and molecular genetics. (This is all documented in UNSCEAR 1972, 1977, 1982, 1984, 1986, 1988; ICRP, 1977; BEIR I Report 1972, BEIR III Report 1980, BEIR V Report (in press); NCRP, 1975, 1980.) There have been no chal-1enges in the peer-reviewed scientific literature to the genetics sections and genetic rirk estimation of the BEIR III Committee - (Genetic Sahcommittee) Report (1980). The 1988 BEIR V Committee with an entirely new group of geneticists. has reviewed the genetics r.ection of BEIR III Committee report (Ge.tetics Subcom-mittee) and included the most recent data available in its own l report. The 1983 committee is in complete agreement with all the scientific conclusions of the genetics section of BEIR III Com- i mittee (Genetics Subcommittee). { Q.93. Is it possible that new knowledge derived from the i most recent Japanese atomic bomb survivor studies may indicate that there are radiat, ion-associated genetic disorders appearing , in exposed human populations? l i l l L _ -_. ..... _.. _ _ _ - . , . - ___ . ~ . . _ _ , - _ . - - - _ . .___ _ __- . - -
A.93. (JIF) The reverse appears to be the case. The most recent data from the Radiation Effects Research Foundation in Hiroshima (Neel et al., 1988) suggest that human beings appear to be less susceptible to the genetic effects of the radiation of atomic bombs than people had feared. This conclusion, first re-leased at an International Congress of Genetics held in August 1988, is the most recent finding of the long-term study that has been exploring how the radiation released by the atomic bombs dropped on Hiroshima and Nagasaki at the end of World War II affected the survivors of the bombings and their children. The study is in its 43rd year. Q.94. If there are no recorded genetic effects found in human populations, what then was measured to assess genetic risk? A.94. (JIF) The new analysis, just reported, compared sev-eral "indicators" of genetic damage in the children of men and women who had been exposed to radiation from the atomic bomb ex-i plosions and in the children of comparable individuals who P.ad 4 not been exposed. There were no significant differences in any of these individual categories between children of exposed and non-exposed individuals. Q.95. How would this finding affect renetic risk estimates? A.95. (JIF) It would increase the "doubling done" for genetic mutations in humans, which in radiation genetics is the amount of radiation required to produce mutations equal in number to those occurring spontaneously in the animal species studied. The currently accepted doubling dose, based on mouse studies, ranges from about 50 to 250 rems for low-LET radiation. From the new Japanese data and the new analysis, a doubling dose in human beings in the range of abcut 145-255 rems would be estimated. Taking all measures into acevunt, Neel et al. conclude that this is rougly four times higher than the doubling dose projected from studies of mice. Q.96. Was the reassessment of the Japanese atomic bomb dosimetry taken into account in this analysis? A.96. (JIF) Yer. Q.97. Whtt does this mean in terms of genetic risk projec-tions from the tritiated water evaporated from the AGW? A.97. (JIF) It may be concluded that the genet.ic risks calculated by the NRC and presented here arc extremely conserva-tive, and tend to overot#.imate considerably any potontial genetic risks of radiation that might be seuimated to occur in human be-ings as a result of evaporation of the AGW. Q.98. What are the genetic risk estimates? A.98. (JIF) On the basis of our present knowledge of , radiation-induced mutations and chromosome aberrations in the mouse and in human beings, attempts have been made to estimate the risks of heritable detriment that are attributable to the l l l l I
different amounts of radiation that the general population re-ceives from various sources. Based on the 1960 BEIR III Report and the UNSCEAR 1977 Report, and on an assumed mutation rate doubling dose of 20-250 rems (in the mouse and in the human), estimates of genetic detriment per million liveborn offspring attributable to a gonadal dose of 1 rem to each parental generation are as follows: Type of Genetic Detriment Natural First Equilibrium , or Disorder Incidence Generation Generations Autosomal traits 10,000 5-65 40-200 (dominant and X-linked) Irregularly inherited traits 90,000 20-900 Recessive traits 1,100 Very few Chromor.cmal aberrations 6,000 Fewer than Increases congenital chromosomal 10 only anor.alies and other slightly congenital anomalies i _ _ _ . -- Total Gene?.ic Health Effects of an Average Population of 1 rom per 30 year generation 5-75 60-1100 Total Natural Incidence 107,100 Q.99. Given the data on the mouse for the various genetic traits that could be associated with radiation exposure, and since there have been no radiation-associated genetic disorders observed in the offpsring of exposed human populations, why is it I I
l necessary to predict what the risks could be in human populations ; exposed to low doses and low dose rates? A.99. (JIF) While no genetic effects are observable in hu- ; mans exposed at low doses at low dose rates, they may neverthe-less occur at a very low frequency that could not be detected ei-ther by direct observation or indirect statistical analysis. For purposes of prudence in radiological protection, such conserva- f f tive risk estimators are useful in establishing radiation protec-e tion standards and bounding possible genetic effects of radia-tion. Q.100. Are any scientific bodies currently reviewing recent data on risks of hereditary harm from radiation, and what are their conclusions? i A.100. (JTF) The UNSCEAR Committee and the National Acade-my of Sciences' BEIR V Committee have both been reviewing recent data on risks of hereditary harm and concluded that previous rick < estimates remain essentially unchanged, although the presentation
- of those risks has been changed. The risk of severe hereditary a
harm in the first two generations of offspring to an exposed individual per unit whole body dose is much leas, about half, than the cancer risk to the exposed individual. Q.101. Does the reassessment of the Hiroshima and Nagasaki dosimetry affect consideration of teratogenesis? A.101. (JIF) No. A recently published report by the Radi-ation Effects Research Foundation updates the information on the induction of severe mental retardation relative to fetal expo-sure2. The data in this report indicate that thresholds of dose (on the order of 25 rads to 50 rads or higher) appear to exist below which mental retardation does not result. The Radiation Effects Research Foundation is still reassessing a relationship between lowering of intelligence, school performance, and fetal exposure. Q.102. Would you expect to find such changes in intelli-gence in a child exposed in utero to tritium radiation as a re-sult of the evaporation of AGW? A.102. (JIF) No. The dosss woe.ld be negligible, and the probability of occurrenco would approach zero. For practical purposes, the risk would be zero. Q.lC3. How would one apply the risk estimates that you dis-cussed above to the situation of evaporation of the AGW? A.103. (JIF) To project the potential risks of radiation exposure, a number of important parameters must he determined. One must first calculate an effective dose equivalent. For the entire two-year period of evaporation of the AGW, the NRC has calculated that the total doses from all radionuclides derived from the evaporation proceso and impacting the maximally exposed individual are: 0.7 mrom to the total body, 0.8 mrem to the bone, and 4 mrem to the thyroid. These three doses can be added to establish a single dose which is termed the "effective dose equivalent." (ICRP 1977) The effective dose equivalent is the sum of the weighted dose equivalents for irradiated tissues and takes into account the relative susceptibility and contribution to stochastic risks (cancer and/or hereditary disorders) of any one tissue relative to the irradiation of the whole body. Rela-tive susceptibility is quantitatively expressed by weighting fac-i tors (WT ) which were established based on experimental findings l by the ICRP (Publication 26) in 1977. The weighting factor val- I ues for bone and thyroid are 0.*5 and 0.03, respectively, rela-tive to the whole body (all tissues) (IRCP, 1977). For example, this implies that a dose of 1 rer.: to che thyroid has the same stochastic health risk (e.g., tumoro) as a dose of 30 mrem whoj,e - body to the whole body (i.e., 0.03 W T x 1,000 mremthyroid = 30 mrom effective dose equivalent). Using the NRC's cal-wbolo body culated doser for tha entire evaporation process of the AGW, the t effective dose equivalent is 0.94 mrem to the maximally exposed individual (determined by applying the appropriate W T V"1"** I # , the tissue at risk). The population which may be potentially affected by the evaporation of processed water is defined by a 50 mile radius around TMI and includes 2.2 million individuals. The average exposure from the radionuclides for this population yielde a dose of 0.00146 mr'..a per individual. The total popula-tion or collective dose is calculated by summing up each individual dose for the all 2.2 million people living within a 50 mile radius of Three Mile Island. This yields a population or i collective dose of 3.21 person-rem, as estimated by the NRC. l I The doses as calculated by GPUN are slightly higher, and therefore the approach is more conservative. GPUN calculated i that the hypothetical maximally exposed individual would receive , 3.6 mrem to the bone and 2.0 mrem total body, which when combined produces an effective dose equivalent of 2.54 mrom to the maxi-1 mally exposed individual. The average exposure for the 2.2 mi - lion population within a 50 mile radius is estimated to be 0.01 mrom per individual and the total population or collective dose i r is rounded up to about 25 person-rem (effective dose equivalent). Q.104. Are these doses of significance in causing any potential health effects in any eFposed populations? - A.104. (JAA) No, the deses are extremaly small. They are [ in fact in the range normally considered de minimis or presenting negligible risk to human health. An illustration of how ex- i l tremely small these doses are is obtained by comparing them with i the radiation doses an individual receives from natura and man-made sources of radiation in everyday life. This comparison is shown in the following table. i I Radiation Doses From Natural and Man-Made Sources l National average background in U.S. (whole body) 300 mrem /yr* s i i Additional whole body dose : from living in a brick house [ instead of a wooden house (whole body) 20 mrem /yr** l l Round trip flight from New I
; York City to Los Angeles ! in a large commercial jet (whole body) 1.9 mrem ** l Diagnostic chest x-rays (series of 2-3 x-rays i to the thorax) (chest) 40 mrem **
} Dental x-ray (per exposure) i to the gum and mouth (month) 2.9 mren** ; Exposure to color television ! . set (wholv body) 1 mrem /yr** t ! Exposure to tritium , watch dial (whole body) 0.5 mrem /yr** l : l
- NCRP Repcrt No. 93. ;
** UNSCEAR 1977, at 13, 51, 03, 99, 310, 319.
As one can see, the dose to the hypothetical maximally exposed l individual from the evaporation of ACW would be loss than one f I l percent of the dose an individual would receive from natucal ^ background radiation each year. It is about 10 percent of an ad- l ditional dose a person would receive from living in a brick building each year, and is comparable to the whole body dose an average individual in the general population receives frcm watching color television each year. The dose to the average individual is many hundreds of times less and thus de minimis.
Q.105. Applying the risk estimates above, what is the prob-ability that members of the public will develop a fatal cancer induced by exposure to the tritium from the evaporated AGW? (JIF) A.105. Applying current total cancer mortality risk
-4 estimates (1 to 2 x 10 / rem) to GPUN's and the NRC's estimates of population dose, the estimates of the total number of excess , cancer deaths among the 2.2 million people living within 50 miles of TMI-2 range from 0.0003 to 0.005. This risk can be restated as an upper-limit of less than one chance in 200 for the possible j occurrence of a single fatal cancer among the 2.2 million people.
The upper limit probability of a fatal cancer for the maximally j exposed individual is less than one chance in 5 million using the NRC's calculated dose and less than one chance in 2 million using l! j GPUN's calculated dose. For all practical purposes, while an ex-
! cess value can be estimated based on modelling and mathematics, in fact no excess fatal cancers will result from the tritium and 4
- the other radionuclides during the evaporation process.
l These risk estimates are based on the ICRP (1977) current i values and do not take into account any new data or revisions of the dosimetry of the atomic bombings. The estimates are also based on the 1980 BEIR III Report. The estimates mLy need to be revised upward somewhat pending revision of the Japanese atomic bomb dosimetry and new statistical procedures presently being I applied to the new data by the 1980 UNSCEAR and 1988 BEIR V Com- ) mittees. It is roughly estimated that the risk coefficient may I. { . 4
---.,.--.--n---- --,_n._ - _ _ , _ . _
be increased overall by a factor of about 1.5 to 1.7, but can be much less, depending on dose, age at the time of exposure, sex, cancer orgar. ar site, end a number of other factors. In some in-stances, these rish estimates will not be revised upward at all. Q.106. Will this have any significant effect on the poten-tial excess cancer risk associated with evaporation of the AGW? A.106. (JIF) No. In simple arithmetic terms, it could raise the estimates of the total number from a range of about 0.0003 to 0.005 up to about 0.00045 to 0.0075. This would have no practical consideration for concern. The risk remains de minimis. Q.107. What is the spontaneous incidence of fatal cancer in a population of 2.2 million persons in the absence of any radia-tion exposure above background levels? A.107. (JIF) The cancer mortality rate in the United States is about 20%, i.e., 20% of all persons in a gen 9ral popu~ lation will die of a fatal cancer. In a population of 2.2 mil- > lion persons, it is estimated about 440,000 persons will eventu-ally die of cancer. Q.108. What is the risk of potential genetic ill health re-sulting from the evaporation of the A0W? A.108. (JIF) The collective gonadal (testes and ovaries) dose to the general population of about 2 million persons living within a 50-mile radius of the Three Mile Island facility is es-timated to be no greater than about 18 person-rems. Rounding up l 3 to 20 person-rems for simplicity, the average exposure is about i i f 0.01 mrem per person in the exposed population. The highest ! t
] gonadal dose to any mmximally exposed individual is taken here to be no greater than 2 mrem. Since the distribution of dose among the population is of no consequence below 100 mrem, the number of 4
j genetic effects may be calculated from the BEIR III estimates by l simple dose proportionality. Thus, the BEIR III first generation ! r i estimate of between 5 and 75 cases becomes 5-75/100,000, or O.00005 to 0.00075 cases per million live births. l It is assumed that the present population of about 2 ; million will be stable in the future and if the generation time ! i j cf populations is taken to be 30 years as an approximation, then . ] we would expect about 30,000 births per year, of which about [ 3,000 (30,000 x 0.107, where 10.7 percent is ths :urrent sponta- t l neous incidence of genetic disorders of all human live Dirths) l t would have been affected at some time in life by genetically re- 7 i j lated ill health irrespective of the AGW. The estimated 0.01 ) mrem average exposure from the evaporation of the A0W would add , i i between about 0.000001 (0.00005 cases per million births x l 30,000/1,000,000) and about 0.00002 induced cases. Expressed an- ; l other way, the incidence of genetically related ill health in the j 50-mile population is estimated to increase as a result of radia-i i tion exposure from the accident generated water by no more than I ! l ) 2
0.0000007 percent (0.00002/3,000 x 100) of the spontaneous inci-dence. In addition to the total population risk, we may also consider the maximum credible risk to the maximally exposed iridi-vidual. As an extreme "worst case," it might be assumed that a couple who each received an individual gonadal dose of 2 mrem subsequently have a child. In the absence of their radiatien ex-posure, the risk that child will experience genetically related ill health at some time in its life is 10.7 percent. From the BEIR III genetic effect estimates of 5 to 75 per million per rem, we may calculate the added risk attributable to the evaporation of AGW is 0.000001 to 0.000015 percent (5-75 x 10-6 x 0.002 rem x 100). In other words, the risk is increased in this "worst case" example from the normal 10.7 percent to a maximum of 10.700015 percent. From the BEIR III equilibrium estimate of between 60 and 1,100 cases per million live birthe per rem of parental expo-sure, we may further conclude that the average parental exposure of 0.01 mrem to the approximately 2 million population within 50 ! miles of the Three Mile Island facility may result ultimately in a total of no more than about one-one hundredth of one additional case of genetically related ill health per million live births , during all future existence. I l 1 l l I
O t-Q.109. In examining the estimation process, the values de-rived and the risk projections, Dr. Fabrikant, how best would you conclude your observations. A.109. (JIF) I agree with the findings of the NCRP Commit-tee that examined the problem of the health impacts of evapora-tion of the TM1-2 AGW, NCRP Commentary No. 4, printed in the PEIS Supp. No. 2 at A.13. First, for purposes of assessing the health impacts of ingesting and inhaling tritium, it is assumed that a uniform whole body dose equivalent of 100 rem will result in average lifetime fatal :ancer risk plus severe genetic risk totalling approximately 2 a 10-2 , Second, this value is somewhat low but not by much. The risk value reflects current estimates of the ICRP (ICRP, 1977), but does not account for potential changes that may result from the completed re-evaluation of the Japanese atomic bomb sur-vivor data. In addition, the quality factor of i for tritium beta radiation is constantly under review by NCRP, and may be re-vised. However, the not effect of both of these reviews and re-visions is unlikely to result in an increase in the risk values by any large facter, and clearly not by an order of magnitude. Third, applying the risk estimates given above to the effective dose equivalent values calculated, it can be concluded that the release will result in a lifetime cancer risk plus a total severe genetic risk to the most highly exposed hypothetical individual of approximately 10-7 , that is, one chance in 10 million. Finally, since these risks are the Negligible Individual . Risk Level of 10-7/ year recommended by the NCRP, and below the risk associated with one day of natural background radiation, the health and safety of the public will be unaffected by the release by evaporation of the AGW from TMI-2. IV. Conclusion Q.llo. As experts in the radiation health field, is it your opinion thst GPUN's proposal to evaporate the AGW is safe? A.llo. (JIF/JAA) Evaporation of the accident generated . water (AGW) from TMI-2 is safe, effective and technically sound. It removes a significant inventory of radioactive materials from the area. It reduces potential exposure at very low risk to the public. It is a major step toward the clean-up of TMI-2. The radiation doses to the public are very icw and should be considered de minimis. Any potential risks are negli-gible compared to normal risks of everyday life in the poten-2 tially exposed population, including that of natural background l l radiation. i Both the NRC's and GPUN's calculations use acceptable models and acceptable individual data values. These models and l data reflect the consensus view of the most authoritative bodies t in the United States and the international radiation protection community. As applied, they ensure that any bias overestimates . l the potential risk. They differ slightly because of the degree t 4 I
i e l- of conservatism they deemed appropriate, but are in basic scien-tific agreement. The issues raised by the Joint Intervenors do not change these conclusions, objective evaluation of their conten- l tions does not reveal any oversight or failure to recognize im-portant considerations by GPUN or the NRC. To the contrary, it , i confirms that existing standards and calculational models proper- . ly reflect an objective analysis /of all available information. This includes the issues and studies identified in contentions 3
- and 5d by the Joint Intervonors.
l i f 4
, o 1
References f i
, Auxier, J.A., Ichiban, ERDA Critical Review Series (1977)
- Baserga, R., and Lisco, H., "Tumor Induction in Mice By Radioac- !
j tive Thymidine," 29 Radiat. Res. 583 (1966) i l Baserga, R., Lisco, H., and Kisieleski, W., "Further Observations on Induction of Tumors in Mice with Radioactive Thymidine" 110 Proc. Soc. Expr. Biol. Med. 687 (1962) Baserga, R., Lisco, H. and Kisieleski, W., "Tumor Induction in , Mice by Radioactive Thymidine," TID-22292 (1965) 2 Batemen, A., and Chandley, A., "Mutations Induced in the Mouse with Tritiated Thymidine," 193 Nature 705 (1962) Bond, V., and Feinendegen, L., "Intranuclear 3 H Thymidine i Dosimetric, Radiobiological, and Radiation Protection As-pects," 12 Health Phys. 1007 (1966) i Butler, H., and LeRoy, J., "Observation of Biological Half-Life of Tritium," 11 Health Phys. 283 (1965) ; Cottier, H., Cronkite, E., Tonna, I. and Nielson, N., I
- "LeukmogenicEffectojW-cytidine"in"CellularBasisandhole-Body with H-thymidine and H Co-y-Irradiat l Aetiology of Late Somatic Effects of Ionizing Radiation," R. I
{ Harris, Ed. (1963) 4 ' Dobson, Level R. gndCooper,M., "Tritium Toxicity: Effect of Low I HOH Exposure on Developing c+aale Germ Cells in the i 'l House," 58 Radiat. Res. 91 (1974) I r I Dobson, R., Kvan, T., and Straume, T., "Tritium Effects on Germ Cells and Fertility," in "European Seminar on the Risks from ( Tritium Exposure," Report EUR 9065 EN (1982) ! Drew, R., and Painter, R., "Action of Tritiated Thymidine on the 1 Clonal Growth of Mammalian Cells," 11 Radiat. Res. 535 t (1959) i Feinendegen, L., "Tritium-Labeled Molecules in Biology and Medi- ! cine" (1967) Furchner, J., "Relative Biological Effectiveness of Tritium Beta-Particles and Co-60 Gamma-Rays Measured by Lethality in CP 1 Mice," 6 Radiat. Res. 483 (1957) s l l l Gray, L., "Some Characteristics of Biological Damage Induced by Ionizing Radiations," 1 Radiat. Res. 189 (1954) Greulich, R., "Deleterious Influence of Orally Administered Tritiated Thymidine on Reproductive Capacity of Mice," 14 Radiat. Res. 83 (1961) Hori, T., a.o Nakai, S., "Usual Dose-Response of Chromosome Aber-rations Induced in Human Lymphocytes by Very Low Dose Expo- j sures to Tritium," 50 Mutation Res. 101 (1978) International Atomic Energy Agency, "A Basic Toxicity Classifica-tion of Radionuclides," Technical Report Series No. 15 (1963) International Commission on Radiological Protection, ICRP Publi-cation 26, "Recommendations of the International Commission on Radiological Protection" (1977) International Commission of Radiological Protection, ICRP Publi-cation 30, "Limits for Intakes of Radionuclides by Workers," Part I (1978) Jacobs, D., "Sources of Tritium and Its Behavior Upon Release to the Environment," AEC Critical Review Series, TID-24635 (1968) Johnson, H., and Cronkite, E., "The Effect of Tritiated Thymidine on Mouse Sper.natogonia," 11 Radiat. Res. 825 (1959) Johnson, H., and Cronkite, E., "Effect of Tritiated Thymidine on Mortality and Tumor Incidence in Mice," 30 Radiat. Res. 488 (1967) Kaplan, W., and Sisken, J., "Genetic and Autoradiographic Studies of Tritiated Thymidine in the Testes of Drosophila Melanogaster," 16 Experientia 67 (1960) Kirchmann, R., "The Conversion to Organic Tritium in Terrestial Plants," in "Proceedings in European Seminar on the Risks from Tritium Exposure," Report EUR 9065 EN (1982) Kirchmann, R., Van Den Hock, J., and LaFontaine, A., "Transfer et Incorporation du Tritium dans les Constituants de l'Herbe et du Lait, en Conditions Naturelles," 21 Health Phys. 61 (1971) Koranda, J. and Martin, J., "Persistence of Radionuclides at Sites of Nuclear Detonations," Report No. UCRL-71867 (U.S. AEC) (1969) i i 1
-4 Koranda, J., and Martin, J., "The Movement of Tritium in Ecological Systems" (1973), in "Tritium," Report No. CONF-710809, A. Moghissi and M. Carter, Eds.
Lambert, B., "Cytological Damage Produced in the Mouse Testes by Tritiated Thymidine, Tritiated Water, and X Rays," 17 Health Phys. 547 (1969) Lisco, H., Baserga, R., and Kisieleski, W., "Induction of Tumors in Mice with Tritiated Thymidine" 192 Nature 571 (1961) Mevissen, D., and Rust, J., "Tumor-Incidence in C57 Black /6 Mice Treated with Tritiated Thymidine" in "Tritium," Report No. CONF-710809, A. Moghissi and M. Carter, Eds. (1973) National Academy of Sciences-National Research Council, Report of the Advisory Committee on the Biological Effects of Ionizing Radiation, "The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation" (1972) (The BEIR I Report) National Academy of Sciences-National Research Council, Report of the Advisory Committee on the Biological Effects of Ionizing Radiation, "The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation" (1982) (The BEIR III Report) National Council on Radiation Protection and Measurements, Report No. 93, "Ionizing Radiation Exposure of the Population of the United States (1987) National Council on Radiation Protection and Measurements, Report No. 91, "Recommendations on Limits for Exposure to Ionizing Radiation" (1987) l National Council on Radiation Protection and Measurements, Report No. 62, "Tritium in the Environment" (1979) National Council on Radiation Protection and Measurements, Report No. 64, "Influence of Dose and Its Distribution in Time on Dose-Response Relationships for Low-LET Radiations" (1980) National Council on Radiation Protection and Measurements, Report No. 43, "Review of the Current State of Radiation Protection Philosophy" (1975) National Council on Radiation Protection and Measurements, Report I No. 63, "Tritium and Other Radionuclide Labeled Organic Com-pounds incorporated in Genetic Material" (1979) Neel, J., Schull, W., Ava, A., Satoh, C., Otake, M., Kato, H., Yoshimoto, Y., "Implications of the Hiroshima-Nakasaki Genetic Studies for the Estimation of the Human ' Doubling 1
a 8 Dose' of hadiation," presented at the XVIth International Congress on Genetics, Toronto, 1988. Oakberg, E., "Sensitivity and Time of Degeneration of Spermatogenic Cells Irradiated in Various Stages of Matura-tion in the Mouse," 2 Radiat. Res. 369 (1955) Painter, R., Drew, R., and Hughes, W., "Inhibition of Hela Growth by Intranuclear Tritium" 127 Science 1244 (1958) Pinson, E. and Lanaham, W., "Physiology and Toxicology of Tritium in Man" 105 Appl. Physiol. 108 (1957) Pinson, E., "Incorporation of Tritium into the Organic Components of various Tissues in the House," Los Alamos Scientific Lab-oratory, Report No. LA-1467 (1952) Radiation Effects Research Foundation, DS86, Final Report (1987) Rall, J., el al., Report of the National Institutes of Health Working Group Publication No. to Develop (Radioepidemological 85-2748 1985) Tables; NIH Seelentag, W., "Two Cases of Death by Panmyelophthisis After In-corporation of Tritium" in "Tritium," Report No. CONF-710809, A. Moghissi and M. Carter, Eds. (1973) Stromnaes, O., "Mutuagenic Effect of C 14 and H3 Labelled DNA Precursors Injected Into Drosophila Melanogaster Males," 4 Can. J. Genet. Cytol. 440 (1962) Thompson, R., and Ballou, J., "Studies of Metabolic Turnover with Tritium as a Tracer," 208 J. Biol. Chem. 833 (1956) Torok, P., Schmahl, W., Meyer, I., Kistner, G., "Effects of a Single Injection of Tritiated Water During Organogeny of the Prenatal and Post Natal Development of Mice," in "Proceed-ings on Biological Implications of Radionuclides Released from Nuclear Industries," IAEA-SM-237/24 (1979) U. S. Nuclear Regulatory Commission, Regulatory Guide 1.109, "Calculation of Annual Doses to Man from Routine Releases of Reactor Effluents for the Purpose of Evaluating Compli-ance with 10 C.F.R. Part 50, Appendix I" (Rev. 1, 1977) . U.S. Nuclear Regulatory Commission, "Programmatic Environmental ( I Impact Statement Related to Decontamination and Disposal of i Radioactive Waste Resulting from March 28, 1979 Accident, Three Mile Island Nuclear Station Unit 2," NUREG-0683, Supp. 2 (1987) I l _ _ _ _ _ , _ _ _ _ . _ _ . _ _ _
< l 4
snited National Scientific Committee on the Effects of Atomic Ra-diation, "Sources and Effects of Ionizing Radiation" (1977) United Nations Scientific Committee on the Effects of Atomic Ra-diation, "Non-stochastic Effects of Radiation" (1982) United Nations Scientific Committee on the Effects of Atomic Ra-diation, "Ionizing Radiation Levels and Effects" (1972) Wylie, K., Zigler, W., and Grove, G., "Biological Malf-Life of Tritium" 9 Health Phys 911 (1963) + i t
, ATTACllMENT 1
- JOHN A. AUXIER, DIP.ECTOR ;
l Education < 1972 Ph.D. in Nuclear Engineering, Georgia Institute of Technology, Atlanta, Georgia i 1952 M.S. in Pb'/ sics, Vanderbilt University, Nashville, Tennessee , i 1951 B.S. in Physics, Berea College, Berea, Kentucky Certification 4 1960 Certified by American Board of Health Physics 1 1 Professional Exnerlence 9/85 - IT/Radioloaical Sciences Laboratory. Oak Ridae. Present Tennescee. Director. Directs approximately 60 i scientists and technicians in Radiation Protection Consultation in all major areas of the radiation associated industries and the Radiological Analytical ! Laboratory. , 9/R3 - Aeolied Science Laboratory. Inc., Oak Ridae. Tennestggt 9/85 President. Directed the formation and development of ; the consulting and analytical laboratory which became
! IT/RSL.
1/83 - Evaluation Research Corooration. Oak Ridae. Tennessee. i 9/83 Chief Nuclear Scientist. Health Physics consultant for ' a wide range of clients, usually in a troubleshooting capacity. 1977 - Oak Ridae National Laboratory. Oak Rida9 Tennessee. Director. Industrial Safety & Aeolied Health Physics ( l 12/82 ) Division. Directed a Program which led to record breaking performance in both Radiation Protection and q Industrial Safety. , 1972 - Oak Ridae National Laboratory. Oak Ridae. Tennessee. ' l 1982 Director Health Physics Division. Gave increased
- emphasis to needs of practicing health physicists.
Strongly encouraged fundamental research in heelth t physics related areas. Directed research in the investigation of pathways of exposure and biological (
)
effects of pollutants (both nuclear and non-nuclear) i and radiation safety.
) 1962 - Qpk Ridae National Laboratory. Oak Ridae. Tennesseem !
i 1972 Chief. Radiation Dosimetry Procram. 1 i ! i j l
JOHN A. AUXIER Page 2 1955 - Oak Ridae National Laboratory. Oak Ridae. Tennessee. 1962 Health Physics Division. Conducted research in ~ radiation physics and dosimetry; participated and ultimately directed successful efforts to obtain radiation doses for survivors of nuclear bombings of Hiroshima and Nagasaki, Japan. 1952 - University of Texas. Coordinated and directed Health 1955 Physics Program. Subsequently appointed Chairman, Department of Physics and Engineering Radiobiological Laboratory. 1944 - U.S. Army Air Corp., Fighter Pilot. 1947 Special Consultant Activities 1976 - Consultant to Radiation Effects Research Foundation, 1987 Japan. 1978 - Member of Advisory Committee to U.S. Department of 1987 Energy for Northern Marshall Islands. Member of i Department of Energy / Defense Nuclear Agency Inspection and Advisory Team for Clean-up of Enewetak Atoll. 1979 Head, Task Group on Health Physics and Radiation i Dosimetry, President's Commission on the Accident at Three Mile Island. 1979 - Member of Dose Assessment Steering Group, U.S. 1987 Department of Energy. '!' 1980 - Member of National Academy of Sciences Panel on 1987 Hiroshima / Nagasaki Occupation Forces. l j 1981 Member of NAS Committee on Emergency Management. 1981 - Member of Safety Advisory Board for Three Mile Island Present Unit 2. 1981 - Member of Advisory Council, Institute of Nuclear Power 1988 Operations. l ) 1988 Listed as an advisory expert in nuclear health effects,
' low-level radiation, occupational safety and waste management in the Media Guide to Nuclear Enerav Experts
- prepared by the U.S. Council for Energy Awareness.
l i
JOHN A. AUXIER Page 3 Professional Societies Health Physics Society, (President-elect, 1976; President, 1977; Managing Editor, Health Physics Journal, 1974-1977; Editor, Health Physics Journal, since its inception in 1958-1974; Chairman, Health Physics Society Presidents' Emeritus committee Chnirman, Research Needs in Health Physics Committee, 1984 , Member, East Tennessee Chapter of the Health Physics Society. American Strategic Defense Association; Society for Risk Analysis; National Academy of Sciences, (Subcommittee on Exposure at Tests of Nuclear Weapons, 1984); National Council on Radiation Protection and Measurements (Member, NCRP; NCRP Scientific Committee 63; NCRP Scientific Committee 57; NCRP Scientific Committee 28; NCRP Scientific Committee 34); International Radiation Protection Association, Charter Member since 1963; French Radiation Protection Society, member of advisory board, 1970 - present. Environmental Associations Earthwatch, Watertown, Massachusetts The Nature conservancy, Arlington, Virginia National Audubon Society, Boulder, Colorado Laboratory of Ornithology, Cornell University Ithaca, New York
JOHN A. AUXIER Page 4
, African Wildlife Foundation Defenders of Wildlife World Wildlife Foundation National Humane Education Society Professional Listinag Who's Who In Technology Today American Men and Women of Science i special Awards 1962 Elda E. Anderson Award, Health Physics Society 1962 National Preparedness Award, National Institute for Disaster Mobilization 1980 Meritorious Public Service Medal, Defense Nuclear Agency 1980 Delivered Eighth Wright H. Langham Memorial Lecture 1984 Fellov, Health Physics Society 1987 Honorary Doctorate of Science, Berea College 1987 Founders Award, Health Physics Society Publications Author or co-author of over seventy-ffva open literature publications in instrumentation, dosimetry, natural environment, radiation physics and radiobiology.
Recipient of the two approved patents. Author of published book in ERDA Prestige Series entitled, ICHIBAN Radiation Dosimetry for the Survivors of the Bombinas of Hiroshima and Nacasaki.
I . JOHN A. AUXIER Page 5 Publications l Auxier, J.A., G. Forman, 52 "Characteristics of X-Ray Excited Phosphorescence of Calcite," Physics, Rev. 87, 107A. 3 Auxler, J.A., P.N. Hensley, G.S. Hurst, W.A. Mills, March 1954, )'
"Neutron Flux and Tissue Dose Studies with Fission Threshold Detector." ORNL-1671.
Auxier, J.A., C. Gentry, S.J. Kaplan, C.M. Rogers, November 1954 "Some Effects of Cumulative Doses of X-Radiation Upon Learning and Retention in the Rhesus Monkey," A.F. School of a Aviation Project 21-3501-0003, Report No. 11, MP-5511. Auxier, J.A., W. Blakely, 1954, "A constant Air Monitor for Alpha Emitting Isotopes," A.F. School of Aviation Project
- 21-3501-0003, Report No. 7.
i
- Auxier, J.A., June 1955, "A High Level Co-60 Irradiation j Facility," A.F. School of Aviation Med. Report AF SAM 55-40.
- Auxier, J.A., G.S. Hurst, June 25-27, 1956, "A Fast Neutron j Insensitive Gamma Dosimeter," Proceedinas of the Health
! Physics society Annual Meetina. Ann Arbor, Michigan, pp. 3-7. Auxier, J.A., G.S. Hurst, R.E. Zedler, "Neutron Insensiti.ve Beta Gamma Dosimeter." U.S. Patent No. 2,974,248. l Auxier, J.A., H.E. Gilbert, T.D. Strickler, "Fast Neutron Scattering from Thick Slabs." Nuclear Science and i Enaineerina 3:11-18. I i Auxier, J.A., G.S. Hurst, R.E. Zedler, 1958, "A Single Ion Detector for Measurcnent of Gamma-Ray Ionization in Cavities," Egalth Physics 1:21-26. Auxier, J.A., "Evaluation of Residential Structures for Shielding ! Against Fallout Radiation," Effects of Nuclear War Hearings l Before the Special Subcommittee on Radiation of the Joint i Committee on Atomic Energy, Congtess of the United States, l pp. 148-151. 1 l Auxier, J.A., J.O. Buchanan, C. Eisenhauer, H.E. Henker, j "Experimental Evaluation of the Radiation Protection i Afforded by Residential Structures Against Distributed l Sources." Atomic Energy Commission, CEX-58.1. I i l l l 1 I i
. JORN A. AUXIER Page 6 Auxier, J.A., R.D dirkhoff, W.D. Dillow, "A Study of Cavity Ionization as a Function of Atomic Number by Use of a Miniature Counter," ORNL-2724 (Master's Thesis - Vanderbilt). Auxler, J.A., G.S. Hurst, "Application of Radiation Dosimetry Studies to the Evaluation of Environmental and Biological Consequences of Nuclear War." Rigloaical and Environmental Effects of Nuclear War. Hearings Before the Special Committee on Atomic Energy, Congress of the United States, pp. 140-147. Auxier, J.A., A.D. Callihan, G.S. Hurst, X.Z. Morgan, R.H. Ritchie, P.W. Reinhardt, F.W. Sanders, E.G. Wagner, "Dosimetric Investigation of ti.e Radiation Accident," Vinca, Yugoslavia, IAEA T0/HS/22, pp. 25-46. Sanders, F.W., J.A. Auxier, J.S. Cheka, 1960, "A Simple Method of Minimizing the Energy Dependence of Pocket Ionization Chambers," Health Physics 2:308-309. Auxier, J.A., T.D. Strickler, "Experimental Evaluation of the Radiation Protection Afforded by Typical Oak Ridge Homes Against Distributed Sources." Atomic Energy Commission, CEX-59.13. Auxler, J. A. , 1961, "Dosimetric Considerations in Criticality Exposure," Diaanosis and Treatment of Acute Radiation Iniury, World Health organization, Geneva, pp. 141-150. Auxier, J.A., C.H. Bernard, W.T. Thornton, 1961, "Silver Metaphosphate Glass for Gamma-Ray Measurements in Co-Existent Neutron and Gamma-Radiation Fields," Selected Tonics in Radiation Dosimetry, IAEA, Vienna, pp. 503-510. Bernard, C.H., W.T. Thornton, J.A. Auxler, 1961, Silver Metaphosphate Glass for X-Ray tcasurements in Coexistent Neutron and Gamma-Radiation Fields," Health Physics 4:236-243. Hurst, G.S., R.H. Ritchie, F.W. Sanders, P.W. Reinhardt, J.A. Auxier, E.B. Wagner, A.D. Callihan, K.Z. Morgan, 1961, "Dosimetric Investigation of the Yugoslav Radiation Accident," Health Physics 5:179-202. Auxier, J.A., F.W. Sanders, P.N. Hensley, 1961, "A Dovice for Determining the orientation of Persons Exposed to Neutron and/or Gamma-Radiation," Health Physics 5:226-227.
JOHN A. AUXIER 3 Page 7 " 24 Auxier, J.A., F.W. Sanders, W.S. Snyder, "Na Activation in the Dosimetry of Nuclear Accidents," Radioactivity in Man, l G.R. Meneely, Editor, Charles C. Thomas, Publisher, Springfield, Illinois, pp. 201-211. Auxier, J. A. , W.T. Thornton, "Some X-Ray and Fast Neutron Response Characteristics of Silver Metaphosphate Glass Dosimeters." ORNL-2912 (Master's Thesis - Vanderbilt). l Auxier, J.A., J.S. Cheka, F.W. Sanders, March 1961, "Attenuation of Weapons Radiation - Application to Japanese Houses - Operation Hardtack, Phase II, Program 39, Projects 39.1, ! 39.2," WT-1725. l Auxier, J.A., J.S. Cheka, F.F. Haywood, F.W. Sanders, f J.H. Thorngate "Technical Concept - Operation BREN." Atomic t
- Energy Commission, CEX-62.01.
I Auxier, J.A., A.D. Callihan, G.S. Hurst, K.Z. Morgan, P.W. Reinhardt, R.H. Ritchie, F.W. Sanders, E.B. Wagner, "Dosimetry," The Vinca Dosimetry Experiment, IAEA Technical Report 6, pp. 25-43. Sanders, F.W., J.A. Auxier, 1962, "Neutron Activation of Sodium i in Anthropomorphous Phantoms," Health Physics 8:371-379. 1 Auxier, J.A., "Dosimetry and Exposures in Nuclear Accidents," r
- Nuclear Safety, 4
- 111-112.
1 i Auxier, J.A., L.W. Gilley, F.F. Haywood, "General Correlative { Studies, Operation BREN," Atomic Energy Commission, .
- CEX-62.03. !
\ i Auxier, J.A., "Ichiban The Dosimetry Program for Nuclear Bomb r I Survivors of Hiroshima and Nagasaki - A Status Report as of l April 1, 1964," Atomic Energy Commission, CEX-64.3. j ) Auxier, J.A., F.F. Haywood, E.T. Loy, "An Experimental j Investigation of the Spatial Distribution of Dose in an j Air-Over Ground Geometry," Atomic Energy Commission, ! CEX-62.14. Auxier, J . A. , G.A. Andrews, C.C. Lushbaugh, "The Importance of Dosimetry to the Medical Management of Persons Accidentally
- Exposed to High Levels of Radiation," Personnel Desimetry j for Radiation Accidents, IAEA, Vienna, pp. 3-16.
.l i Auxier, J.A., 1965, "The Health Physics Research Reactor." I i Health Physics, 11:89-93. I i i ! l i
- _ . . - . - . __ _ _ _ . _ _ . _ - . - ..-_.-_. -. - . ~ --. _ - _ . _ _
I JOHN A. AUXIER Page 8 Auxier, J.A., "Nuclear Accident at Wood River Junction," Nuclear Safety, 6:298-301. J Auxier, J.A., F.F. Haywood, "Technical Concept-Operation HENRE," Atomic Enerqy Commission, CEX-65.02. Auxler, J.A., F.F. Haywood, T.G. Provenzano, "Operation Plan-Operation HENRE," Atomic Energy Commission, CEX-65.03. Auxier, J.A., "Ichibant The Dosimetry Program for Nuclear Bomb 1 Survivors of Hiroshima and Nagasaki," Proceedings of the SynDosium on Protective Structures for Civilian Poculations. NAS-NRC, Washington, pp. 121-126.
! Auxier, J.A., J.S. Cheka, F.F. Haywood, T.D. Jones, i J.H. Thorngate, 1966, "Free-Field Radiation Dose Distributions from the Hiroshima and Nagasaki Bombings,"
Health Physics 12:425-429. i Auxier, J.A., R.T. Boughner, M.D. Brown, T.D. Jones, W.D. Snyder, i
"Distribution of Dose and Dose Equivalent in an Anthromorphic Phantom Resulting from Broad-Beam Sources of
. Monoenergetic Neutrons," Transactions of American Nuclear Society 9:357. j Auxier, J.A., R.T. Boughner, M.D. Brown, T.D. Jones, W S. Snyder, j November 1966, "Distribution of Dose and Dose Eg , valent in j an Anthropomorphic Phantom Resulting from Broad Beam Sources i of Monoenergetic Neutrons," Proceedinos of_ Conference on
! Radiation TransDort and Biolocical Effects, CONF-661125, pp. 25-45.
I l Auxier, J.A., "Dosimetry and Exposures in Nuclear Accidents," Nuclear Safety 8:382-385. i i Auxier, J.A., 1967, Multilaboratory Intercomparisons of Neutron j Dosimetry Systems," Neutron Monitoring, IAEA, Vienna, pp. 625-630. Auxier, J.A., "Physical Problems of Dosimetry of Neutrons and Protons. Accidental Irradiation at Place of Work," EURATOM, } S. A. Vaillant-Carmannge, Liege, Belgium, pp. 181-194. ] l Auxier, J.A., "Special Methods in Radiation Dosimetry," l Prir,4 gles of Radiation Dosiretry, K.Z. Morgan and J.E. ar, Editors, John Wiley and Sons, Inc., New York, ! Chapts. ,, pp. 215-241. l I
JOHN A. AUXIER Page 9 Auxior, J.A., F.F. Haywood, S. Holf, J.H. Thorngato, "Energy and Angular Distribution of Neutrons and Gamma Rays - Operation BREN," Atomic Energy Commission, CEX-62.12 Auxier, J.A., Erpceedinast Lona-Rance Biomedical and Psychosocial Effects.of Nuc1 car War, Volume 1, First Interdisciplinary Conference, Defense Nuclear Agency, DASIAC Special Report 67. Auxier, J. A. , 1967, "Radiation Propagation and Shiolding Experiments at the BREN Tower," Trans American Nuclear Society 101726. Auxior, J.A., K. Becker, E.M. Robinson (Editors), September 23-26, 1968, proceedinas of the Second International Conference on Luminescence Dosimetry, Gatlinburg, Tennessee, CONF-680920, 1021 pages. Auxior, J . A. , M. D. Brown, 1966, "Neutron Crois-Scctions and Reaction Products for H, C, N, and O for the Energy Range from Thornal to 15 MoV," Proceedinas of the First International _Conaress of Radiation Proter, tion, Pergamon Press, New York, Volume 2, pp. 853-858. Auxior, J. A. , T. D. Jones, W.S. Snyder, "Neutron Interactions and Penetration in Tissue," Radiation Dosimetry, F.H. Attix and W.C. Roesch, Editors, Academic Press, New York, Chaptor 6, pp. 275-316. Auxier, J. A. , T.D. Jones, D.R. Johnson, J.W. Poston, September 5-10, 1966, "Doco Distribution Functions for Neutrons and Gamma-Rays in Anthropomorphous and Radiological Phantoms," Proceedinas of the First IntSrnational Concrer.s of Radiatign Protection, Rome, Italy, Pergamon Press, Volume 2, pp. 1461-1467. Auxier, J.A., Thorngate, J.H., "Fast Neutron Spectrometry for Radioprotection," gr11ocue d'Elgetronique Nuc1caire et Radioprotection, Tome 1, University of Toulouse, Volume 1 of 4, (27 pagos). Auxier, J.A., 1969, "Kerna Versus First Collision Dose: The Other Side of the Controversy," Health Physics 17:342-343. Auxier, J.A., K. Becker, "Progress in Luminescence Dosimetry," Epience 164t974-978. Auxier, J.A., "Multi-Laboratory Intercomparisons and Standardizations: Nuclear Accident Dosimetry Systems IAEA, Vienna, IAEA-PL-329/13, pp. 153-164.
. - . . _. . _ . -_. =. _ . _ - - _ _ _ _.
l JORN A. AUXIER Page 10 Auxier, J. A. , H.H. Hubbell, Jr. , T.D. Jones, November 11-14, 1969, "Review of Depth-Dose Calculation and
. Experimentation," Proceedinos of the Symoosium on Neutrana ' ) in Radiobioloav, Oak Ridge, Tennessee, CONF-691106, pp. 73-94. j i Auxier, J.A., K. Fukushima, S. Fujita, T. Ichimaru, S. Jablon,
{ November 11-14, 1969, "REB or Neutrons in Japanese
] Survivors," Proceedinas of the Syroosium on Neutrons in Radiobioloov, Oak Ridge, Tennessee, CONF-691106, pp. 547-579.
k Johnson, D.R., J.W. Poston, J.A. Auxier, D.G. Brown, W.A. Gramly, W.D. Gibbs, } .D. Hodges, D.R. Davy, "' Total' and
' Exchangeable' Sodium Studies in Swine and Sheep Using l Activation Analysis and Izatopic Dilution," Health Physics ! 18t729-731.
Auxier, J.A., "The Outcry Cver Exposure Guidelines," Englgar Safety 2:456-460. Jones, T.D. , J. A. Auxier, 1971, "Neutron Dose, Dose Equivalent, an6 Linear Energy Transfer from 252-Cf Sources," Health ] Physics 20:252-258. Auxier, J.A., K. Becker, E.M. Robinson, D.R. Johnson, e R.H. Boyett, C.H. Abner, 1971, "A New Radon Progeny d Personnel Dosimeter," Health Physics 21:126-128. Auxier, J.A., B.G. Auxier, 1971, "Review of the Story of Radioactivity," Health Phys (q3 21:129. ! Jones, T.D. , W.S. Snyder, J. A. Auxier, 1971, "Absorbed Dose, Dose j Equivalent, and LET Distributions in Cylindrical Phantoms .1 Irradiated by a Co111 mated Beam of Moncenergetic Neutrons," ] Health Physics 21:252-272. l Brown, D.G., D.F. Johnson, J. A. Auxier, 1971, "Unilateral and i Bilateral Exposure of Swine to Fission Neutrons," Health Physics 21:537-545. I Auxier, J.A., 1971, "Review of Personnel Dosinetry Systems _ int j External Radiation Exoosure, IAEA Technical Report No. 109," Health Physics 213613. i Auxler, J. A. , F.F. Haywood, "Unusual and Unexpected Radiation j Sources," Safety Newsletter of the National Safety Council. Auxier, J.A., J.H. Thorngate, "Advances in Dosimetric Instrumentation," American Nuclear Society TransactioDa,
- 14
- 408-409.
i 4 l 3
JOHN A. AUXIER Page 11 Auxier, J . A. , Z.G. Burson, R.L. French, F.F. Haywood, L.G. Mooney, E.A. Straker, "Nuclear Weapons Free-Field Environment Recommended for Initial Radiation Shielding calculators," ORNL-TM-3396. Auxier, J. A. , T.D. Jones, "Local Dose from Neutron Produced Recoil Ions in the Region of a Therapeutic 252-Cf Needle," Radioloov 104:187-189. Turner, J.E. , J. A. Auxier, 1972, "Symposium on Radiation Standards and Regulations," Health Physics 23:445-446. Auxier, J. A. , "Concluding Summary," Neutron Monitorina for Radiation Purposes, IAEA, Vienna, pp. 495-498. Auxier, J. A. , "Developments in Neutron Dosimetry for Radiation Protection," Neutron Monitorina for Radiation Protection Pu rposes , IAEA, Vienna, IAEA-SM-167/26, Volume 1, pp.3-12. Auxier, J. A. , R.O. Chester (Editors), 1972, "Report of the Clinch Valley Study, May 15-June 2, 1972." ORNL-4835. Auxier, J. A. , D.J. Christian, T.D. Jones, G.D. Kerr, P.T. Perdue, W.H. Shinpaugh, J.H. Thorngate, "Contribution of Natural Terrestrial sources to the Total Radiation Dose to Man." ORNL-TM-4323 (Ph.D. Thesis - Georgia Tech.). Jones, T.D. , J. A. Auxier, W.S. Snyder, G.G. Warner, 1973, "Dose to Standard Reference Man from External Sources of Honoenergetic Photons," Health Physics 24:241-255. Perdue, P.T., W.H. Shinpaugh, J.H. Thorngate, J.A. Auxier, 1974, "A Convenient Counter for Measuring Alpha Activity of Smear and Air Samples," Health Physics 26:114-116. Auxier, J. A. , W.H. Shinpaugh, G.D. Farr, D.J. Christian, 1974, "Preliminary Studies of the Effects of Sealants on Radon Emanation from Concrete," Health Physics 273789-391. Auxier, J. A. , P.T. Perdue, W.H. Shinpaugh, J.H. Thorngate, Determination of Radon in Air, U.S. Patent No. 3,805,070. Jones, T.D. , J. A. Auxier, J.S. Cheka, G.D. Kerr, 1975, "In Vivo Dose F.stimates for A-Bomb Survivors Shielded by Typical Japanese Houses," Health Physics 28:367-381. Auxier, J. A. , 1976, "Respiratory Exposure in Buildings Due to Radon Progeny," Health Physics 31:119-125.
JOHN A. AUXIER Page 12 Auxier, J.A., "Physical Dose Estimates for A-Bomb Survivors - Studies at Oak Ridge, U.S.A.," Journal of Radiation Research 11, Supplement:1-11. Auxier, J.A., 1976, "Studies Directed Toward the Spatial Resolution of the Distribution of Plutonium in Bono," Health Effects of Plutonium and Radium, Webster, S.S. Jee (Ed.), The J.W. Press, Salt Iake City. Auxier, J.A., 1976, Ichibant Radiation Dosimetry for the i Survivors of the Bombinas of Hiroshima and Naaasaki, ERDA l Prestige Series. l t Auxier, J.A., 1977, "Need for Improved Standards in Neutron l Personnel Dosimetry," National Bureau of Standards Special ; Publication 493, Proceedings ?f the International # Specialists Symposium on Neutron Standards and Applications, i held at the National Bureau of Standards, Gaithersburg, MD, , March 28-31, 1977. , Auxier, J.A., 1977, "Radiation Safety," Twenty-Fourth National Conference on Camous Safety, Monograph No. 39, Safety Monographs for Schools and Colleges, University of Hawaii at Manoa, Honolulu, Hawaii, June 9-16, 1977, pp. 58-60. Auxier, J. A. , 1977, "The regulatory pendulum, or, a matter of : common sense...," American Industrial Hvaiene Association j Journal (38), 12/77. , Auxier, J.A., 1977, "Brief Synopsis of Symposium," IAEA ; International Symoosium on National and International Standardization in Radiation Dosimetry, Atlanta, GA, December 5-9, 1977. Auxier, J.A., 1978, "A Brief Synopsis of the Symposium," National and International Standardization of Radiation Dosimetry, Volume II, IAEA, Vienna. Auxler, J.A., C.D. Berger, C.M. Eisenhauer, T.F. Gesell, A.R. Jones, M.E. Masterson, October 1, 1979, "Report of the Task Group on Health Physics and Dosimetry," Presidents commission on the Accident at Three Mile Island. Jones, T.D., D.G. Jacobs, J.A. Auxier, G.D. Kerr, 1979, "Risk of Cancer Based on Promotion from Cytotoxicity," EE2Seedinas of a Conference on Neutrons from Electron Medical Accelerators (H.T. Heaton, II and R. Jones, Eds.) NBS Special Publication 554.
JOHN A. AUXIER Page 13 Eichholz, G.G., J.W. Poston, M.F. Fair, J.A. Auxier, May 1980, "Cost-Benefit Effects of Conversion to SI Units in Hecith Physics," Oak Ridge National Laboratory, NUREG/CR 1419; ORNL/NUREG-68. Auxier, J.A., W.F. Ohnesorge, June 1980, "Gamma Exposure Rates Due to Neutron Activation of soil Site of F. cod Detonation, Operation Plumbbob," Oak Ridge National Laboratory, ORN L/TM-7 4 06. Auxier, J.A., K. Z. Morgan, 1983, "Radiation, Ionising: Detectors and Portable Survey Instruments," EncycloDedia of OccuDational Health and Safety, Volume II, ILO, Geneva, 1983. Auxier, J.A., H.W. Dickson, 1983, "Guest Editorial: Concern Over Recent Use of the ALARA Philosophy," Health Physics 44:595-600. Auxier, J.A., "The Windscale Accident," AMA Radiation Conference, Washington, D.C., November 19, 1986, in press.
1 D ATTACHMENT 2 s CURRICULUM VITAE JACOB 1. FABRIKANT Birth February 9, 1928 U.S.A. Educetion 1948-52 McGill University, Montreal Faculty of Arts and Science B.Sc. (magna cum laude; Chemistry) 1952-56 McGill University, Montreal Faculty of Medicine M.D., C.M. 1961-64 University of London, England Faculty of Science Ph.D. (Biophysics) 1978 American College of Radiology F. A.C.R. (Fellov, Radiology) Academic Appointeents 1956-57 Duke University Hospital and School of Medicine, Durham Intern in Surgery 1957 Duke University Hospital and School of Medicine Assistant in Pathology 1957-56 Duke University Hospital and School of Medicine Fellov in Surgery 1958-61 The Johns Hopkins Hospital, Baltimore Resident in Radiology 1958-61 The Johns Hopkins Hospital. School of Medicine, Baltimore Fellov in Radiology 1961-64 Department of Physics Institute of Cancer Reseerth Advanced Fellov in Academic University of London, England Radiology of the James Picker Foundation, National Academy ot Sciences-National Research Council 1964-65 The Johns Hopkins University School of Medicine and School Advanced Fellov in Academic of Hygiene and Public Health. Radiology of the James Picker Baltimore Foundation, National Academy of Sciences-National Research Council 1964-68 The Johns Hopkins University School of Medicine Assistant Professor of Radiology 1964-70 The Johns Hopkins Hospital Radiologist 1965-68 The Johns Hopkin: University School of Hygiene and Public Assistant Professor of Health Radiological Science
s i* Page 2 . 1 1968-70 The Johns Hopkins University J School of Medicine Associate Professor of Radiology
' 1969-70 The Johns Hopkins University School of Hygiene and Public Associate Professor of !
Health Radiological Science i 1970-75 The University of Connecticut School of Medicine, Farmington Professor and Head i Department of Radiology 1973-75 The Royal Society I London, England Special Consultant for the !
- Advisory Committee on the l Biological Effects of Ionizing ,
- Radiations, National Academy of ;
, Sciences-National Research Council 1973-75 Royal Postgraduate i Medical Schreol Picker Sabbatical Study Year ' University of London, England James Picker Toundation ! National Acaddemy of Sciences-National Research Council 1973-75 Royal Postgraduate Medical School Visiting Colleague i University of London, England Department of Diagnostic Radiology ; } j 1973-75 Hammersmith Hospital Royal Postgraduate Honorary Consultant Radiologist Department of Diagnostic Radiology ! Medical School, London, England 1975-78 McGill University I Faculty of Medicine Professor of Diagnestic Radiology l Montreal, Canada Department of Diagnostic Radiology 1975-78 The Montreal General Hospita) j Montreal, Canada Diagnostic Radiologist-in-Chief ! Department of Diagnostic Radiology ! 1976-78 l McGill University ! i Taculty of Medicine Professor and Chairman Department of Diagnostic Radiology i
! Diagnostic Radiologist-in-Chief l 1978- University of California
- Professor of Radiology t i San Francisco School of Medicine i f
! 1978-80 University of California,
- Scientist j
Burkeley, Donner Laboratory 1 Invrence Berkeley Laboratory [ .' 1979 ltesident's Commission on the Director l Ac:Ident at Three Mile Island, The White House, Vashington, D.C. Public Health and Safety ! { 3 1 i I k , r I a
, Paga 3 1980- University of California Senior Scientist Berkeley, Donner Laboratory Lavrence Berkele.y Laboratory 1980- University of California Professor of Radiology Berkeley Graduate Group in Biophysics Departrent of Biophysics and Medical Physics Academic and Professional Organizations American College of Radiology,1972- Member, 1972-78: Fellov, 1978-Society of Chairmen of Academic Radiology Departments, Member, 1970-75: 1976-78 Association of University Radiologists, Member, 1967-British Institute of Radiology, Member, 1961-Society of Nuclear Medicine, Member, The Academic Council, 1970-76 Canadian Association of Radiologists, Member, 1975-80 Committee on Basic Research, Member, 1975-78 The New England Roentgen Ray Society, Member, 1972-78 Radiological Society of Connecticut, Member, 1971-75 Radiation Research Society. Member, 1965-Councillor in Medicine, 1973-76 Association for Radiation Research (U.K.), Member, 1964-American Association for the Advancement of Science, Member, 1966-75 New York Academy of Selences, Member, 1958-70 American Institute of Biological Science, Member, 1968-75 The Johns Hopkins Medical and Surgical Association, Member, 1965 Connecticut State Medical Society, Member, 1971-75 Maryland Medical and Chirurgical Society, Member, 1958-70 Society of Sigma XI, Member, 1971-Cell Kinetics Society, Member, 1978-Alpha Omega Alpha Monorary Medical Society, Member, 1955-Nu Sigma Nu Medical Fraternity, Member, 1953-Academic H,onors Alpha Omega Alpha Honorary Medical Society, McGill University Faculty of Medicine, Montreal, 1955 Vood Gold Medal, McGill University Faculty of Medicine, Montreal 1956 Advanced Fellov in Academic Radiology of the James Picker Foundation, National Academy of Sciences-National Research Council 1961-65 Special Consultant, Committee on the Biological Ef fects of Ionizing Radiations.
National London, England, Academy1973-75 of Sciences-National Research Council The Royal Society, Picker Sabbatical Study Year Award of the James Picker Foundation, National Academy of Sciences-National Research Council, 1973-75 Visiting Colleague in Diagnostic Radiology, Royal Postgraduate Medical School, London, England, 1973-75 Fellov of the American College of Radiology (F.A.C.R.), Elected. 1978 Member of the Royal Society of Medicine, Great Britain, Elected. 1984 Distinguished Visiting Lecturer in Radiation Biology and Protection, TN0 Radiobiological Institute, Rijsvijk, The Netherlands, 1988
Page 4 Extramural Research and Education Reviev Committees National Academy of Sciences-National Research Ceuncil, Division of Medical Sciences, Committee on Radiology, Member, 1967-74 U.S. Atomic Energy Commission, Division of Biology and Medicine, Consultant, 1968-75 National Science 1970 Foundation, Division of Developmental Biology, consultant, State of Connecticut, Commission on Higher Education, Standing Committee on Accreditation, Connecticut Council on Higher Education, Consultant, 1971-73 Connecticut Caneer Epidemiological Program, Planning Committee, Member. Secretary, 1412-73 American Cancer 1972-73 Society, Connecticut Division, Board of Directors, Member, U.S. Energy Research and Development Agency Consultant, 1975-76 National Academy~~of Selences-National Research Council Scientific Advisory Committees ~ Committee on Radiology, Division of Medical Sciences. Assembly of Life Sciences. National Academy of Sciences-National Research Council, Member, 1967-74 Committee on the Biological Effects of Ionizing Radiations (BEIR 1), Division of Medical Sciences, Assembly of Life Sciences, National Academy of Sciences-National Research Council, Member, 1969-72: Subcommittee on Somatic Effects, Member, 1969-72 Committee on the Biological Effects of Ionising Radiations (BEIR II), Division of Medical Sciences. Assembly of Life Sciences, National Academy of Sciences-National Research Council, Member and Vice Chairman, 1973-77 Subcommittee on Medical Radiation, Chairman, 1973-77 Cosmittee on the Biological Effects of Ionizing Radiations (BEIR !!!), Division of Medical Sciences, Assembly of Life Sciences National Academy of Sciences-National Research Council, Member, 1977-80: Subcommittee on Somatic Effects, Member, 1977-80: Ad hoc Subcommittee (Subcommittee on Somatic Effects), Chairman, 1979-80 Committee on Federal Research on the Biological and Health Effects of Iontring Radiatian, Division of Medical Sciences, Assembly of Life Sciences. National Academy of Sciences-National Research Council, Consultant, 1980-81 Board of Radioactive Vaste Management, National Academy of EnEineering, National Research Council, Consultaat 1981-82 Committee to Reviev the Portsmouth Naval Shipyard Cytogenetics Protocol, Division of Medical Sciences, Commission on Life Sciences, National Acadery of Sciences-National Research Council Member, 1982
- Fage 5 Oversight Committee on the Radioepidemiologic Tables, Division of Medical Sciences. Commission on Life Sciences, National Academy of Sciences-National Research Council, Member, 1983-85 Board on Radiation Effects Research, Commission on Life Sciences, National Academy of Sciences-National Research Council, Member, 1983- ;
Committee on the Biological Effects of lonizing Radiations (BEIR IV), Board of Radiation Effects Research, Commission on Life Sciences, National Academy of Sciences-National Research Council, Member and Chairman, 1985-87 Committee on the Biological Effects of Ionizing Radiations (BEIR V), Board of Radiation Effects Research, National Academy of Sciences-National Research Council, Member, 1986 Additional National and International Scientific Advisory Committees commission on Radiation and Infection, Armed Forces Epidemiological Board, Department of the Army, Liason Member, 1965-66 X-Ray Image Production and Related Facilities Advisory Committee Bureau of Radiological Health. Department of Health, Eduation and Velfare. United States Public Health Service, Member, 1968-69 Medical Radiation Advisory Committee, Bureau of Radiological Health Food and Drug Administration, Department of Health, Education and Velf are, United States Public Health Service, Member, 1969-74 Long-Tern Radiation Effects Advisory Committee Bureau of Radiological Health. Food and Drug Administration Department of Health, Education and Velfare, United $tttes Public Health Service, Member, 1969-74 Neurology Study Section, National Institutes of Health. Department of Hes.th. Education and Velfare, United States Public Health Service. Member, 1969-72 Committee on Genetic and Carcinogenic Effects. Division of Radiotherap+utic Research, Commission on Radiation Therapy American College of Radiology. Member, 1972-76 Committee on Medisal Uses of Radiation and Radiation Exposure cf Fatients, National Radiological Protection Board, creat Britain, Member, 1974-75 Associate Committee on Scientific Criteria for Environmental Quality, Subccamittee on Physical Erergy, National Research Council, Canada. Member. 1976 78 Come!'. tee on Radiation Risks to Space Verkers (Satellite Pover Systems). National Aeronautics and Space Administration. Herber, 1979 81 Committee on Federal Research into the Biological and Health Effects of Iontring Radiation, National Institutes of Health, Department of Health. Education and Valfare, United States Public Health Service, Neeber, 1975-80
. Page 6 President's Director of Public Health and Safety, 1979 Commission on the Acciden International Effects, Member, 1980-Commission on Radiological Protection, Committee 1 on Ra l Safety Advisory Board, Three Mile Island Unit-2, Member,1981- Radiation !
Hazards Panel, Member,1981 , canirman,1985- ' Committee on Radiological Health Effsets Model Nuclear Regulstory Commission Harvard 1982-87 University School of fublic Health. Advisory Committee Member, t National Council on Radiation Protection and Measurements, Member,1985-Cor.mittee American College of Radiology, Member, 1985-on Biologletl and Healti l Committee Americanon Radiologic College Units, Member, of Radiology, Standards and Protection. Commission on Physic! 1985-Committee t Subpanelon on Interagency Radiation Research and Policy Coordination, Science Pre-Disaster Planning for Human Health Effects Research, ! Consul tan t , 198 7- ' i University Research and Education Reviev Committees ! The Johns 1966-70 Hopkins Medical Institutions, Radiation Control Committee, Member. TheCoesittee, UniversityChairman. of Connecticut 1970-73Health Sciences Center, Radiation Control i McGill University, University Senate, Senator, 1976-78 McGill i The Graduate Council. Councillor. 1975-78 University. Taculty of Graduate Stu McGill University. Faculty of Medicine, Postgraduate Training Conittee. Member. 1375-78 McGill University. Postgraduate Training Committee. Program1976-78 1.avrence Director, Faculty of Medicin Drug Research Consittee, Member,1979-Berkeley1 Chairman, 1981-86 1.aboratory, Univers University of California, Berkeley, Committee on the Protection of Huran Subjects, M.eber,1983-Visitint Professorships ap Lectureships Bovman Visiting Gray School of Medicine, Visiting Professor of Radiology 1968 Hospital. Clinical Canter Program. 1969 Professor of Oncolor/ Georgetov Aretican Institute of Biological Sciences, Visiting Radiation Biologist, 1969-75
--,P J .
Fago 7 1 . ; i University of Minnesota School of Medicine and Hospitals, Villiam O'Brien l
) Professor of Radiation Science, 1970 i
University of Vermont College of Medicine, Visiting Professor of Radiology, 1970, 1977, 1978 i L.H. Gray Laboratory, Cancer Research Campaign Mt. Vernon Hospital England, Visiting Scientist, 1971
) Cambridge University Medical School, Addenbrooke's Hospital, Cambridge, J
England Visiting Lecturer, 1971 University of South Florida College of Medicine, Visiting Frofessor of ) j
- Radiology, 1973 i
d University 1977 of Montreal Faculty of Medicine, Visiting Professor of Radiology, ) [ i j Oxford University Medical School, The Radcliffe Infirmary, Oxford, England. ' Visiting Lecturer, 1979, 1980, 1981 University of London Institute of cancer Research, London, England, Visiting Lecturer, 1979, 1981 i Royal Postgraduate Medical School, Hammersmith Hospital, London, England, i d Visting Lecturer, 1959 ) National Radiological Protection Board Harve11 England, Visiting Scientist, ! L l 1979, 1981 1 Middlesex Hospital Medical School, Department of Radiotherapy and Oncology, Visiting Lecturer, 1981 Brown University Division of Biology and Medicine, Providence, Visiting j l Professor of Radiation Medicine, 1979, 1980, 1981, 1982, 1983, 1984, 1985, i 1987 j i Valter H. Herbst Memorial Symposium, Invited Lecturer, University of California i l San Francisco School of Medicine, 1981 Tartu University Faculty of Medicine, Tartu, Estania, U.S.S.R., Visiting 1 l Lecturer, 1984 Estor.lan Academy of Sciences, Tallin, Estonia, U.S.S.R., Visiting Lecturer in [ i ' Physics, 1984 [ University of California, Graduate School of Business Administration, The Berkeley Business School, Executive Program. Faculty, 1985, 1986, 1987, 1988 Shanghai Medical University, Institute of Radiation Medicine, Shanghai, China, i Visiting Professor, 1986 j i Academy of Military Medical Sciences, Institute of Radiation Medicine, Beijing, i i China, Visiting Frofessor, 1986 ! j rarolinska Institute, Departrents of Hecatology and Radiological Frotection and j i Neurosurgery, Stockholm, Vist.ing Lecturer, 1987 University of Usea Faculty of Medicine, Umea, Sweden, Visiting Le turer, 1987 l University of U University Academic Hospital, Departt at of [ Neurosurgery,ppsala, Visiting Lecturer, 1987 ( Svedish Agricultural University, Department of Radioecology, Visiting Lecturer, f 1987 j TNO Radiobiological Institute, Rijsvijk The Netherlands, Distinguised Visiting I l Lecturer in Radiation Biology and Protection, 1988 i ! t t k
. Page 8 Scientific Journal Reviev cell and Tissue Kinetics, 1968- ; Member, Editorial Board, 1972-85 Investigative Radiology, 1973- ; Member, Editorial Board, 1973-76 Journal of the Canadian Association of Radiologists, 1976-78; Member, Editorial Board, 1976-78 McGill Medical 1954-55; Journal, Editor, Member, Editorial Board, 1952-56; Managing Editor, 1955-56 i Cancer Research, 1968-Science, 1970 ' Biology of Reproduction, 1970-Medicine, 1970-Bioscience, 1970-Cancer, 1971-Radiation Research, 1972-International Journal of Applied Radiation and Isotopes, 1973-New England Journal of Medicine, 1982-International Journal of Radiation Oncology Biology Physics,1987-Hospital Appointments 1964-70 The Johns Hopkins Hospital Radiologist Baltimore, Maryland 1970-73 University of Connecticut Hospital liead, Department of Radiology Hartford, Connecticut 1973-75 University of Connecticut Hospital Attending Radiologist Hartford, Connecticut 1970-73 Veterans Administration Hospital Acting Chief, Department of Nevington, Connecticut Radiology Consultant in Radiology 1971-75 New Britain General Hospital Consultant in Radiology New Britain, Connecticut 1971-75 Villiam V. Backus Hospital Consultant in Radiology Norwich, Connecticut 1972-75 Mount Sinal Hospital Consultant in Radiology Hartford, Connecticut 1973-75 Hammersnith Hospital Honorary Consultant Radiologist London, England Department of Diagnostic Radiology 1975-78 The Montreal General Hospital Diagnostic Radiologist-in-Chief Montreal, Canada Department of Diagnostic Radiology 1975-78 The Montreal General Hospital Director, Department of Montreal, Canada Diagnostic Radiology 1978- Covell Memorial Hospital present Physician University of California, Berkeley
{ 1978- University of California Medical
- present Center, San Francisco Radiologist, Cllnical Faculty L ,
I
\ .
Page 9 Certification 1962 American Board of Radiology Medical Licensure 1957 1958 National MarylandBoard of Medical Examiners (No. 36999) (No. D1511) 1971 Connecticut (No. 14808) 1973-75 Great Britain 1976-78 Quebec, Canada (No. 76-033) 1978 California (No. G 36656) Military Service United States Navy, Vorld Var II, Veteran Marital _ Status Irene B. Fabrikant, Vife B.Sc. (McGill University) M.Sc. (McGill University, Bacteriology and Immunology) Ph.D. (University of Maryland, Microbiology) 1966-70 Instructor, Department of .-icrobiology University of Maryland Schu si of h'edicine 1970-75 Assistant Professor of Medicine, Department of Medicine The University of Connecticut School of Medicine 1973-75 Honorary Research Fellov (Immunology) Department of Zoology and Comparative Anatomy University College,. London, England 1975-78 Assistant Professor, Department of Microbiology & Immunology Faculty of Medicine, McGill University, Montreal 1977-78 Executive Secretary, McGill University Biohazards Committee McGill University, Montreal 1978-79 Research Fellow, U.S. Public Health Service, DHEV Center for Disease Control, San Juan Laboratories, Puerto Rico 1979-80 Research Associate, University of California, Berkeley, School of Public Health, Department of Biomedical & Environmental Health Sciences 1981-82 Associate Research Immunologist, University of California School of Medicine, San Francisco, cancer Research Institute 1985- Scientific Consultant, Crosby, Heafey, Roach, and May, , present Oakland, California I l i
. Page 10 BIBLIOGRAPHY
- 1. Fabrikant, 1955, J.I. The Osler Society. (Editorial) McGill Med. J. 24:128, 2.
Fabrikant, J.I. The Dean (Editorial) McGill Med. J. 24:180, 1955, 3. Fabrikant, 24:201-207,J.I. 1955. A concept of the term "anxiety". McGill Med. J. 4. Fabrikant, McGill Med.J.I. J. Pediatric problems 24:114-115, 1955. in clinical practice. (Book Reviev) 5. Anylan, V.G. , Delaughter, G.D. , Jr. , Fabrikant, J.I. , Sullenberger, J.V. and Veaver, V.T. 168:725-729, The management of acute venous thromboembolf sm. JAMA 1958. 6. Anylan, V.G. , Baylin, G.J. , Fabrikant , J.I. and Trumbo, R.B. Stu jics in coronary angiography. Surgery 45:8-18, 1959. 7. Fabrikant, J.I. Colostomy--A short review. II. Quart. 2:23-33, 1959. 8. Sullenberger, J.V. , Veaver, V.T. , Fabrikant, J.I. and Anylan, V.G. A study of the pressor effects of serotonin and its possible role in massive thromboembolism. Surgical Forum 9:127-130, 1959. t 9. Fabrikant, J.I. Reflections on illness. Il Quart. 3:6-8, 1959 10. Fabrikant, J.I. , Anlyan, V.G. , Baylin, G.J. and Trumbo, R.B. A comparison of various techniques arteriography. Surgical for a safe and reliable method of coronary Forum 9:233-237, 1959.
- 11. Fabrikant, J.I., Anlyan, V.G. and Creadick, R.N. The management of radiation 1959.
injuries to the intestines. South. Med. J. 52:1186-1191, 12. Fabrikant, J.I. The ileal bladder. II. Quart. 3: 43-47, 1959.
- 13. Fabrikant, of techniques for visualization of the coronary arteries. Ame Roentgenol., Rad. Therapy and Nuclear Med. 81:764-771, 1959.
14. Fabrikant, J.I. The vet colostomy. II. Quart. 4:1-5, 1959.
- 15. Koehler, P.R.,
Fabrikant, J.I. and Dana E.R. Gastric retention during oral cholecystography due to underlying lesions of the stomach and duodenum. Surg. Gynec. and Obstet. 110:409-412, 1960,
- 16. Fabrikant, J.I., Anlyan, V.G. and Creadick, R.N. Management of intestinal injuries caused by pelvic irradiation. Modern Med. 28:117-118, 1960 .
17. Fabrikant, J.I. An 89:416-418, 1960.improved 11eortomy appliance. AMA Arch. Surg.
t Page 11
)
- 18. Anlyan, V.G., Baylin, G.J., Fabrikant, J.I. and Trumbo, R.B. Studies in coronary arteriography. (In) Year Book of Radiology, Holt, J.F. ,
Whitehouse, V.M. , Jacox, H.V. and Kligerman, M.M. , eds. , pp. 123-125, Year Book Medical, Chicago, 1960.
- 19. Fabrikant, J.I. Specialists at your service: The radiologist. II. Quart.
5:29-32, 1961.
- 20. Fabrikant , J.I. , Richards, G.J. , Jr. , Brack, C.B. and Goodvin, P.N. A vaginal applicator for radium therapy of carcinoma in the vagina.
Radiology 77:987-989, 1961.
- 21. Fabrikant, J.I. , Cockey, T.B. and Goodvin, P.N. A simple pituitary localizer for radiation therapy. Amer. J. Roentgenol., Rad. Therapy and Nuclear Med. 86:649-650, 1961.
- 22. Fabrikant, J.I. Reflections upon illnsss. Nursing News 12:3-5, 1961.
- 23. Fabrikant, J.I. , Anlyan, V.G. , Baylin, G.J. and Isley, J.K. Isotope studies for the evaluation of venous disease of the lover extremity.
J. Nuclear Med. 2:136-148, 1962.
- 24. Koehler, P.R., Fabrikant, J.I. and Dickson, R.J. Observations on the behavior of testicular tumors with comments on racial incidence. J.
Urol. 87:577-579, 1962.
- 25. Fabrikant , J.I. , Richards, G.J. , Jr. , Tucker,, G.F. , Jr. and Dickson, R.J. Contrast laryngography in the evaluation of laryngeal neoplasms.
Amer. J. Roentgenol. , Rad. Therapy and Nuclear Med. 87:822-835, 1962.
- 26. Fabrikant , J.I. , Richards, G.J. , Jr. , Tucker, G.F. , Jr. and Dickson, R .J.
Aid to diagnosis of laryngeal cancer. Modern Hed. 31:212, 1962.
- 27. Fa kant, J.I. Radiological changes in experimental animals fe'41oving administration of bone-seeking radionuclides. (ab) Intern. Congr.
Rh ' tion Res. 2:212, 1962.
- 28. Fabrikant, J.I. Cellular response and cell population kinetics under continuous irradiation. Radiologic changes in bone following irradiation. (In) James Picker Foundation. Annual Report, pp. 23-25, New York, 1962.
- 29. Fabrikant, J.I. and Dickson, R.J. Contrast cinefluorographic studies of the larynx (ub) Intern. Congr. Radiolcgy 10:261, 1962.
- 30. Fabrikant, J.I. and Dickson, R.J. Clinical observations on radiation carcisiogenesis. (ab) Intern. Congr. Radiology 10:243, 1962.
! 31. Fabrikant, J.I. and Smith, C.I..D. Radiological changes in experimental animals following the administration of bone-seeking radionuclides. (In) Radiation Effects in Physics, Chemistry, and Biology, Ebert, M. and Hovard, A. , eds. , p. 472, North-Holland, Amsterdam,1963.
. Page 12 32. Fabrikant, Research:J.I. Regenerating liver (In) Report of the Institute of Cancer Royal Cancer Hospital, Annual Report, p. 122, London, 1963.
- 33. Fabrikant, J.I. , Richards, G.J. , Jr. , Brack, C.B. and Goodvin, P.N.
Vaginal applicator for radium therapy of carcinoma in vagina. (In) Year Book of Radiology, Holt, J.F., Vhitehouse, V.M., Jacox, H.V. and Kligerman, M.M. , eds. , p. 315, Year Book Medical, Chicago,1963. 34. Fabrikant, J.I. Studies of cellular response and cell population kinetics under continuous Report, pp. 26-27, Nev irradiation. York, 15,3.(7m) James Picker Foundation Annual 35. Fabrikant, irradiatedJ.I. Cell and proliferation studies in normal, continuously malignant the Institute of Cancer Research: tissues. Regenerating liver. (In) Report of Royal Cancer Hospital, British Empire Cancer 41:152-153, Campaign for Research, Annual Report, London, 1964. 36. Fabrikant, J.I. and Smith, C.L.D. Radiographic changes following the-administration 37:53-62, 1964. of bone-seeking radionuclides. Brit. J. Radiol. 37. Fabrikant, J.I. and Roylance, P.J. Cinefluorographic anatomy of the larynx 1964. 33:25, and hypopharynx. Proc. Anat. Soc. Great Britain and Ireland 38. Fabrikant, J.I. Investigation of cellular response and cell population kinetics Foundation, in Annual tissues under Report, pp.continuous irradiation. 28-29, New York, 1964. (In) James Picker 39. Fabrikant, J.I. Studies of cell proliferation in the regenerating liver and the effect University of prior1964. of London, continuous irradiation. Ph.D. Thesis,
- 40. Fabrikant, J.I., Dickson, R.J. and Fetter carcinogenesis at the clinical level. Brit. B.F.
J. Mechanisms Cancer 18: 459-477, of radiation 1964. 41. Fabrikant, J.I. and Dickson, R.J. The use of cinefluorography for the radiological examination of the larynx and hypopharynx in cases of suspected carcinoma. Brit. J Radiol. 38:28-38, 1965. 42. Fabrikant, of the normal J.I. and andRoylance, diseased larynx.P.J. Cinefluorographic J. Anat. functional anatomy 99:209, 1965.
- 43. Fabrikant, J.I. and Koburg E. R6ntgen-Kontrastuntersuchungen von Larynx und Praxis Hypopharynx 13:16-19, 1965. in Verbindung mit Bildverstarkung. HNO Vegv. f. f ach.
44. Fabrikant, J.I. and Lamerton, L.F. The ef f ect of prior continuous irradiation Intern Congr. on89:347, cell proliferation 1965. in the regenerating liver. Exc. Med.
Page 13
- 45. Fabrikant, J.I.,
Dickson, R.J. and Fetter, B.F. Mechanisms of radiation carcinogenesis J.F., at clinical level. (In) Year Book of Radiology, Holt, Whitehouse, V.M and Latourette, H.B., eds., pp. 384-386, Year Book Medical, Chicago, 1966. 46. Fabrikant, J.I. Cell cy:le of regenerating hepatocytes after continuous irradiation (ab) Intern. Congr. Radiation Res. 3:79, 1966. 47. Fabrikant. J.I. Cell population kinetics in the regenerating liver in normal Res. and1966. 3:80, continuously irradiated mice. (ab) Intern. Congr. Radiation 48. Fabrikant, J.I. Radiation-induced chromosome abberations in the regenerating liver under continuous irradiation. (ab) Intern. Congr. Radiation Res. 3:80, 1966. 49. Fabrikant, J.I. and Dickson, R.J. Use of einefluorography for radiologic examination of larynx and hypopharynx in cases of suspected carcinoma. (In) Year Book of Cancer, Clark, R.L. and Cumley, R.V., eds., pp. 384-387, Year Book Medical, Chicago, 1966.
- 50. Fabrikant, J.I.
The spatial distribution of parenchymal cell proliferation 120:137-147, 1967. regeneration of the liver. J. Hopkins Med. J. during 51. Fabrikant, J.I. The effect of prior continuous irradiation on the G 3, M and liver.SRadiation phases of proliferating Res. 31:304-314, parenchymal 1967. cells in the regenerating 52. Fabrikant, J.I. Radiation sterilization in man. JAMA 200:201-202, 1967. 53. Fabrikant, J.I. The kinetics of cellular proliferation in conditional cell renewal 15:24, Radiologists systems1967. under continuous irradiation. (ab) Assn. Univ.
- 54. Fabrikant, lov dose-rate exposure. RadiologyJ.I. 88:767-774, The accumulation of chromoso 1967. !
55. Fabrikant, J.I. The ileal bladder. Colorado St. Dept. Public Health, Suppl., pp. 1-4, Denver, 1967. l 56. Lamerton, L.F. and Fabrikant, J.I. Repair of cellular radiation injury in the liver of continuously irradiated C57BL mice. 31:664-665, 1967. (ab) Radiation Res. 57. Fabrikant, J.I. The effect of radiation-free intervals after continuous exposure liver. (ab) on the yieldRes. Radiation of chromosome 31:665, 1967. aberrations in the regenerating 58. Fabrikant, J.I. Cell proliferation in the regenerating liver of continuously irradiated mice. Brit. J. Radiol. 40:487-495, 1967. 59. Fabrikant, J.I. and Visseman, C.L., III. Cell proliferation in normal and malignant 3 Radio 1, Soc. N. Amer.37:41, tissues. I. In vitro incorporation of thymidine-H 1967. . (ab)
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- 60. Fabrikant, J.I. Cell proliferation in the regenerating liver and the ef fect 1967.
of prior continuous irradiaton Radiation Res. 32:804-826, 61. Fabrikant, J.I. , Peterson, V.E. and Donner, M.V. Biographical note. (In) Russell H. Morgan, A Tribute. Fabrikant, J.I. and Donner, H.V. , eds. , pp. xi-xil, duPont, Vilmington, Delavare, 1967. 62. Fabrikant, J.I. The analysis of cell population kinetics in a conditional renewal system under continuous irradiation. (In) Russell H. Morgan, A Tribute, Vilmington,Fabrikant , J.I.1967. Delavare, and Donner, M.V. , eds. , pp. 93-100, duPont ,
- 63. Fabrikant, J.I.
34:311-315, 1967. Kinetic analysis of hepatic regeneration. Growth 64. Ho reels, C.L. Jr., Cherry, J. and Fabrikant, J.I. Ossified arytenoid cartilage masquerading as a foreign body; A case report. Amer. J. Roentgenol., Rad. Therapy and Nuclear Med. 101:837-838, 1967. t 65. Fabrikant, J.I. The liver. J. Cell. Diol.kinetics of cellular 36:551-565, 1968.proliferation in regenerating
- 66. Fabrikant, J.I. and Visseman, C.L., III. In vitro incorporation of tritiated thymidine 90:361-363, 1968. in normal and neoplastic tissues. Radiology 67.
Morreels, Modern C.L.Med. ,36:103, Jr., Cherry, 1968. J. and Fabrikant, J.I. Masqurader. (ab) 68. Fabrikant, J.I. Rate Brit. J. Radiol. of cell 41:71, proliferation in the regenerating liver. 1968. I 69. Foster, B.R. and Fabrikant, J.I. Studies on lymphoid cell proliferation in the normal and continuously irradiated mouse thymus by repeated labeling with tritiated thymidine. (ab) Radiation Res. 35:486, 1968. - 70. Fabrikant, J.I. Cell proliferation during lymphopolesis in normal and continuously irradiated mice. (ab) (In) Symposium on the Effect of Radiation Vienna, SM-103/41,on Cellular 1968.Proliferation and Differentiation, I.A.E.A., 71.
- Fabrikant, J.I. Radiation effects on a conditional cell reneval system
- under continuous Therapy and Nuclear lovMed.
dose rate exposure. Amer. J. Roentgenol., Rad. 102:811-821, 1968. 72. Fabrikant, J.I. Cell proliferation in normal and malignant human tissues. (In) James York, 1968. Picker Foundation, Annual Report, 1967, pp. 44-45, Nev 73. Fabrikant, J.I. Cell proliferation during lymphopolesis in normal and continuously irradiated mice. (In) Symposium on Effects of Radiation on I.A.E.A Cellular Prolif 1968.
, Vienna, eration and Dif ferentiation, SM-103/41, pp.1-24 1
1
Pege 15 74. Fabrikant, J.I. Influence of cell cycle stage on radiation response in vivo. (ab) Assn. Univ. Radiologists 16:27, 1968. 75. Fabrikant, J.I. Cell proliferation in the regenerating liver of continuously irradiated mice; Effect of a radiation-free interval. Brit. J. Radi.l. 41: 369-374, 1968.
- 76. Fabrikant, J.1, . Vitak, M.J. and Visseman, C.L. , III. The kinetics of cellular proliferation in human tissues. IV. Nucleic acid synthesis and the cell cycle in relation to normal, inflammatory and neoplastic grovth. (ab) Radiol. Soc. N. Amer., 54:214-224, 1968.
77. Hoopes, J.E. and Fabrikant, J.I. Objective evaluation of clef t palate speech. Plast. Reconstr. Surg. 4? 214-224, 1968. 78. Fabrikant, J.I. The kinetics of lymphoid cell proliferation under continuous irradiation. (ab) Radiol. Soc. N. Amer. 54:180, 1968. 79. Knudson, D.M. and Fabrikant, J.I. Radiographic eve'.uation of radiation induced bone tumors. (ab) Radiol. Soc. N. Amer. 54:180, 1968. 80. Fabrikant, J.I. Cell proliferation during lymphopoiesis in the thymus of continuously irradiated alce. (In) Effects of Radiation on Cellular Proliferation 1968. and Differentiation, pp. 269-393, I . A.E. A. , Vienna ,
- 81. Fabrikant, J.I., Visseman, C.L., III, and Vitak, M.J. The kinetics of
- cellular proliferation in normal and malignant tissues, II. An in vitro method for incorporation of tritiated thymidine in human tissues. Radiology 92:1309-1320, 1969.
82. Fabrikant, J.I. Studies on cell population kinetics in regenerating liver. (In) Human 30:169-183, 1969. Tumor Cell Kinetics, Nat. Cancer Inst. Monogr. No. 83. Fabrikant, J.I. and Cherry, J. The kinetics of cellular proliferation in normal Ann. and, Rhinol, 0101. malignant tissues. III. Cell proliferation in the larynx. Laryngol. 78:326-341, 1969. 84. Hoopes, J.E., Dellon, A.L. , Fabrikant, J.I. and Soliman, H. The locus of levator veli palatini function as a measure of velopharyngeal incompetence. Plastic Reconstr. Surg. 44: 155-160, 1969. 85. Fabrikant, J.I. and Foster, B.P. The kinetics of lymphoid cell proliferation during radiation lymphomogenesis in C578L mice. Radiation Res. 39:544, 1969. 86. Fabrikant, J.I and Cherry, J. The kinetics of cellular proliferation in normal and malignant tissues. V. Analysis of labeling indices and potential Oncol. doubling 1:27-51, times in human tumor cell populations. J. Surg. 1969. 87. Fabrikant Cell Res., J.I55:277-279, Size of proliferating 1969. pools in regenerating liver. Exp.
. Page 16 88.
Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo. Amer. J. Roentgenol., Rad. Therapy and Nuclear Hed. 105:734-745, 1969. 89. Fabrikant, J.I. Studies on cell population kinetics in radiation leukomogenesis. Assn. Univ. Radiologists 17:88, 1969. 90. Fabrikant, J.I. and Foster, B.R. Cell cycle of lymphocytes in mouse thymus. Die Naturvissenschaften 57:567, 1969. 91. Fabrikant, J.I. Lell proliferation in continuously irradiated mammals: Effect of age. (In) Radiation Biology of the Fetal and Juvenile Mammal, Sikov, M. and Mahlum, D.D., eds. USAEC, CONF. 621-678, Oak Ridge, Tennessee, 1969. 690501, pp. 92. Hoopes, J.E. , Dellon, A.L. , Fabrikant, J.I. , Edgerton, H.T. and Soliman, A.H. Cineradiographic definition of the functional anatomy and ' pathophysiology 42, Houston, Texas, of 1969.the velopharynx. (ab) Intern. Congr. Cleft Pala:s, 93. Fabrikant, J.I. The kinetics of cellular proliferation in the seminiferous epithelium under continuous irradiation. XII Intern. Congr. Radiology 12:98, 1969. 94. Fabrikant, J.I. Radiation effects on lymphopolesis under continuous lov dose-rate exposure. Radiology 93:877-893, 1969. 95. Hoopes, J.E. and Fabrikant, J.I. Objective evaluation of clef t palate speech. (ab) Clef t Palate J. 6:181, 1969. 96. Fabrikant, J.I. Research on cell proliferation in normal and malignant human 45-50, New tissues. York,(In) James Picker Foundation Annual Report, 1968, pp. 1969. 97. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malignant tissues. VIII. Studies on cell population kinetics in normal,Radiology Congr. inflammatory and neoplastic tissues in man. (ab) XII Intern. 12:442, 1969. 98. Fabrikant, J.I. Cell proliferation in normal and malignant human tissues. (In) James 1969. Picker Foundation Annual Report, 1969, pp. 40-42, New York, l 99. Fabrikant, J.I. and Visseman, C.L., III. In vitro incorporation of tritiated thymidine in normal and neoplastic tissues. (In) Year Book of Radiology, Holt, J.F. , Vhitehouse, V.M. and Latouret te, H.B. , eds. , pp. 383-384, Year Book Medical, Chicago, 1969. 100. Fabrikant, J.I. The kinetics of cellular proliferation in human tissues. IX. Estimation of DNA synthesis time in normal and malignant tissues. (ab) Radiol. Soc. N. Amer. 55:44, 1969. 101. Fabrikant, J.I. Tumor cell population kinetics during radiation lymphogenesis. (ab) Radiol. Soc. N. Amer. 55:124, 1969. 1 i
. Page 17 102. Hoopes, J.E., Dellon, A.L., Fabrikant, J.I. and Soliman, A.H.
Cineradiographic assessment of combined island flap pushback and pharyngeal flap in the surgical management of submucous cleft palate. Brit. J. Plast. Surg. 23:39-44, 1970. 103. Fabrikant, J.I. and Kovar, D.S. Spermatogonfal cell reneval under contin-uous irradiation at 1.8 rads / day. (ab) Radiation Res. 18:233, 1970. 104. Dannenberg, A.M., Jr., Shima, K., Chandrasekhar, S. and Fabrikant, J.I. macrophage proliferation, maturation, and function in rabbit BCG lesions. (ab) Fed. Proc. 29:501, 1970. 105. Fabrikant, J.I. Thymus cell population studies during radiation leukemo-genesis 729-735,Amer. 1970. J. Roentgenol., Rad. Therapy and Nuclear Hed. 108: 106. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malignant tissues. XI. Estimation of DNA synthesis time in human tissues. Radiology 95:691-693, 1970. 107. Hoopes, J.E. , Dellon, A.H. , Fabrikant, J.I. and Soliman, A.H. idiopathic hypernasality: Cineradiographic evaluation and etiologic considerations. J. Speech Hearing Dis. 35:44-50, 1970. 108. Fabrikant, J.I. The kinetics of cellular prollferation in normal and malignant tissues. Invest. Radiol. VI. 1970. 5:281, Nuclec acid synthesis in human tissues. (ab) 109. Hoopes, J.E. , Dellon, A.L. , Fabrikant, J.I. and Soliman, A.H. The locus of levator palatini function as a measure of velopharyngeal incompetence. (ab) Cleft Palate J. 7:357, 1970. 110 Fabrikant, J.I. and Cherry, J.I. The kinetics of cellular proliferation in normal and malignant tissues. X. Cell proliferation in respiratory epithelium of the nose and adjoining cavities. Ann. Otol., Rhinol., Laryngol. 79:572-578, 1970.
- 111.
Fabrikant, J.I. Environmental radioactivity Inclusion at the cellular level. Environmental Radioactivity Symposium, Clopton, J.C. , ed. , pp. 36-106, The Johns Hopkins University Press, Baltimore, Maryland, 1970. 112. Fabrikant. J.I. Report of the United Nations Scientific Committee on the Effects of Atomic Radiation. Supplement 13, 1969. (Book Reviev) Social Biol. 17:238-241, 1970. 113. Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo. (ab) Radiology 94 247, 1970, 114. Fabrikant, J.. Human tumor cell kinetics. (In) Time and Dose Relation-ships in Radiation Biology as Applied to Radiotherapy, Bond, V.P., Suit. H.D. and Marcial, V. , eds. , pp. 334-337, BNL 50203(C-57) Brook-haven national Laboratory, Upton, New York,1970. i l
. Page 18 , 1 115. Hoopes, J.E., Dellon, A.L., Fabrikant, J.I. , Edgerton, M.T. and Soliman, A.H. Cineradiographic definition of the functional anatomy and pathophysiology of the velopharyn. Cleft Palate J. 7:443-454, 1970. ) 116. Fabrikant, J.I. Cell proliferation in the seminiferous epithelium under continuous Chime Rayon.irradiation. 4:68, 1970.(ab) IV Congr. Intern. Radiobiol. Physico-117. Fabrikant, J.I. Ef fects of rapidly and slovly proliferating cell reneval systems. Sixth Annual San Francisco Cancer Symposiu.7, (ab) 5:26, 1970. t 118. Dannenberg, A.M. , Jr. , Shima, K. , Kambara, T. , Meyer, 0.T. , Es terly, J.R. 1 and Fabrikant, J.I. Immunity in tuberculosis, illustrated by its pathogenesis. 7, 1970. (ab) Tuberculosis Conference, NIAID, US-Japan Program, 119. Hoopes, J.E., DcIlon, A.L., Fabrikant, J.I. and Soliman, A.H. Cineradiographic definition of the anatomical variable responsible for cleft palate speech. Brit. J. Plast. Surg. 24:158-162, 1971. 120. Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo. (In) Year Book of Radiology, Holt , J.F. , Whi tehouse, V.M. and Latourette, H.B., eds., p. 392, Year Book Medical, Chicago, 1970. 121. Fabrikant, J.I. The kinetics of cellular proliferation in human tissues. VII. DeterminationBrit. autoradiography. of duration of DNA synthesis using double labeling J. Cancer 24:742, 1970. 122. Fabrikant, J.I. Thymus cell population studies during radiation leukemogenesis. (ab) Radiology 97:742, 1970. 123. Fabrikant, J.I. Radiation effects on cell reneval systems. (ab) (In) Frontiers 1970. of Radiation Therapy and Oncology, Vaeth, J.H. , ed. , 5:6-8, 124. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malignant tissues. XII. In vitro label. (In) The Grovth Kinetics of Solid Tumors, Villiamsburg, Va., February 8-11, 1971, Summary Report of the Meeting. Hendelsohn, H.L. and Shackney, S.E. The grovth kinetics of solid tumors. Cell Tissue Kinet. 3:401-414, 1971. 125. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malignant tissues. XV. A review of methodology and the analysis of cell population Therapy kinetics and Nuclear Hed.in human tissues. Amer. J. Roentgenol., Rad. 111:700-711, 1971. 126. Fabrikant, J.I. Spermatogonfal cell renewal. (In) Symposium on Cell Renewal Systems. (ab) Radiation Res. 19:46-47, 1971. 127. Delhunty, J.E. and Fabrikant, J.I. Experimental laryngeal arterlography. Ann. Otol., Rhinol., Laryngol. 00:744-749, 1971. 128. Fabrikant, J.I. Cell population kinetics in thymus lymphocytes under continuous irradiation. (In) Biological Aspects of Radiation
Page 19 Protection, Sugahara, E. and Hug, 0. , eds. , pp. 74-80, Igaku Shoin. Tokyo, Japan, 1971. 129. Fabrikant, J.I. Biological effects of small doses of radiation. (ab) Amer. Assn. Physicists Med. Quart. Bull. 5:115, 1971. 130. Fabrikant, J.I. Spermatogonial cell reneval under continuous lov dose irradiation. Invest. Radiol. 6:343, 1971. 131. Fabrikant, J.I. Radiation Biology of the Fetal and Juvenile Mammal. Proc. Ninth Ann. Hanford Biol. Symposium. (Book Reviev). Radiology 97:659-660, 1971. 132. Fabrikant, J.I. and Foster, B.R. The cell cycle and growth kinetics during radiation leukemogenesis in C57BL mice. (ab) Radoll. Soc. N. Amer. 57:244, 1971. 133. Chandrasekhar, S. , Shima, K. , Dannenberg, A.M. Jr. , Kambara, T. , Fabrikant, J.I. and Roessler, V.G. Radiation, infection and macrophage function. IV. Effect of radiation on the proliferative abilities of mononuclear phagocytes in tuberculosis lesions of rabbits. Infection and Immunity 3:254-259, 1971. 134. Fabrikant, J.I. and Cherry, J. The kinetics of cellular proliferation in normal and malignant tissues. XIII. Doubling times in primary and metastatic tumors in the same patient. (ab) Radiol. Soc. N. Amer. 57:46, 1971. 135. Fabrikant, J.I. , Visseman, C.L. , III and Vi tak, M.J. The kinetics of cellular proliferation in normal and malignant tissues. VI Nucleic acid metabolism in relation to the cell cycle in human tissues. Growth 36:173-183, 1972. 136. Fabrikant, J.I. The ef fects of small doses of radiation. (In) Reduction of Radiation Dose in Diagnostic X-Ray Procedures, pp. 3-32. Proceedings of a Symposium held in Houston, Texs, July 8, 1971. Amer. Assoc. Phys. Hed., USDHEV Publ. No. (FDA) 73-8009, Bureau of Radiological Health, Rockville, Md., 1972. 137. Fabrikant, J.I. Spermategonlai cell reneval under continuous lov dose irradiation. Amer. J. Roentgenol., Rad. Therapy and Nuclear Med. 114 7920802, 1972. 138. Fabrikant, J.I. Radiation effects on rapidly and slovly proliferating cell reneval systems. Discussion. Front. Radiation Ther. Oncol. 6:524-526, 1972. 139. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonf al cell reneval under contin-uous lov level irradiation. VII. Kinetics of cellular depopulation under 45 rads per day. (ab) Radiation Res. 51:544, 1972. 140. Fabrikant, J.I. and Foster, B.R. Lymphoid cell reneval under lov-level irradiation. XI. The cell cycle and growth kinetics during radiation leukemogenesis of C57BL mice. Radiology 104: 203-204, 1972.
~ _ _ . _ _ _ _ -.
Page 20 l 141. Fabrikant, ! cell reneval systems. (In) Frontiers of Radiation Therapy and Oncology, Vaeth, J.M., eds., Vol. 6, pp. 57-78, Karger, Basel, 1972. 142. Fabrikant, 105:434,J.I. Medical Radiation Biology. (Book Reviev). Radiology 1972, 143. Fabrikant, J.I. Cell population kinetics in the seminiferous epithelium under continuous lov dose rate irradiation. (In) Advances in Radiation l Research. eds. Biology and Medicine. Vol II. Duplan, J.F. and Chapiro, A. , pp. 805-814, ' Gordon and Breach, New Y0rk, 1972. 144. Fabrikant, J.I. and Foster, B.R. Cell population kinetics in mouse and rat thymus. J. Hopkins Med. J. 130:208-215, 1972. 145. Fabrikant, J.I. Lymphoid cell reneval under lov level irradiation. XII. Regulation of thymus cell proliferation under continuous exposure. (ab) Radiation Res. 51:471, 1972. 146. Fabrikant , J.I. , Hsu, T.H.S. , Knudson, D.H. and Smi th, C.L.D. Ef fec t of LET on radiation carcinogenesis. Comparison of single and fractionated doses of plutonium-239, americium-241, phosphorus-32 and x-rays on the production of osteosarcomas in rats. (ab) 12th Banford Biology Symposium 1972. on Radionuclide Carcinogenesis, Richland, Vash., May 11-13, 147. Fabrikant, J.I. and Cherry, J. The kinetics of cellular proliferation in . normal and ealignant tissues. XIV. Analysis of tumor cell kinetics in primary and metastatic lesions. (ab) Assn. Univ. Radiologists 20:34, 1972. Invest. Radiol. 7:436-437, 1972. 148. Fabrikan t , J.I. , Hsu, T.H.S. , Knudson, D.H. and Smi th, C.L.D. LET and radiation carcinogenesis. The effects of fractionation of dose of plutonium-239, americium-241, phosphorus-32 and x-rays on the production of osteosarcomas in rats. (In) Radionuclide Carcinogenesis, 12th Hanford Biology Symposium, pp. 322-346, C.L. Sanders, R.H. Busch, J.E. 1973.Ballou, D.D. Hahlum, eds. , CONF-720505, USAEC. Oak Ridge, Tenn. 149. Fabrikant, J.I. Public health considerations of the biological effects of small Puerto Juan, doses of medical radiation. (ab) Health Physics Society, San Rico, 7:4, 1972. 150. Fabrikant, J.I. Radiation dosimetry of heavily irradiated sites in patients treated for ankylosing spondylitis. (In) The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation. Report of the Advisory pp. 190-195. Committee on Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Academy Press Vashington, D.C., 1972. 151. Fabrikant, J.l. The kinetics of cellular proliferation in normal and malignant tissue. XVI. Cell population kinetics in primary and metastatic tumors. (ab) Europ. Soc. Radiation Biol., Rome. 9:47, 1972. I I i
-.,-r
l l l . Page 21 1 152. Fabrikant, J.I. Lymphoid cell reneval under lov level irradiation. XIII. Homeostatic control of cell reproduction under continuous exposure. (ab) Europ. Soc. Radiation Biol., Rome, 9:48, 1972. 153. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonial cell reneval under lov level irradiation. VII. Cellular response and cell population kinetics in the seminiferous epithelium during recovery af ter continuous exposure 1972, at 45 rads / day. (ab) Europ. Soc. Radiation Biol., Rome, 9: 49, 154 Shima, K. , Dannenberg, A.M. , Jr. , Ando, M. , Chandrasekhar, S. , Seluicki, J. and Fabrikant, J.I. Macrophage accumulation, division, matura: ion, and digestive and microbial capacities of tritiated thymidine and their content of lysomal enzymes and bacilli. Amer. J. Pathol. 66:143, 1972. 155. Delahunty, RadiologyJ.E. and Fabrikant, 103:227, 1972. J.I. Experimental laryngeal arterlography. 156. Fabrikant, J.I Lymphoid cell reneval under continuous low level irradiation. XIV. Regulation of cell proliferation and differentiation. (ab) Radiol. Soc. N. Amer. 58: 47, 1972. 157. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonf al cell reneval under lov level irradiation. X. Cellular response and cell population kinetics during recovery of the testes after continuous irradiation at 45 rads / day. (ab) Radiation Res. 55:560, 1973. 158. Fabrikant, J.I. and Foster, B.R. Lymphoid cell reneval under lov level irradiation. XVII. Cell kinetic analysis of radiation leukemogenesis. (ab) Radiation Res. 55:587, 1973. 159. Fabrikant, J.I. Public health considerations of the biological effects of small doses of medical radiation. (In) Health Physics in the Healing Arts, pp. 31-42, DHEV Publication (FDA) 73-8029, Food and Drug Administration, 1973. Bureau of Radiological Health, NTIS, Springfield, Va., 160. Fabrikant, J.I., Hsu, T.H.S., Kovar D.H. and Snith, C.L.D. Radiation-induced osteosarcomas in rats. Delayed effects of bone-seeking radionuclides and x-rays. Invest. Radiol. 8:269, 1973. 161. Fabrikant, J.I. Tumor cell population kinetics under continuous irradiation. (In) Symposium on the Radiobiological Effect and RBE of Minimum
- p. 473, Madrid,DosesSpain, of Radiation.
1973. (ab) Proc. XIII Intern. Congr. Radiology, 162. Fabrikant, J.I. Lymphoid cell renewal under lov level irradiation. XV. Regulation of lymphopoles!s under continuous exposure. (In) Symposium on Long-Term Effects--Lov Level Radiation Doses. Proc. XIII International Congress of Radiology, p. 518, Madrid, Spain, 1973. 163. Hsu T.H.S., Fabrikant, J.I. and Kovar, D.S. Spermatogonfal cell reneval
. Pa2e 22 under lov level irradiation. XII. Effect of dose rate on cellular Radiology Sec., Baltimore, Md., 1973. response under continuous 164.
Fabrikant, J.I. The cell cycle in lymphoid tissues. (ab) (In) The Cell Cycle in Malignancy and Immunity. Thirteenth Hanford Biology Symposium, Richland, Vash. 13:59-60, 1973. 165. Hsu, T.H.S., Kovar, D.S. and Fabrikant, J.I. Spermatogonfal cell renew kinetics in mice. (ab) Rdiat. Res. Soc. Vork-in Progr Tventy-third Ann. Mtg., St. Louis, Mo., May 1, 1973. , 166. Fabrikant, J.I. Some implications of the 1972 Report of the Advisory Committee on the Biological Effects of Ionizing Radiations (The BEIR Report) of the National Academy of Sciences-National Research Counc (In) Report of the Eleventh Meeting of the Medical Radiation Advisor y Committee, Bureau September 13-14, 1973.of Radiological Health, FDA, DHEV, Rockville , Md., 167 Fabrikant, J.I. The cell cycle in lymphoid tissues and the immune ed., Thirteenth Hanford 81 ology Symposium, NTIS, Springfield, Va., 1974. pp.J., 504-530,(CONF-731005) respons 168. Fabrikant, J.I. The biological effects of lov levels of radiation dose Course The Faculty of Radiologists, London, Engla 169. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonial cell renewal under Radiatoin Res., Seattle, Vash., July 1974. continuous irradia 170. Fabrikant, J.I. Tumor cell population kinetics under continuous 1973, pp. 585-589, irradiation. Proc. XIII Intern. Congress , Spain, Radiology, Excerpta Medica, Amsterdam, 1975, 171. i Fabrikant, J.I. Medical Radiation. Second Report to the Advisory Academy D.C., 1974 of Sciences-National Research Council , 172. Fabrikant, J.I. Concepts: Report cost-benefit analysis and eedical radiation. to3,the Advisory Committee on the Biological Effects of Ionizing Radiatior: National pp. , Vashington, C C.Academy
. ,1975. of Sciences-National Research council, 18 173.
Hsu, T.H.S. and Fabrikant, J.I. Spermatogonial cell reneval under continuous the Sym irradiation at 1.8 and 45 rads per day. (In) Proceedings of Agency IAEA-AM-202/214, posium on Lov Level Radiation, International Atomic Energy Chicago, Ill., 1975. 174. Fabrikant, J.I. The significance to diagnostic radiology of the effects 33:172-179, 1975.of exposure to lov levels of ionizing radiations. Clinical R I L
P:gt 23 175. Fabrikant, J.I. Benefit-Risk-Cost Analysis for Medical Radiation. Chapte VI. (In) Considerations of Health Benefit-Risk-Cost Analysis for Activities Involving Ionizing Radiatio.. Exposure and Alternatives . Radiations National Academy of Sciences-Nationa 147 pp., National Academy Press, Vashington, D.C., 1976. 176. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonfal cell renewal under continuous irradiation at 1.S ind J.5 rads per day. (In) Biological and Environmental Effects of Lov-Level Irradiation. Vol.1, pp.157-168, IAEA-SH-202/214, 1976. International Atomic Energy Agency, Vienna, 177. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonial cell renewal under lov-level irradiation. 70:620, 1977. XVI. Stem cell proliferation. (ab) Radiatioon Res. 178. Hsu, T.H.S. and Fabrikant, J.I. Kinetics of spermatogonial cell reneval under continuous irradiation at 1.8 and 4.5 rads per day. (ab) Radiation Res. 70:620, 1977. 179. Fabrikant, J.I. and Hilberg, A.V. Benefit-cost analysis for medical radiation. (ab) Radiation Res. 70:670-671, 1977. 180. Fabrikant, J.I. Benefit-cost analysis in diagnostic radiology. (In) Panel Radiology. James Picker Foundation Conference, The Society--Pospects and Problems for the 1980s. April 1977. Kay Biscayne, Florida, 181. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonf al cell reneval under low-level irradiation. XV. Stem cell proliferation in the seminiferous Radiology, Rio de Janeiro, Brasil, 1977. epithelium under 1.8 ra 182. Fabrikant, J.I. and Hilberg, A.V. Benefit-cost analysis for diagnostic radiology in medicine. (In) Symposium on Risks and Benefits in Medical Radiation de Janeiro,Applications. Brasil, 1977.XIV International Congress of Radiology, Rio 183. Fabrikant, J.I. and Anderson, N.D. Immunohematopoietic cell reneval under lov level irradiation. XVIII. Hematopoietic stem cell kinetics. (ab) (In) Symposium on Immunological Consequences of Radiotherapy. XIV Intern. Congr. Radiology, Rio de Janeiro, Brasil, 1977. i 184. Fabrikant, to humanJ.I. and Hilberg, A.V. The effects of lov level radiation dose populations: XIV Intern. Congr. Radiology. Rio de Janeiro, Brasil,1977.The signific 185. Fabrikant, J.I. Lymphoid cell reneval under lov level irradiation. XIX. Cell proliferation in the spleen germinal center during the primary immune reaction under 45 rads per day. (ab) XIV Intern. Congr. 3 Radiology, Rio de Janoiro, Brasil, 1977.
l Pege 24 186. Fabrikant, J.I. and Hilberg, A.V. Hammography: Benefit-cost analysis of mass screening Janeiro, procedures. (ab) XIV Intern of Radiology, Rio de Brasil, 1977. 187. Fabrikant, J.. Respiratory function in ischemic myocardial disease The value of pulmonary radiology. (ab) XIV Intern. Congr. Radiology, Rio de Janeiro, Brasil, 1977. 188. P Fabrikant, J.I. Radiation protection and safety in diagnostic ultrasound. (ab) XIV Intern. Congr. Radiology, Rio de Janeiro, Brasil, 1977. 189. Fabrikant, J.I. Safety in Diagnostic Ultras.und. (In) CRC Critical Reviews in Diagnostic Imaging, Vang, Y , ed., CRC Press, Vol. 10, pp. 219-234, 1977. 190. Fabrikant, J.I. Ferspectives of de-'-'~ . making and estimation of risk in i populations exposed to lov levels of ionizing radiation. (In) Symposium on Epidemiology Studies of Lov Level Radiation Exposure. AAAS Annual Meeting, Houston, Texas, January 1979. , 191. Fabrikant, J.I. Cell cycle of spermatogonia in mouse testes. Invest. Radiol. 14:189-191, 1979. 4 192. Fabrikant, J.I. The 1979 report of the Advisory Committee on the Biological Effects of Ionizing Radiation (The BEIR Report): The Effects on Populations to Exposure to Lov Levels of Ionizing . Radiation. Implications for Nuclear Energy and Medical Radiation. (In) Symposium on Knovn Effects of Lov Level Radiation Exposures, (National Cancer Institute), Pittsburgh, Pennsylvania, April 1979, Lavrence Berkeley Laboratory Report, LBL-9084, pp.1-42. , 193. Fa' .4kant, J.I. and Anderson, N.D. Immunohemptopoletic cell reneval under low level irradiation. XIX. CFU stem cell kinetics. (ab) VI Inter-national Congress of Radiation Research, p. 309. Tokyo, 1979. 194.
- Fabrikant, J.I. Spermatogonial stem cell reneval following irradiation.
(In) Symposium on Radiation and Stem Cells, (ab) VI Intern. Congr. Radiation Research, p. 44, Tokyo, 1979. 195. Fabrikant, J.I. spermatogonfal stem cell reneval folloving irradiation. (In) Symposium on Radiation and Stem Cells. VI Intern. Congr. , Radiation LBL-8667, 1979. Research. Proceedings of the Congress Tokyo, Hay, 1979, 196. l Fabrikant, J.I. and Hilberg, A.V. Benefit-risk analysis for diagnostic >
- radiology.
1979. (ab) VI Intern. Congr. Radiation Research, p. 183, Tokyo, } 197. ! Lyman, J.T. and Fabrikant, J.I. Estimation of absolute risk of leukemias l and cancers of heavily irradiated sites in single-course radiotherapy i patients treated for ankylosing spondylitis in England and Vales. (ab) VI Intern. Congr. Radiation Research, p. 180, Tokyo, 1979. l l l
Page 25 198. Tobias, C. A. , Ben ton, E.V. , Holley, V.R. , Fabrikan t , J.I. , and Henke, R.P. Heavy-lon computed tomography. (ab) VI Intern. Congr. Radiation Research, p. 135, Tokyo, 1979. 199. Vi tak, M.J. , Hsu, T.H.S. , Kovar, D. , and Fabrikan t , J.I. Lymphoid cell reneval under lov level irradiation. XX. B-cell population kinetics of the cellular immune response. (ab) VI Intern. Congr. Radiation Research, p. 212, Tokyo, 1979. 200. Fabrikant, J.I. Degeneration and regeneration of the spermatogonal stem-cell system af ter exposure to ionizing radiation. Lavrence Berkeley Laboratory Report No. LBL-8850, pp.1-25, Uriversity of California, Berkeley, California, February 1979. 201. Fabrikant, J.I. Perspectives of decision-making and estimatioa of risk in populations exposed to lov levels of ionizing radiations. (In) Symposium on Epidemiology Studies of Lov-Level Radiation Exposure, AAAS Annual Meeting, Houston, Texas, January 3-8, 1979; Lavrence Berkeley Laboratory Report LBL-8667, pp. 1-40, January 1979. 202. Fabrikant, J.I. Fertility. Somatic Effects: Effects Other Than Cancer. The Ef fects on Populations of Exposure to Lov Levels of Iontring Radiation: 1980. Chapter V, pp. Report of the Commit tee on the
- Biological Effects of Ionizing Radiations. National Academy of Sciences-National Research Council, National Academy Press, Vashington, D.C., 1980, Lavrence Berkeley Laboratory Report LBL-8704, January 1979.
203. Fabrikant, J.I. Salivary Glands. Somatic Effects: Cancer. (In) The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter V, pp. 392-396, Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 392-396, National Academy of Sciences- National Research Council, National Academy Press, Vashington, D.C.,1980, Lavrence Berkeley Ls.boratory Report LBL-8708, January 1979. 204. Fabrikant, J.I. and Lyman, J.T. Estimates of radiation doses in tissues and organs in the single-course radiotherapy patients treated for ankylosing spondylitis in England and Vales. Somatic Effects: Cancer. (In) The Ef fects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter V, pp. 160-167, Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Academy Press, Vashington, D.C.,1980, Lavrence Berkeley Laboratory Report LBL-8708, January 1979. 205. Fabrikant, J.I. and Land, C.E. Pancreas. Somatic Ef fects: Cancer. (In) The Ef fects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter V, pp. 384-389, Report of the Commi'.ur, on the Biological Effects of Radiations, National Academy of Sciences-National Research Council, National Academy Press, Vashington, D.C.,1980 Lavrence Berkeley Laboratory Report Lb M10, January 1979.
Page 26 206. Fabrikant, J.I. Pharynx, hypopharynx, and larynx. Somatic Effects: Cancer. (In) The Ef fects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter V, pp. 389-392, Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Academy Press, Vashington, January 1979.D.C. ,1980, Lavrence Berkeley Laboratory Report LBL-8711, i 207. Fabrikant, J.I. Somatic Ef fects - Cancer. II. Introductory Material. A. Mechanisms of Radiation Carcinogenesis. B. Concepts of Somatic Effects. (In) The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. pp.1-14. Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Academy Press, Vashington, January 1979. D.C. , Lavrence Berkeley Laboratory Report LBL-8715, 208. Fabrikant, J.I. Ovary. Somatic Effects: Cancer. The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter V, op. 406-409, Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, Natioal Academy Press, Washington, D.C.,1980, Lawrence Berkeley Laboratory Report LBL-8743. January 1979. 209. Fabrikant, J.I. Degeneration and regeneration of the spermatogonial stem-cell system after exposure to ionizing radiation. Presented at the Symposium on Radiation and Stem Cells, VI Intern. Congr. Radiation Research, Tokyo, Japan, May 13-19, 1979. Lavrence Berkeley Laboratory Report LB1-8850, pp. 1-25. February 1979. 210. Fabrikant, J.I. Health effects of lov-level ionizing radiation. Presented before the U.S. Senate Committee on Human Resources, Subcommittee on Health and Scientific Research. Official Record of the U.S. Senate Hearings of April 4,1979, GPO, Vashington, D.C. Lavrence Berkeley Laboratory Report LBL-9018. April 1979. 211. Fabrikant, J.I. Applications of dose-response functions to observed data. Scientific Principles of Radiation Effects. (In) The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. Chapter II. Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Academy Press, Vashington, D.C. ,1980. 4 212. Fabrikant, J.I. Perspectives of decision-making and estimation of risk in populations exposed to lov levels of ionizing radiation. Presented at the AAAS Annual Meeting. Symposium of Epidemiology Studies of l Low-Level Radiation Exposure, Houston, Texas. January 3-8, 1979. Report LBL-8667, pp.1-40, Lavrence Berkeley Laboratory, University of California, Berkeley, California, January 1979. 213. Tobias, C.A., Fabrikant, J.I., Holley, V.R., and Benton, E.V. Heavy-lon radiography. pp. 63-67. 1979. Lavrence Berkeley Laboratory Report, LBL-10022. UC-48, ; l 1
I Pogo 27 214. Holley, V.R. , Henke, R.P. , Gauger, G.E. , Jones, B. , Ben ton, E.V. , Fabrikant, J.I., and Tobias, C.A. Heavy particle computed tomography. (In) 1979. Sixth Symposium on Computer Radiology, 1979 IEEE, pp. 64-70, June 215. Fabrikant, J.I. Summ ry of the Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island (In) Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island. (Fabrikant, J.I. , ed. ) 32 pp. , Government Printing Of fice, Vashington, D.C., October 1979. 216. Axelrod, D., Bluestone, M., Densen, P.H., Fabrikant, J.I., Johnson, K.G. , Jones, E.V., and Seltser, R. Technical Staf Fovinkle E.V., f Analysis Report on Public Health and Epidemiology. (In) Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island. (Fabrikant, J.I. , ed. ) 147 pp. , Government Printing Office, Vashington, D.C., October 1979. 217. Abrahamson, S., Bair, V.J., Bender, M.A., Bloom. A.D., Bond, V.P., Casaret t, G.V. , and Fabrikant, J.I. Technical Staf f Analysis Report on Report of the Radiation Health Effects Task Group. (In) Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island. (Fabrikant, J.I., ed.) 98 pp., Government Printing Office, Vashington, D.C., October 1979. 218. Fabrikant, J.I. The BEIR-III Report and the health effects of lov-level radiation. (In) Symposium on Nuclear Reactor Safety: A Current Perspective. AAAS, San Francisco, 1980. Science. Lavrence Berkeley Laboratory Report LBL-10383, January 1980. 219. Fabrikant, J.I. The 1979 Report of the Advisory Committee on the Biological Effects of Ionizing Radiation (The BEIR Report). The Ef fects on Populations of Exposure to Lov Levels of Ionizing Radiation. Implications for Nuclear Energy and Medical Radiation. (In) Knovn Ef fects of Lov Level Radiation Exposure Health Impilcations of THI Accident (Shrivastava, P.N., eu.) pp. 79-104. Division of Cancer control and Rehabilitation of the National Cancer Institute, Mideast Center for Radiological Physics, Pittsburgh, Pennsylvania, April 25, 1979 NIH Publication 80-2087, 1980. Lavrence Berkeley Laboratory Report LBL-9084. 1980. 220. Fabrikant, J.I. The BEIR-III Report and its implications for radiation protection and public health policy. (In) Proceedings of the International Radiation Protection Association, Fifth International Congress, Jerusalem, March 9-14, 1980. Lavrence Berkeley Laboratory Report LBL-10494, 1980. 221. Fabrikan t , J.I. , Tobias, C. A. , Benton, C.V. , and Capp, M.P. Heavy ion imaging applied to medicine, (ab) (In) Proc. SPIE, IEEE, Medicine VIII, p. 64, Las Vegas, Nevada. April 1980. 222. Fabrikant, J.I. Current understanding of the relation between radiation exposure and the induction of developental disabilities. (In)
PagG 28 Symposium on Prevention of Mental Retardation: Opportunities and Obstacles 1980, III. Environmental Hazards; Special Concerns, American j 1 Association Hay 14, 1980.on Hental Deficiency, 104th Annual Meeting, San Francisco, i 1 i 223. Fabrikant, J.I., Tobias, C.A., Capp, M.P., Benton, E.V. and Holly, V.R. Heavy-lon imaging applied to medicine. Application of Optical Instrumentation in Medicine VIII, SPIE Vol. 233, pp. 255-263, 1981. Lavrence Berkeley laboratory Report LBL-10543, 1981. 224. Fabrikant, J.I. Health ef fects of the nuclear accident at Three Mile Island. (In) Conference on Environmental Regulation of the Nuclear Industry: A New Decade. Atomic Industrial Forum, San Francisco, California, May 18-21, 1980. 225. Fabrikant, J.I. The BEIR-III controversy. Radiation Research Society, Nev Orleans, Louisiana. June 1,1980. University of California, LBL-11268, June 1980. 226. Fabrikan t , J.Y. Tobias, C. A. , Capp, H.P. , Benton, C.V. , and Holley, V.R. i Heavy-ion imaging applied to medicine. Amer. J. Roentgenol., Nuclear Medicine and Rad. Therapy, 1981. 227. Tobias, C. A. , Fabrikant, J.I. , Benton, E.V. and Holley, V.R. Projection radiography and tomography. (In) Biological and Medical Research with Accelerated Tobias, Heavy Ions at the Bevalac 1977-1980. (Pirrucello, H. and C.A., eds.) pp. 335-346. Lavrence Berkeley Laboratory Report LBL-11220, 1980. 228. Fabrikant , J.I. , Tobias, C. A. , Capp, H.P. , Holley, V.R. , Voodruf f, K.H. i and Sickles, S. A. Heavy-lon rammography and breast cancer. (In) Biological and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1980. (Pirruccello, H. and Tobias, C. A. , eds. ) pp. 347-357. Lavrence Berkeley Laboratory Report LBL-11220,1980. 229. Chen, G.T.Y. Fabrikant, J.I. , Holley, V.R. , Tobias, C. A. and Castro, J.R. Hesvy-lon radiography applied to charged particle radiotherapy. (In) Biological and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1980. (Pirruccello, M. and Tobias, C. A. , eds. ) pp. 359-366. Lavrence Berkeley Laboratory Report LBL-11220.1980. 230. Llacer, J. , Chu, V.T. , Tobias, C. A. , Fabrikant , J. I. , and Alonzo, J.R. Active heavy-lon radiography and computerized tomography. (In) Biological and Medical Research vith Accelerated Heavy Ions at the Bevalac 1977-1980. (Pirruccello, H. and Tobias, C. A. , eds. ) pp. 367-374. Lavrence Berkeley Laboratory Report LBL-11220.1980. 231. Fabrikant, J.I. Budinger, T.F. , Tobias, C. A. , and Born, J.L. Focal lesions in the central nervous system. (In) Biological and Medical Research vith Accelerated Heavy Ions at the Bevalac 1977-1980. (Pirruccello, H.and Tobias C. A. , eds. ) pp. 399-405. LAvrence Berkeley l Laboratory Repor t LBL-11220,1980. l l
Page 29 232. Fabrikant , J.I. , Beebe, G.V. , Bender, M. A. , Brill, A.B. , Land, C.E. , Hoeller, D.V., and Vebster, E.V. Estimating the Total Cancer Risk of Lov-Dose, Lov LET, Vhole-Body Radiation. (In) The Effects on Populations of Exposure to Lov Levels of Ionizing Radiation, 1980. Chapter V, Section 3, pp. 176-226. Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, National Acacemy Press, Vashington, D.C., 1980. 233. Fabrikant, J.I. Health ef fects of the nuclear accident at Three Mlle Island. Health Phys. 40:151-161, 1981. Lavrence Berkeley Laboratory Report LBL-11297, 1980. 234. Fabrikant, J.I. The BEIR-III controversy. Radiation Res. 84:361-368, 1980. 235. Fabrikant, J.I. The contribution of modern medical imaging technology to radiation health effects in exposed populations IEEE Transactions on Nuclear Science, Vol. NS-28, No.1, pp. 40-46, February 1981. Lavrence Berkeley Laboratory Report LBL-11728, November,1980. 236. Fabrikant, J.I. Public health implications and decision-making during nuclear reactor accidents---the Three Mile Island experience. (In) Symposium on Preparing for the Issues of the 1980's. Annual Meeting, Association of State and Territorial Health Officials, Atlanta, Georgia, April 1980. 237. Fabrikant, JI. The BEIR-III Report: Origin of the controversy. AJR 136:209-214, 1981. Lavrence Berkeley Laboratory Report LBL-13409, 1981. 238. Fabrikant, J.I. and Lyman, J.T. Estimates of absolute risk of excess leukemias and cancers arising in heavily irradiated sites in the single-course radiotherapy patients treated for ankylosing spondylitis in England and Vales. Lavrence Berkeley Laboratory Report LBL-13999, 1981. 239. Fa'orikant, J.I., Tobias, C.A., and Pirruccello, H.C. Medical imaging using heavy-lon radiography. (In) Proceedings of the Conference on Biological Imaging, Scripps Clinic and Research Foundation, La Jolla, California, November 1980. Lavrence Berkeley Laboratory Report LBL-12517, 1981. 240. Fabrikant, J.I. Risk estimation and decision-making: Implications of the 1980 BEIR-III Report. (In) Proceedings of the Conference on Radiation Exposure on Pediatric Dentistry, American Academy of Pedodontics, Cincinnati, Ohio, April 1981. Pediatric Dentistry, 3:400-41, 1981. 241. Fabrikant, J.I. Epidemiological studies on radiation carcinogenesis in human populations following acute exposure: Nuclear explosions and medical radiation. (In) Proceedings of the Symposium on Effects on Humans of Exposure to Lov Levels of Ionizing Radiation, Yale University School of Medicine, New Haven, Connecticut Hay 1981. Lavrence Berkeley Laboratory Report LBL-13416, 1981.
1 l Page 30 l 242. Fabrikant, J.I. The effects of lov-level radiation on human health: Epidemiological studies. The Valter V. Herbert Memorial Symposium: Is Lov-dose Radiation Harmful? (In) Diagnostic Radiology 1981. (Margulis, A.R. and Gooding, G.A., eds.) pp. 451-455. University of California, San Francisco, 1981, j i 243. Fabrikant, J.I. and Tobias, C.A. Heavy-fon radiography and cancer. Donner Laboratory, Lavrence Berkeley Laboratory, University of California, Berkeley, PUB-5051. February 1981. 244. Fabrikant, J.I. Impact of the 1980 BEIR-III Report on lov-level radiation: Risk assessment. radiation protection guides, and public health policy. (In) Proceedings, Selected Topics in Reactor Health Physics, Fourth Annual HPS Summer School, Lexington, Kentucky, June 1981. NUKEG/CP-0039, pp. U1-U30, USNRC, Vashington, D.C. , December, 1982. Lavrence Berkeley Laboratory Report LBL-13408,1981. 245. Fabrikant, J.I. Biological effects of ionizing radiation: Epidemiological surveys and laboratory animal experiments. Implications for risk evaluation and decision processes. (In) Proceedings of the Seminaire des Evcluations des Risques et Processus de Decision, National Academy of Sciences-National Research Council (USA) and Mouvement Universal de la Responsibilite Scientifique-Academie MURS, 1983. Francais, Orsay, France, December 17-19, 1980. Lavrence Berkeley Laboratory Report LBL-12555,1981. 246. Fabrikant, J.I. Nuclear energy, public health and public policy. Amer. ' Public Health Assn, Los Angeles,1981. Lavrence Berkeley Laboratory Report LBL-13469, 1981. 247. Fabrikant, J.I. Influence of dose and its distribution in time on dose-response relationships for lov-LET radiations. NCRP Report 64 National CouncilPhysics, Reviev). Health on Radiation Protection 42:392-393, 1981,and Measurements (Book 248. Fabrikant, J.I. Mathematical models and epidemiological surveys: their value in risk assessment of the health effects on populations of exposure to lov levels of ionizing radiation. Lavrence Berkeley Laboratory Report LBL-13348, September 1981. 249. Fabrikant, J.I Nuclear Energy, public health, and public policy. Lavrence Berkeley Laboratory Report LBL-13469. November 1981. 250. Fabrikant, J.I. Is nuclear energy an unacceptable hazard to public health? Lavrence Berkeley Laboratory Report LBL-13586, November 1981. 251. Fabrikant, J.I. Epidemiological studies on radiation carcinogenesis in human populations following acute exposure Nuclear explosions and medical radiation. Yale J. Biol. Med. 54:457-469, 1981. i 252. Holley, V.R. , Tobias, C. A. , Fabrikant, J.I. , Llacer, J. , Chu, V.T. and Benton, 283-293, E.V. Computerized heavy-lon tomography. SPIE Vol. 273, pp. Application of Optical Instrumentation in Medicine IX,1982. Lavrence Berkeley Laboratory Report LBL-12304, 1982. ' i l
f Page 31 253. Fabrikant, J.I. Controversial issues confronting the BEIR-III Committee---implications for radiation protection. Thirteenth Annual National Conference on Radiation Control, Lit tle Rock, Arkansas, May 1981. Lavrence Berkeley Laboratory Report LBL-13444, 1981. (In) Proceedings, pp 60-80, U.S. Department of Health and Human Services, USPHS, FDA, Vashington, D.C., 1982. 254. Fabrikant, J.I. and Lyman, J.T. Estimates of radiation doses in tissues and organs and risk of excess cancer in the single-course radiotherapy patients treated for ankylosing spondylitis in England and Vales. Lavrence Berkeley Laboratory Report LBL-13999, February 1982. 255. Fabrikant, J.I. and Hilberg, A.V. Cost-benefit analysis in decision making for diagnostic radiology. Lavrence Berkeley Laboratory Report LBL-14000, February 1982. 256. Fabrikant, J.I. Radiation carcinogenesis in man: Influence of dose-response models and risk projection models in the estimation of risk coefficients following exposure to lov-level radiation. Lavrence Berkeley Laboratory Report, LBL-14016, February 1982. 257. Fabrikant, J.I. Decision-making and radiological protection at Three Mile Island: Response of the Department of Health, Education, and Velf 1982.are. Lavrence Berkeley Laboratory Report, LBL-14021, February 258. Holley, V.R. , Fabrikant, J.I. , Tobias, C. A. , and Benton, E.V. The physics of heavy-lon radiography and heavy-ion computerized tomography. Lavrence Be:keley Laboratory Report LBL-14316, March 1982. 259. Fabrikant, J.I. Risk estimation and decsion-making: The health effects on population of exposure to lov levels of ionizing radiation. Pediatric Dentistry 3:400-413, 1982. 260. Fabrikant, J.I. Estimation of risk of cancer induction in populations exposed to lov-level radiation. Invest. Radiol. 17:342:349, 1982. 261. Fabrikant, J.I., Holley, V.R., McFarland, E.V., and Tobias, C.A. e Heavy-lon radiography and heavy-lon computed tomography. Lawrence Berkeley Laboratory Report LBL-14001, February 1982. 262. Fabrikant, J.I. Radiation carcinogenesis in man: Influence of 3 ' dose-response models and risk projection models in the estimation of risk coefficients folloving exposure to lov-level radiation. (In) Proceedings Third International Symposium: Society for Radiological Protection. Radiological Protection---Advances in Theory and Practice, Vol. 1. pp. 175-180, Inverness, Scotland, 1982. 263. Fabrikant, J.I., Holley, V.R., McFarland, E.V., and Tobias, C.A. Heavy-lon radiography and heavy-lon computed tomography. (In) Proceedings, Third International Symposium: Society for Radiological Protection, Radiological Protection---Advances in Theory and Practice, Vol. I, pp. 175-180, Inverness. Scotland, 1982.
Paga 32 264. Fabrikant, J.I. and Lyman, J.T. Estimates of radiation doses in tissues and organs and risk of excess cancer in the patients treated for ankylosing spondylitis in England and Vales. (In) Proceedings, Third International Symposium: Society for Radiological Protection. Radiological 428-435, Inverness, Scotland, 1982. Protection---Advances in Theory and Practice, Vol. I, pp. ' 265. Fabrikant, J.I. and Hilberg, A.V. Cost-benefit analysis in decision l 4 making for diagnostic radiology. (In) Proceeedings Third International Symposium: Society for Radiological Protection. Radiological 428-435, Inverness, Protection---Advances Scotland, 1982. in Theory and Practice, Vol. I, pp. 266. Fabrikant, J.I. Decision-making and radiological protection at Three Mile Island: Response of the Department of Health, Education, and Velfare. (In) Proceedings Third International Symposium: Society for Radiological and Practice, Protection. Radiological Protection---Advances in Theory Vol. II, pp. 756-763, Inverness, Scotland,1982. i 267. Fabrikant, J.I. The health ef fects in women exposed to lov levels of ionizing June, radiation. Lavrence Berkeley Laboratory Report LBL-14198, 1982. 268. Fabrikant, J.I. The BEIR-III Report and its implicatiens for radiation protection and public health policy. (In) Radiation Protection, A Syteaatic Oxford, Approach to Safety, Vol. I, pp. 1213-1232 Pergamon Press, 1981, 269. Fabrikant, J.I. 4 Carcinogenesis and lov level ionizing radiation with ' special reference to lung cancer and exposure to radon daughters. Lavrence Berkeley Laboratory Report LBL-14772, April 1982. e 270.
- Benton, E.V. , Henke, and Henshav, D.L. R.P. , Tobias, C. A. , Holley, V.R. , Fabrikant , J.I. ,
Charged particle radiography and computed tomography. (In) Solid State Nuclear Track Detectors, Fowler, P.H. and Clapham, V.M., eds., pp. 661-666, Pergamon Press, Oxford, 1982. ' 271. Fabrikant, J.I. Vomen and ionizing radiation: Sex- and age-dependency j affecting 1982. risks of lov-level exposure. (ab). Health Phys., p. 75, June , ] 272. Hosobuchi, Y. , Fabrikant , J.I. , and Lyman, J.T.
- Stereotactic 1
heavy-particle irradiation of intracerebral arteriovenous j malformations (AVM). (ab) 28th Annual Meeting, Vestern Neurological Society, San Francisco, September 1982. ' 273. Holley, V.R., Fabrikant, J.I., Tobias, C.A., and Benton, E.V. The I physics of heavy-lon radiography and heavy-lon computed tomography. (In) Proceedings of the International Vorkshop on Physics and Engineering Angeles, 1982. in Medical Ir. aging, IEEE, Computer Society Press, Los l l i i i
\
l
. Page 33 274.
Fabrikant, J.I. Epidemiological Studies on radiation carcinogenesis in human populations folloving acute exposures Nuclear explosions and medical radiation. Lavrence Berkeley Laboratory Report LBL-13416 (Revised), August 1982. 275. Tobias, Holley, C. A. , Chu, V. , Cha t terj ee, A. , Benton, E.V. , Fabrikant, J.I. , V.R., Schmidt, J., Blakely, E., and Hayes, T.L. Special topics in heavy lon research. (In) Pion and Heavy-Ion Radiotherapy: Preclinical and Clinical Studies. pp. 169-193, Skarsgaard, L., ed. Elsevier Science Pubishing, New York / Amsterdam, 1982. 276. Fabrikant, J.I. The effects of the accident at Three Mile Island on the mental health behavioral responses of the general population and nuclear vorkers. Health Phys. 45:579-586, 1983. 277. Fabrikant, J.I. ! Is nuclear energy an unacceptable hazard to health? Health Phys. 45:575-578, 1983. ' f 278. Fabrikant, J.J. Phys. 46:739-744, Nuclear 1983.energy, public health and public policy. Health 279. Fabrikant, J.I. Radiation and health. Vest. J. Med. 138:387-390, 1983. 280. Fabrikant , J.I. , Lyman, J.T. , and Ensobuchi, Y. Stereotactic heavy-lon Bragg peak radiosurgery for intracranial vascular disorders: Method of treatment for deep arteriovenous malformations. Brit. J. Radiology 57:479-490, 1984. 281. Voodruf f, K.H.J.I. Fabrikant, , Lyman, J.T. Lavrence, J.H. , Tobias, C. A, Born, J.L. , and Pathol. 15:48-54, Delayed 1984. sequelae of pituitary irradiation. Human 282. Lyman, J.T. , Fabrikant, J.I. , and Frankel, K. A. Charged-particle stereotactic 1107-1110, 1985. radiosurgery. Nuclear Instruments Methods B 10/11: i i I 283. Fabrikant, J.I. , Lyman, J.T. , and Hosobuchi, Y. Stereotactic heavy-ion i l I Bragg peak radiosurgery for intracranial vascular disorders. (In) Neurosurgery. Vilkins. R.H., ed., pp. 1128-1132, McGrav-Hill, Nev t York, 1985. 284. . Hecht, Norman,S.T. D.,
, Fabrikant, J.I. , Lyman, J.T. , Frankel, K. A. , Newton, T.H. ,
and Brant-2avadzki, H.N. Stereotactic heavy-icn Bragg peak radiosurgery for treatment for treatment of deep arterio-venous l malformations. Amer. Soc. Neuroradiology, New Orleans, February,1985. ( ) 285. O'Donohue, J. , Marshall, V.H. , Enzmann, D.R. , Fabrikant, J.I. , and l l Silverberg, G.D. i The AVH vascular steal phenomenon demonstrated by the xenon CT blood flov method. Amer. Soc. Neuroradiology Nev ' Orleans, February 1985. ! l 286. Fabrikant , J.I. , Lyman, J.T., and Frankel, K. A. Heavy charged-particle i Bragg { Res., peak radiosugery1985. 104:S-244-S-258, f or intracranial vascular disorders. Radiat. I l i c-.. - - _. - _ _ ___ , _ - - - _ _ _ .__- -____ _ _ - _ _ - - - _ - - - _ . _ _ -
f . I Page 34 i 287. Lyman, J.T., Kanstein, L., Yeater, F., Fabrikant, J.I., and Frankel, K.A. A hslium-ion beam for stereotactic radiosurgery of central nervous system disorders. Medical Phys. 13:695-699. 1986. 288. Fabrikant, J.I. Radiation Hordiesis. Report to Comr.d t t ee 1 of the International Israel, Commission November 1986. on Radiological Protection. 4 pp., Jerusalem, 289. Fabrikant, J.I. , Land. C.E. , Schull, V.J. Risk Coefficient for Radiation-Inductd Bladder Cancer. Report to Committee 1 of the : International Commission en Radiological Protection. 8 pp. Jerusalem, Israel, November 1986. 290. Glicksman, A.S., Fcbrikant, J.I. Analysis of post-irradiation sarcomass correlation of clinical data with experimental results. (In) International Symposium on Biological Effects of Lov Level Radiation. Vei, L. , Vu, D.C. , Vang, X.H. , eds. , pp. 4-22. Society of Radiological Medicine and Protection, Chinese Medical Association, Nanjing, China, 1986. 291. Fabrikant, J.I. Application of consensus reports used in litigation --- BEIR, NCRP, ICRP. (In) Basic Concepts of Radiation for Attorneys. l Ricks, R., ed. REAC/TC Oak Ridge Associated Uriversities, Oak Ridge, Tennessee, 1986. , 292. Glicksman, A.S. and Fabrikant, J.I. Analysis of post-irradiation t sarcomas: Correlation of clinical data vith exprimental results. (In) Proceedings, International Symposium on Biological Effects of Lov Level Radiation. Vel, L., Vu, D.C., Vang, J.X.H., Eds., pp. 124-142, Nanjing, China, 1987. . I 293. Fabrikant, J.I. Adaptation of cell reneval systems under continuous irradiation. Health Phys. 52:561-570, 1987. [' 294. Fabrikant, J.I., Frankel, K.A., Phillips, M.H., Lyman, J.T. Foster, M.L. Heavy chargid-particle Bragg peak stereotactic radiosurgery for ; intracranial vascular disorders. (In) Radiation Research, Fielden. E.M., Fowler, J.F., Hendry, J.H., Scott, D., : Taylor & Francis, London, 1987. eds., (ab) Vol. 1 p. 323, l t 295. Phillips, M.H., Tobias, C.A., Frankel, K.A., and Kuhl, T. Fabrikant, J.I., Kraft G., [ Induced electrical birefringence measurements of DNA strand breaks in SV 40 virus. (In) Radiation Research Fielden, E.M., ' Fowler, J.F. , Hendry, J.H. , Scot t , D. , eds. , (ab) Vol 1. , p. 320, Taylor & Francis, London, 1987. ' l 296. Fabrikant, J.I., Ellett, V.H., Cooper, R.D., Brovn, S.L. The 1987 BEIR l IV Reporti Internally deposited alpha emitters. (In) Radiation Research, Fielden, E.M., Fowler, J.F., Hendry, J.H., Scott, D., eds., (ab) Vol.1, p. 356, Taylor & Francis, London,1987. LBL-24173,1987. j 297. Frankel, K. A. , Phillips, M.H. , Lyman, J.T. , and Fabrikan t , J.I. ! Treatment planning for stereotactic radiosurgery for intracranjstl i i
Pega 35 vascular disorders. (In) Radiation Research, Fielden, E.M., Fovler, J.F., hendry, J.H., Scott, D., Francis, London, 1987. eds., (ab) Vol. 1, p. 77, Taylor & 298. Rosander, K., Frankel, K.A, Cerda, H., Fabrikant, Fabrikant, J.I. I.B., Lyman, J.T. and DNA damage of the endothelial cells of the mouse brain after E.M., Fovler,heavy ion irradiation. (In) Radiation Research, Fielden, J.F., Hendry, J.H., Scott, D., 322, Taylor & Francis, London,1987. eds., (ab) Vol. 1, p. 299. Phillips, M.H. , Tobias, C. A. , Ludevigt, B., Vong, H. Schimmerling, V., Frankel, K.A., and Fabrikant, J.I. Multiple scattering of fast heavy ion beams for biomedical uses. (In) Third Vorkshop on Heavy Charged Particles in Biology and Medicine, Kraf t, G. , Grundinger, U. , eds. , (ab) GSI Report CSI-87-11, July 1987. 300. Rosander, K. Frankel, Cerda, K.A., H., Fabrikant, I.B., Lyman, J.T., Fabrikant, J.I. DNA damage in the endothelial cells of the mouse brain after heavy ion irradiation. (In) Radiation Research, Fielden. E.M., Fowler, J.F. , Hendry, J.H. , Scot t , D., (eds.) vol. 1, pp. 322 Taylor
& Francis, London, 1987.
301. Marks, K.A.,H.P. , DeLaPaz, R.L. , Enzmann, D.R. , Fabrikant, J.I. , Frankel, Phillips, M.H., Levy, R.P. Imaging of charged particle stereotactic radiosurgery for intracranial vascular malfo;eations. (ab) Radiological Society of North America, Chicago, IL, (if press, 1987). 302. Marks, H.P. , DeLaPaz, R.L. , Enzmann, D.R. Fabrikant, J.I. Imaging of heavy-ion Bragg peak radiosurgery for intracranial arteriovenous malformations. (ab) Vestern Neuroradiology Society, 1987. 303. Fabrikant, J.I. The Chernobyl disaster An internaticnal perspective. Industrial Crisis Quart., 1:1-10, 1988. 311. Harks, H.P., DeLaFar, R.L., Enzmann, D.R., Fabrikant, J.I., Frankel, K.A., Phillips H.H., Levy, R.P. Imaging of charged particle stereotactic radiosurgery for intracranial vascular malformations. (ab) Radiological Society of North America, Chicago, IL, (in press, 1987). 304. Fabrikant, J.I. Estimation of risks of radiation-induced cancer in exposes human populations --- technical difficulties and uncertainties. (In) Proceedings, International Symposium on Biological Effects of Lov Level Radiation. Vel, L., Vu, D.C., Vang, J.X.H., eds., pp. 101-123, Nanjing, China, LBL-24395, 1988. 305. Fabrikant, J.I. Radon and lung cancer risks: implications for radiological protection. Toronto, 1987 submitted, Presented, Soelety of Nuclear Medicine, J. Nucl. Hed., 1988, LBL-24393, 1988. 306. Fabrikant, J.I. Application of consensus reports used in radiation litigation: Ricks, R., 1987. (In) Basic Concepts of Radiation for Attorneys. Tennessee, ed., REAC/TC, Oak Ridge Associated Universities, Oak Ridgc, 1987. LBL-24391, 1988.
Page 36 307. Fabrikant, J.I. Particle beams for brain studies. Lavrence Berkeley Laboratory. TID (Submitted J. Nucl. Med., 1988) 308. Fabrikant, J.I., Bond, V.P., Modan, B., and Upton, A.C. Probability of causation. Report to Committee 1 of the International Commission on Radiological (in press, 1988). Protection. 33 pp. Jerusalem, Israel, November 1986, LBL 309. Fabrikant, J.I. Probability of Causation: Implications for radiological protection and dose limitation (In) Proceedings Annual Conference, Canadian Radiation Protection Association, Saskatoon, Saskatchavan, 1987 (in press). LBL-24392, 1988. 310. Fabrikant, J.I. Radiation effects on sking Implications for radiological control and radiation protection. Presented, Health Physics Society, Salt Lake City, Utah,1987 (submitted to Health Physics,1988). LBL-24389, 1988. 311. Fabrikant, J.I., Frankel, K.A., Phillips, M.F. and Foster, M.L. Heavy charged-partic1r a tgLevy, R.P. , Lyman, J .T. , peak stereotactic radiosurgery for intracranial arteriovr m $ me1 formations. (In) Third Workshop on Heavy Charged Particle in e.-logy and Medicine, Kraft G., Grundinger, U., eds., (ab). CSI Report GSI-87-11, July 1987. LBL-34390, 1988. 312. Fabrikant, J.I. Health effects of radon and other internally-deposited alphr-emitters: BEIR IV Chinese Journal of Radiation Medicine and Radiological (in press, 1988). Protection (in Chinese, transl. by Prof. Chen Xing-an) i , 313. Fabrikant, J.I., Ellett, V.H., Cooper, R.D., Brovn, S.L. The 1987 BEIR j Report: Alpha Emitting Radionuclides. (In) Proceedings, Eighth International Congress of Radiation Research, Fielden E.M., Fowler, J.F. , Hendry, J.H. , Scot t, D. , eds. , Taylor & Francis, London,1987, LBL-24178, 1988. 314. Ellett, V.H.. Fabrikant. J.I., Cooper, R.D. The BEIR IV Committee estimates of lung cancer rortality associated with exposure to raden progeny. (In) Proceedings The Fourth International Symposium on the Natural Radiation Environment, December 7-11, 1987, Lisbon. (in press, 1988). 315. Marks, M.P. , PetaPaz, R.L. , Fabrikant , J.I. , Frankel, K. A. , Phillips, M.H. , Levy, R.P. , Enzmann, D.R. Imaging of charged-particle radiosurgery for intracranial arteriovenous malformations. Submitted to Radiology. (in press, 1988). 316. Marks, M.P. , O'Donahue, J. , Fabrikant , J.I . , Frankel, K. A. , Phillips, M.H. , DeLaPaz, R.L., Enzmann, D.R. Cerebral blood flov evaluation of arteriovenous malformations with stable xenon computed tociograph). Submitted to Neuroradiology (in pres', 1988).
t . Page 37 I 317. Steinberg, G.K. , Silverberg, C.D. , Fabrikant , J.I. , Shuer, L.M. , Frankel, K. A. , Phillips, M.H. , Levy, R.P. , Marks, M.P. Preliminary results of heavy particle radiation for arteriovenous malformations of the brain. (ab) 13th International Joint Conference on Stroke and Cerebra circulation, San Diego, (in press, 1988). ! i 318. Fabrikant, J.I. Health effects of radon and other internally-deposited alpha-emitters: BEIR IV Chinese Journal of Radiation Medicine and ' Radiological (in press, 1988).Protection (in Chinese, transl. by Prof. Chen Xing-an) i l 1 i i l 6 I i t i 6 l l I
?
Pagt 38 BOOKS AND CHAPTERS
- 1. Fabrikant, J.I.
Studies on Cell Proliferation in the Regenerating Liver and the Effect of Prior Continuous Irradiation. Ph.D. Thesis, University of London, London, 1964.
- 2. Fabrikant, J.I. and Donner, M.V., eds. Russell H. Morgan, A Tribute, duPont, Vilmington, Dslavare, 1967.
- 3. Fabrikant, J.I.
of Irradiation.The Effects of Continuous Irradiation. (In) Pathology Berdjis, C.C., ed., Chapter 4, pp. 50-85. Villiams and Vilkins, Baltimore, Maryland, 1971.
- 4. Fabrikant, J.I.
The Effects of Irradiation on the Kinetics of Proliferation in Cell Reneval Systems. (In) CRC Critical Reviews in Radiological Sciences. Vang, C., ed. Vol. 2, pp. 525-576, CRC Press, Cleveland, Ohio, 1971.
- 5. Fabrikant, J.I. Radiobiology.
Illinois, 1972. Year Book Medical Publishers, Chicago,
- 6. Fabrikant, J.I.
The Kinetics of Cell Proliferation in Normal Tissue, Malignant Tumors of the Upper Air Passages. (In) The Biological and Clinical Basis of Radiosensitivity. Friedman, M. , ed. , Chapter 13, pp. 274-313, Charles C. Thomas Publishers, Springfield, Illinois, 1974.
- 7. Casarett, G., Abrahamson, S., Alpen, E.L., Baram, M.S., Brovn. J.M.,
Comar, C.L. , Eden M. , Falk, H.L. , Gregg, E.C. , Hut chison, G.B. , Fabrikant , J.I. , Kru tilla, J.V. , Levis, E.B. , Ne tschert, B.C. , Rall, D.P. , Rall, J.E. , Russell, V.L. , Smi thers, O. , Upton, A.C. Considerations of Health Benefit-Cost Analysis for Activities Involving Iontring R9diation Exposure and Alternatives ~. A Report of i Advisory Committee on the Biological Ef fects of Ionizing Radiations. j National D.C., Research Council, National Academy of Sciences, Vashington, 1977. i
- 8. Fabrikant, J.I.
Safety in Diagnostic Ultrasound. (In) CRC Critical Reviews in Diagnostic Imaging. Vang, C., ed. Vol.10, pp. 219-234, CRC Press, Cleveland, Ohio, 1977.
- 9. Fabrikant, J.I., ed. Report of the Public Health and Safety Task Force of i,
' The President's Commission on The Accident at Three Mile Island.
Government Printing Office, Vashington, D.C., October 1979. 10. l Fabrikant, J.1. Summary of the Public Health and Safety Task Force Report to The President's Commission on The Accident at Three Mile Island. 32 pp. Government Printing Office, Vashington, D.C., 1979. '; 11. Axelrod, D. , Blues tone, M. , Densen, P.P. , Fabrikant J.I. , Fovinkle, E.V., Johnson, K.G., Jones, E.V., and Seltser, R. Technical Staff ' Analysis Report on Fublic Health and Epidemiology. (In) Report of the Public Health and Safety Task Force Report to The President's i i e
(. Page M i i Commission on The Accident at Three Mile Island. 132 pp.. Government Printing Office, Vashington, D.C., 1979.
- 12. Abrahamson, S. , Balr, '1.J. , Bender, M. A. , Bloom, A.D. , Bond, V.P. ,
Casarett, G.V., and Fabrikant, J.I. Technical Staff Analysis Report onReport of the Radiation Health Effects Task Group. (In) Report of , the Public Health and Safety Tack Force Report to The President's Commission on The Accident at Three Mile Island. 98 pp. Government . Printing Office, Vashington, D.C., 1979. t i
- 13. Auxler, J. A. , Berger, C.D. , Eisenhauer, C.M. , Gesell, T.F. , Jones, A.R. , i and Masterson, cf.E. Report of the Task Group on Health Physics and I Dosimetry. (In) Report of the Public Health and Safety Task Force to The President's Commission on The Accident at Three Mlle Island (Fabrikant, J.I., ed.) 196 pp. Government Printing Office, i Vashington, D.C., 1979.
- 14. Dohrenvend, B.P. , Dohrenvend, B.S. , Fabrikant, J.I. , Kasl, S.V. , and Varheit, G.J. Technical Staff Analysis Report on Behavioral Effects.
(In) Report of the Public Health and Safety Task Force to The; President's Commission on The Accident at Three Mile Island ; (Fabrikant, J.I., ed.) 81 pp. Government Printing Office, Washington, D.C., 1979.
- 15. Radford, E.!'. , Abrahamson, S. , Beebe, G.V. , Bender, M. A. , Brdl, A.B. ,
Brovn, R.F. , Cleary, S.F. , Comar, C.L. , Dennis ton, C. , Fabrikant J.I. , Ingram. M., Land, C.E., Mays, C.V., Moeller, D.V., Parker, D.R., Rossi, H.H. , Russell, L.B., Russell, V.L. , Selby, P.B. , Sloan, M.H. , 3 I Trimble B.K. , Vebster, E.V., and Vellman, H.N. The Effects on ! Populations of Exposure to Lov Levels of Ionizing Radiation: 1980. National Academy of Sciences-National Research Council, National I Academy Press, Vashington, D.C., 1980.
- 16. Fabrikant, J.I. , Beebe, G.V. , Bender, M. A. , Brill, A.R. , Land, C.E. , t Moeller, D.V., and Webster E.V. Estimating the Total Cancer Risk of Lov-Dose, Lov-LET, Whole-Body Radiation. Chapter V., Section 3. (In) .
The Ef fects on Populations of Exposure to Lov Levels of Ionizing ( Radiation: 1980. Report of the Committee on Biological Effects of ! Ionizing Radiations, pp. 176-226, National Academy of l Sciences-National Research Council, National Academy Press, l Vashington, D.C., 1980.
- 17. Lyman, J.T., Ainsvorth, E.J., Alpen, E.L., Bond, V.P., Curtis, S.B.,
Fabrikant , J.I. , Fry, R.J.M. , Jackson, K.L. , Nachtvay, S. , sondhaus, C., and Tobias, C.A. Ionizing Radiation Risks to Satellite Pover ' Systems (SPS) Vorkers in Space. DOE / NASA Satellite Pover System Concept Development and Evaluation Program, LBL Berkeley, CA, DOE /ER-0094, 1980. i
- 18. Volff, S., Bender, M.A., Breven, J.G., Fabrikant, J.I., Greenberg, B.G.,
Lagakos, S.V. , Mendelsohn, M.L. Schull, V.J. , and Vel, L.J. ; Evaluation of Portsmouth Naval Shipyard Cytogenetics and i Spermatogenesis Protocol. National Academy of Sciences-National ; Research Council. National Academy Press, Vashington, D.C., 1982. ; i
.i l
. Page 40 19. Mos teller F. , Fabrikant , J.I. , Fry, R.J.M. , Lagakos, S.V. , Miller, A.B. , Saenger, E.L. , Schot tenfeld, D. , Scot t , E.L. Van Rytin, J.R. , and Vebster, E.V. Assigned Share for Radiation as a Cause of Cancer. Reviev of Assumptions and Methods for Radioepidemiologic Tables. National Academy of Sciences-National Research Council, National Academy Press, Vashington, D.C., 1984. 20. Mos t eller, F. , Fabrikant , J.I. , Fry, R.J.M. , Lagakos, S.V. , Hiller, A.B. , Saenger, E.L. , Schot tenfeld, D. , Scot t, E.L. , Van Ryzin, J.R. , and Vebster, E.V. Assigned Sh6re for Radiation as a Cause of Cancer. Reviev of Radioepidemiologic Tables Assigning Probabilities of Causation. D.C.,Press, National Academy National Academy of1985. Vashington, Sciences-National Research 21. Goldman, M. , Anspaugh L. , Catlin, R.J. , Fabrikant , J.I. , and Gudiksen, P. The Nuclear Reactor Accident at Chernobyl. Interim Report of the Committee on Assessment of Radiological Effects and Consequences. Prepared for the Office of Health and Environmental Research, U.S. Department of Energy, Vashington, D.C., July 1986. 22. Goldman, M. , Anspaugh, L. , Catlin, R.J. , Fabrikant , J.I. , and Gudiksen, P. Assessment of the Dosimetric and Health Implications of the Chernobyl Reactor Accident. Interim Report of The Committee on the Assessment of Radiological Effects and Consequences (CAREC). Prepared for The Of fice of Health and Environmental Research, U.S. Department of Energy, Vashi'igton, D.C. , August 1986. 23. Goldman, P. M. , Anspaugh, L. , Catlin, R.J. , Fabrikant, J.I. , and Gudiksen, Health and Environmental Consequences of the Chernobyl Nuclear Power Plant Accident. Report to the United States Department of Energy from the Interlaboratory Task Group on Health and Environmental Aspects of the Soviet Nuclear Accident. Prepared by the Cor.mit tee on the Assessment of Health Consequences in Exposed Populations. U.S. Department of Energy, Vashington, D.C., January 1987. 24 Fabrikant, J.I., Bair, V.J., Bender, M.A., Bor'..t. C. , Ccoer P., J. , Huir Lubin, Vaxveller, D.R. , Pierce, D. Roesch, V. , Samei, J. , Schlender, R. , and Deposited Alpha-Emitters:The Health BEIR IV. Effects of Radon and Other Internally National Academy of Sciences-National Research Council National Academy Press, Vashington, D.C., 1988,
- 25. Fabrikant, J.I., Frankel, K.A., Phillips, M.H., and Levy, R.P.
Stereotactic heavy charged particle Bragg peak radiosurgery for intracranial vascular malformations. (In) Vol. 2. Cerebral Vascular Diseases in Childhood and Adolescence. H.J., Edvards, H.S.B and Hoffman, eds. , Villiams I, Vilkins, Baltimore, Maryland,1988 (in press).
c e 9 7 GPU Nuclear Corporation kUC1GM Post Office Box 480 Route 441 South Middletown, Pennsylvania 17057 0191 717 944 7621 TELEX 84 2386 Writer's Direct Olal Number: (717) 948-8461 October 7, 1988 4410-88-L-0168/0428P US Nuclear Regulatory Commission Attn: Document Control Desk
!!ashington, DC 20555
Dear Sirs:
Three Mile Island Nuclear Station, Unit 2 (TMI-2) Operating License No. DPR-73 Docket No. 50-320 Processed Water Disposal System Technical Evaluation Report Attached for your review and approval is a copy of the Processed Water Disposal System Technical Evaluation Report. The purpose of this report is to provide a description of the processed water disposal system and its interfaces with other plant systems; to provide a technical evaluation of the system's conformance to applicable codes, standards, and regulatorv reouirements; and to provide a safety evaluation of the system and its operation. This report concludes that the Processed Water Disposal System does not constitute an unreviewed safety Question and that the system can be operated as designed without undue risk to the public health and safety. Further, it concludes that the envirornental irtpacts of the system operation and potential accidents involving the system fall within the bounds of activities previously evaluated by the NRC staff in their Prograrcatic Environmental Impact Statecent and its supplements. Per the reouirements of 10 CFR 170, an application fee of $150.00 is enclosed. Sincerely,
/s/ M. B. Roche M. B. Roche Director, TMI-2 .
DHW/m!<k
Enclosure:
GPU Nuclear Corp. Check No. 01755 GPU Nuclear Corporation is a subsidiary of the General Public Utilities Corporation
Docu5ent Control Desk October 7, 1988 '. 4GO-88-L-0168 cc: R. J. Conte - Senior Resident Inspector, TMI W. T. Russell - Regional Administrator, Region I J. F. Stolz - Director, Plant Directorate IV L. H. Thonus - Project Manager, THI Site -
GPU NUCLEAR TER 3232-019 REY. O ISSUE DATE_ October 10, 1988
/ X/ ITS
/ / NSR
/ / NITS DIVISION TECHNICAL EVALUATION REPORT FOR PROCESSED WATER DISPOSAL SYSTEM Cognizant En0ineer --> - J Date M . 7 s g RTR 3%__ - /I/ II _* m Date /o.7-PP COG ENG MGR, < m- Date /o -7.- BB DOCUENT PAGE 1 0F 38
l GPU NUCLEAR l No. 3232-019 Rev. O
Title:
Technical Evaluation Report for the l Processed Water Disposal System l Pace 2 of 38 I I I , Rev. I
SUMMARY
OF CHANGE I Approval i Oate i I I O l Initial Issue for Use i I l l l l l l l l l l l l l l l l l l l l l l 1 1 I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I i 1 I I I I I I I I I l l I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I , 1 I l I I I 0225H/13H
TER 3232-019 Revo O Page 3 of 38 TABLE OF CONTENTS
- g. TION PAGE 1.0 INTRODUCB ON 5 1.1 Backgtnund 5
1.2 Purpose and Scope
5 t 2.0 SYSTEM DESCRIPTItN 6 2.1 General 6 2.2 Mr.in Evaporator 6 2.3 Auxiliary Evaporstor 8 2.8 Flash Vaporizer 8 . 2.5 Blender /Oryer 9 l 2.6 Packaging System 9 2.7 Ancillary Equipment 10 l 2.7.1 Enclosure Building 10 1 2.7.2 Cooling Water System 11 2.7.3 Electrical System 11 2.7.4 Plant System Tie-ins 11 2.7.5 Fire Protection 12 j 3.0 SYSTEM OPERATION AND CONTROL 12 3.1 General Operation 12
- 3.2 Operational Modes 13 i
3.2.1 Coupled Operation 13 3.2.2 Decoupled Operation 15 3.3 Influent Limits 16
- 3.4 System Instrumentation and Control 19 3.4.1 Liouid Level Controls 19 .
. 3.4.2 Flow Measurements 20 3.4.3 Conductivity Monitors 20 3.4.4 Radiation Monitor 21 3.4.5 Other Instrumentation 22
4.0 TECHNICAL EVALUATION
23 4.1 Codes, Standards, and Engineering Specifications 23 4.2 System Response to Upset Conditions 26 4.2.1 Loss of Electrical Power 26 4.2.2 Loss of Service Air 26 4.2.3 Tank or Pipe Rupture 26 4.2.4 Severe Weather Conditions 27 0225H/13H
TER 3232-019 Rev. O Page 4 of 38 TABLE OF CONTENTS (Continued) SECTION PAGE S.0 ENVIRONMENTAL AND RADIOLOGICAL ASSESSMENT 27 5.1 Environmental Assessment 27 5.2 Radiological Assessment 30 5.2.1 Of f-si te 30 5.2.2 On-site Occupational Exposure 31 6.0 SAFETY EVALUATION 32 TABLES AND FIGURES Table 1 - Identification of Radionuclides in the Processed Water 34 Table 2 - Processed Water Disposal System Influent Limits and the Resulting Environmental Release Rates 35 Figure 1 - Evaporator Flow Block Diagram 36 Figure 2 - Site Plan Showing Location of the Processed Water Disposal System 37 ATTACHMENTS (3) Figure 3 - Piping and Instrument Diagram, Plant System Tie-in Figure 4 - Piping & Instrument Diagram, Processed Water Disposal System Figure 4a - List of Speciality Symbols 38 0225H/13H
TER 3232-019 Revo O Page 5 of 38
1.0 INTRODUCTION
1.1 Background The TMI-2 accident resulted in the production of large volumes of contaminated water. Direct releases of reactor coolant during the accident filled the reactor building basement to a depth of about 3-1/2 feet. In the two years following the accident, cdditional water was added to this inventcry by primary coolant leakage and inleakage of river water through the reactor building air coolers. In 1980, an agreement was executed between the City of Lancaster, Pennsylvania, GPU Nuclear Corporation, and the Nuclear Regulatory Comission (NRC) which prevented discharge or disposal of this accident generated water, even after treatment to reduce its radionuclide content to within regulatory limits, prior to an environmental evaluation by the NRC. In mid 1981, treatment of this water through the Submerged Demineralizer System (SDS) and EPICOR II System was begun. Since 1981, the total inventory of this accident generated water has increased to the current volume of 2.15 million gallons due to continued additions from defueling and decontamination activities and condensation from the reactor building air coolers. With the projected additions to this volume of water through the end of the defueling and decontamination of the facility, the total volume of water that will require disposal is anticipated to be about 2.3 million gallons. Most of this accident generated water has already been processed to very low levels of radionuclide contamination and is commonly referred to as Processed Water. This water is continuously recycled for use in cleanup activities and is subsequently reprocessed. Some of the water, such as the approximate volume of 66,000 gallons in the reactor coolant system, will require some form of processing prior to disposal. The method of disposal that is proposed is to process the water through a closed cycle evaporator, reheat the purified distillate, and discharge it as a vapor containing essentially all of the tritium and a small fraction of the particulate contamination to the atmosphere in a controlled and monitored manner via a 100 ft high exhaust stack. The remaining particulate contamination will be concentrated in the evaporator bottoms, collected, and further concentrated to a dry solid that can be shipped off-site for disposal by burial at a commercial low level radioactive waste facility.
1.2 Purpose and Scope
The purpose cf this report is to provide a description of the processed water disposal system and its interfaces with other plant systems; to provide a technical evaluation of the system's conformance to applicable codes, standards, and regulatory requirements; and to provide a safety evaluation of the system and its operation. This report concludes that the Processed Water Disposal System does not constitute an unreviewed safety question and that the system can be operated as designed without undue risk to the 0225H/13H
TER 3232-019 Revo 0 Page 6 of 38 public health and safety. Further, it concludes that the environmental impacts of the system operation and potential accidents involving the system fall within the bounds of activities previously evaluated by the NRC staff in their Programmatic Environmental Impact Statement and its supplements. 2.0 SYSTEM DESCRIPTION 2.1 General The processed water disposal system consists of: (1) a vapor recompression distillation unit (main evaporator) that will distill i the processed water feed in a closed cycle process and collect the i purified distillate for subsequent release by vaporization; (2) an auxiliary evaporator that will further concentrate the bottoms from l the main evaporator; (3) a flash vaporizer unit that will heat and ] vaporize the purified distillate from the other evaporation and drying systems and release the vapor to the atmosphere in a
, controlled and monitored manner; (4) a waste dryer that will further evaporate water from the concentrated waste and produce a dry solid; and (5) a packaging system that will prepare the dry solid waste in containers acceptable for shipment and for burial in a commercial low level radioactive waste disposal site. A block diagram of the process is shown in Figure 1.
2.2 Main Evaporator l The main, or VC-300, evaporator is a vapor recompression type I distiller that can be operated in either a climbing film or spraying film mode. The heating section consists of a horizontal shell and tube type heat exchanger that is 24 inches in diameter and 120 inches long. The heat exchanger is of a patented design known as a Bayonet Augmented Tube (BAT) heat exchanger. The evaporator feed enters the bottom of the heat exchanger shell
. where it is heated to boiling by steam condensing in the tubes. The. ! heated vapors along with a significant Quantity of entrained liquid exits the shell through two 12 inch diameter vapor risers and enters l the separator / vapor dome section. The majority of the entrained liquid is collected in the bottom of the 24 inch diameter separator.
l The remainder of the entrained liquid is removed from the vapor as it
- rises into the vapor dome through two stages of woven wire demister j screens. The liquid collected in the bottom of the vapor dome is i drawn off by a pump along with a portion of the 11auid from the heat j exchanger section and returned to the main (VC-300) concentrate j tank. The dried vapors exit the vapor dome through a 14 inch steam
- line and enter the suction side of a motor driven mechanical vapor i recompressor. The compressor will increase the temperature and l pressure of the steam and discharge it to the tube side of the heat j exchanger in the evaporator heating section. The vapor condenses in 1
(, 0225H/13H
TER 3232-019 Rev. 0 . , Page 7 of 38 l the tubes, giving up its superheat and latent heat to the boiling liquid in the shell. The condensate, or distillate, is removed from i the tubes by a vacuum eductor and discharged to the VC-300 distillate tank. The system is designed to operate under a vacuum and will boil the feed liquid at a temperature of about 150' F. The mechanical vapor recompressor will raise the temperature of the vapor to about 170* F. The compressor will supply all the heat needed for steady state operation, operating on the principal of continuous reclamation , and reuse of the latent heat of vaporization of the steam produced by ,
!, evaporation. The cycle is basically a refrigeration cycle as :
i employed in conventional heat pumps, but it uses water as the heat ' transfer fluid. The heat necessary for system start-up is supplied
, in the form of steam from the auxiliary evaporator which is described
- in Section 2.3.
1 Processed water will be fed to the VC-300 concentrate tank at a rate of no more than 5 gpm. The liquid is moved by vacuum from the coricentrate tank to the evaporator heat exchanger shell at a rate of , about double the evaporation rate. The excess feed is carried over with the vapor, removed in the vapor separator section, and returned : along with a portion of the concentrated liquid from the heat exchanger shell to the concentrate tank for recycle. The liquid level in the heat exchanger shell is maintained high enough to cover i about one third of the heat exchanger tubes. The vigorous foaming action during boiling, which is typical of waste water streams, will i i ensure continuous wetting of the rest of the tubes to provide good : heat transfer characteristics, while the low liquid level in the ! shell provides a low hydrostatic head. If the foaming action is i insufficient to adequately wet the tubes, the system can be operated in a spraying film mode. In the spraying film mode, a portion of the i feed enters the top of the heat exchanger shell and is sprayed over the tubes to provide a constantly wetted film on the heat transfer i surfaces. A small flow, on the order 0.5 gpm for a 5 gpm evaporator feed rate, of the concentrated liquid gravity drains from the VC-300 concentrat.e j ] tank to the auxiliary (C-30) evaporator concentrate tank for further j concentration ind processing. When the VC-300 evaporator is supplied ;
- with processed water containing about 3,000 ppm boron, it will i produce a concentrated solution of about 30,000 ppm boron. The l concentration of other soluble and particulate contaminants, 1 including radionuclides, will be increased by the same proportion. v The final concentration ratios can be varied to suit the pre m sing needs or to optimize the process as experience dictates. The purified distillate will contain nearly all of the tritiated water but will be essentially free of other contaminants since less than '
O.1% of the soluble and particulate contaminants in the processed l water will be carried over in the VC-300 distillate. The distillate i will be collected in the distillate tank for further staging in an ! on-site storage tank or for direct feed to the flash vaporizer, j 0225H/13H l
)
TER 3232-019 Rev. O Page 8 of 38 2.3 Auxiliary Evaporator The auxiliary (C-30) evaporator is similar in design to the VC-300 evaporator, but it is smaller and does not use a vapor recompressor. The heating section is a 6 inch diameter horizontal shell and tube heat exchanger and the separator section is 8 inches in diameter. The auxiliary evaporator is fed by recirculation from its concentrate tank (C-30 concentrate tank) and will further concentrate the 30,000 ppm discharge from the main evaporator to a concentration of between 30 and 50 percent total solids, depending on operational needs. The C-30 evaporator heat exchanger operates on the submerged tube principle with liquid level being maintained by an overflow weir in the discharge end of the shell. The heat source to the auxiliary evaporator is waste heat from the hot distillate in the VC-300 distillate tank supplemented by two thermostatically controlled 30 kW electric heaters. Distillate is pumped from the VC-300 distillate tank through the electric heaters which heat it to about 170*F. It flows to the tube side of the shell and tube heat exchanger portion of the auxiliary evaporator where it heats the boiling liquid on the shell side. The distillate then exits the tubes and returns to the VC-300 distillate tank. During system start-up, vapor from the auxiliary evaporator is used to provide a heat source to the main
- evaporator. Once the main evaporator is heated up and in operation, a valve in the vapor line to the main evaporator is closed and the vapors are routed to the auxiliary condenser. The condensate is removed from the condenser by an eductor and discharged to the C-30 distillate tank. It is then transferred by pump to the VC-300 concentrate tank for reprocessing. A portion of the concentrated l liquid is pumped from the C-30 concentrate tank to the blender / dryer transfer tank for subsequent drying and packaging.
1
- 2.4 Flash Vaporizer i The flash vaporizer will perform the final evaporation of the l purified distillate and will release the resultant vapor to atmosphere through a 100 foot high exhaust stack. Distillate will be J
pumped to the system at a rate of no more than 5 gpm. It will enter, ' the system flow stream at the suction of a 500 gpm recirculation pump. The recirculation pump forces water through three 300 KW electric heaters where the temperature and pressure are raised to , about 240' F and 10 psig respectively. The heated water discharges through a bleed / orifice valve into the 24 inch diameter by 60 inch high cylindrical flash tank where the reduced pressure results in immediate vaporization of a portion of the heated water. The vapors exit the top of the tank through a 10 inch thick demister screen into a 3 inch diameter by 100 foot high exhaust stack and are released to
- the atmosphere. A small amount of liquid will be drained from the flash tank as a continuous blowdown and returned to the VC-300 concentrate tank. Any condensate that forms in the exhaust stack will be drained through a steam trap to the VC-300 distillate tank.
0225H/13H
TER 3232-019 Rev. O Page 9 of 38 2.5 Blender / Dryer a The blender / dryer will receive the liquid or slurry product from the
- auxiliary evaporator at a concentration of 30 to 50 percent total solids, evaporate the remaining water, and produce a dry solid waste. The water removed by the dryer in the form of vapor will be condensed in a heat exchanger and returned to the VC-300 concentrate tank for reprocessing. The body of the dryer consists of a cylindrical horizontal vessel that is about 10 feet long by 3 feet in diameter with a holding capacity of 50 cubic feet. It is equipped with three sets of electrical strip heaters (100 KW per set) in direct contact with the outside surface of the shell. The outside of this heated surface is covered with a layer of insulating material. ,
The inside surface of the dryer is continuously scraped by a rotating helical ribbon agitator that removes and mixes the material that dries on the inside surface of the shell. The liquid or slurry is pumped into the dryer in batches through two (2) 2 inch feed connections located on the dryer side near each end of the unit. As the material comes in contact with the heated shell surface, the remaining water is evaporated. The rotating helical ribbon agitator scrapes the dried material from the surface, continually blends the material, and conveys it toward the center of the dryer body. When a batch has been dried, it will be discharged through a four inch
- pneumatically operated ball valve into the blender / dryer discharge J
hopper. > 2.6 Packaging System ! The dry solid waste from the blender / dryer discharge hopper is ' transferred by a fully enclosed screw conveyor to the pelletizer feed hopper. The pelletizer is a standard Model 200 Blount/Ferrel-Ross i I laborotory "ellet mill. The dry product flows by gravity from the i 1 feed hoppe. Into the center of a cylinderical extrusion die. The i ! product which enters as a powder is pressed or extruded through ; l radial holes in the die, forming a compacted solid material. As it - exits the die, the material will be cut off to pellets about 3/8 inch 1 in diameter and about 1/2 inch long. The pellets then drop through ,a
- shroud into a DOT Specification 17-C shipping container. The i pelletizer is integrally mounted on top of an enclosure around the DOT Specification 17-C container. A ventilation blower, which discharges to the building atmosphere, draws a constant suction through a HEPA filter on the enclosure to ensure that the enclosure i and the pellet mill are maintained under a negative pressure while in l use. This will prevent leakage of material that could cause an airborne radioactivity proble'n in the building. All handling of the
- open solid waste containers such as installation of lids and wiping of the exterior surfaces will be performed with the drum in the l ventilated drum enclosure.
[ I l 0225H/13H
- i i
TER 3232-019 Rev. O Page 10 of 38 2.7 Ancillary Equipment 2.7.1 Enclosure Building The entire processed water disposal system will be enclosed in a modular building 26'X30'X14' high located as shown on Figure 2. The primary purpose of the building is to shield the equipment and operators from the environment and to t contain the process liquid in the extremely unlikely event of ' catastrophic failure of the system tanks or pipi9g. The building is constructed of are-fabricated interlocking panels that lock together with hoot devices. The panels are laminated construction consisting of an insulating foam material sandwiched between sheet metal. The panels are painted on their interior and exterior surfaces for easy cleaning. Attached to the building is 10'X12' office area , that will serve as an operating control point. In addition, it will provide a controlled point of entry into the equipment building which will be a radiologically controlled area. The building will be placed on a poured, reinforced foundation and slab which will be curoed to contain any liquid spilled, and sloped to channel spilled liquid to a sump. The curbing is of sufficient size to contain the entire volume of liquid that could be contained in the system. The foundation and slab will be coated with an epoxy base sealant to facilitate decontamination, as needed. The building will be provided with the necessary lighting and ; telephone communication to facilitate efficient operation. In addition, portable heaters can be installed if needed during periods of shutdown if cold weather presents a possibility of freezing, , The building will be ventilated by an exhaust fan that will provide 2,500 CFM air flow out through the building exhaust. This will provide about 15 air exchanges per hour. 1 An ambient air sampler will be operated within the evaporator. i building to evaluate airborne radiological conditions. Airborne radiological concentrations will be controlled to ! less than or equal to 25 percent of Maximum Permissible , Cor. centration (WC) to personnel. ' If atrborne concentrations exceed 25 percent of WC to personnel, decontamination or other radiological condition improvements will be made within 1 hour, during which time t period the airborne radiological concentration will not exceed 25 percent to 50 percent W C. If af ter 1 hour, mitigation of the release is not achieved, the evaporator building exhaust will be shut down, and evaporator operations will be - terminated until acceptable radiological conditions can be ' restored. 0225H/13H w _
t TER 3232-019 Revo 0 : Page 11 of 38 If operating experience shows that airborne concentrations of less than 25 percent of >PC to personnel cannot be achieved through radiological controls, then engineered controls including a building exhaust monitor, will be instituted. 2.7.2 Cooling Water System Cooling water for the processed water disposal system will be supplied from and returned to a closed cycle chilled water system. The self contained chiller and chilled water system will be located adiac.9nt to the evaporator building and will provide about 20 gpm of cooling water at a temperature of : about 50' F to the C-30 condenser and the main evaporator compressor oil cooler. 2.7.3 Electrical System The evaporator system requires a 480V, 3 phase, 60 Hz main power feeder capable of supplying 1600 KVA to the evaporator building switchgear. This is provided by a single 13.2 KV primary from an existing HET-ED junction pedestal at the NE end of the 230 KV substation. This is routed through existing underground duct banks to a 2500 KVA step-down transformer i (13.2 KY - 480f/277V). The sten-down transformer is installed on a concrete pad adjacent to the evaporator building and is i surrounded by a block wall to prevent the spread of possible fire due to a transformer oil leak. The switchgear is supplied by the evaporator vendor as part of the system, l : 2.7.4 Piant System Tie-ins Operation of the evaporator system requires connection to existing plant systems for various service needs. These plant tie-ins are shown schematically in Figure 3. The figure shows the connections to the contractor supplied evaporator system , as well as the modifications to the existing systems necessary I to facilitate the tie-ins. , The existing Processed Water Storage Tanks (PWSTs) will be the primary feed source to the evaporator. The tie-in to the PW System allows pumping from either of the 500,000 gallon PWSTs i to the evaporator. Evaporator distillate can also be returned to either tank. The Auxiliary Building Emergency Liquid Cleanup System (ALC) will be modified to allow using the ,
- existing 85,000 gallon CC-T-1 in the EPICOR !! system as a distillate staging tank. This tank can receive distillate I from the evaporator or it can transfer liquid as either feed
! to the vaporizer or feed to the evaporator. Cross connect j valves between the source tanks and the evaporator and 0225H/13H
TER 3232-019 Reva O Page 12 of 38 vaporizer feed connections are capable of being locked closed to prevent inadvertently feeding raw water to the vaporizer. They will be locked and controlled per GPUN procedures. In addition, the tie-ins are designed so that any tank being used to feed the system will be isolated from all sources that may add any water to that tank while in service as a feed source. Similarly, any tank used as a staging tank to receive distillate will be isolated from any other sources of water. Domestic water is supplied to the evaporator system for equipment flushing and cleaning. It is supplied from the plant Domestic Water (00) System. Service air is supplied to the evaporator building from the existing plant Instrument Air (IA) System. It supplies the air driven building sump pump, the blender / dryer transfer pump, and the air operated blender / dryer discharge valve. All piping containing liquids that is outside the building is
-heat traced to prevent freezing in cold weather. Process connections to the vendor supplied system from plant liquid systems will be bolted flanged connections.
2.7.5 Fire Protection Fire protection will be provided by portable fire extinguishers installed in the building in accordance with National Fire Protection Association Codes and Standards and the Plant Fire Protection Plan. 3,0 SYSTEM OPERATION AND CONTROL 3.1 General Operation The processed water disposci system is designed to operate at a steady state feed rate of no more than 5 gpm. The currently projected disposal program will process the entire 2.3 million gallons of water over a period of two years with about half of the total inventory being processed in each of the two years. The projection of 1.15 million gallons per year is based on current estimates of water availability and estimated system down time. If operational availability of the evaporator system permits, and progress of defueling, decontamination, and preprocessing of water improves the availability of water, it is feasible to dispose of the entire 2.3 million gallons of accident generated water in as little as 16 months. This estimate is based on operating the evaporator 7 days per week with 25 percent down time. Regardless of the overall length of the operating program, the systrm will be operated and controlled in such a manner that the environmental impacts of the
.a 0225H/13H
TER 3232-019 Rev. O Page 13 of 38 project will be no more than the minimal impacts projected and evaluated in the NRC Staff's Progrannatic Environmental Impact Statement, Supplement 2. This section of the report describes the modes of operation of the system, the instrumentation and controls used in the system, and describes the basis for the operating limits imposed on the system to assure that the resulting environmental impacts are within those analyzed. 3.2 Operational Modes The processed water disposal system is designed with the flexibility to operate the evaporator and vaporizer as a coupled unit or to separate the two units and operate them independently. In the coupled mode, the evaporator and vaporizer are operated in series in a continuous flow operation. The distillate from the evaporator is i fed directly to the vaporizer for atmospheric discharge. When decoupled, the evaporator and vaporizer are operated separately with the vaporizer influent independent of the evaporator effluent. The distillate from the evaporator is pumped to a separate staging tank and the feed to the vaporizer is supplied from an independent staging i tank. These modes are described in detail in Sections 3.2.1 and 3.2.2. Operation of the processed water disposal system will be under direct
! control and supervision of GPUN operations staff. The personnel performing the operation will be contractor personnel provided by Pacific Nuclear Incorporated, the vendor and owner of the system.
, These personnel will receive the training required by plant ! procedures for access to the facility's protected area and radiation
- work permit areas and will perform all operations under the control of GPUN approved operating procedures. Radiological controls, chemistry, and effluent sampling and analysis needed to support system operation will be provided by GPUN staff.
3.2.1 Coupled Operation ! In this configuration the evaporator and vaporizer will be coupled and operated as a continuous cycle system. The primary control over environmental effluents tvill be established by strict control over the process influents. The
- body of water to be processed will be isolated from all other i possible sources of contamination, the source tank will be I recirculated to assure homogeniety, and then sampled. A
- chemical and radicchemical analysis for the principal
- radionuclides will be performed as presently done on-site and the analytical results compared to the influent criteria discussed in Section 3.3 Once conformance to the influent criteria is confirmed, water may be processed. Water will be supplied at a rate of no more than 5 gpm to the VC-300 incentrate tank from where it is fed and recirculated through c?in evaporator. The main evaporator will increase the 0225H/13H
TER 3232-019 Rev. O Page 14 of 38 concentration of dissolved solids, including the particulate radionuclides, by a factor of about 10. The concentrated liquid is continuously drawn from the VC-300 concentrate tank and sent to the C-30 evaporator. The C-30 evaporator will produce a further concentrated liquid that is about 30 to 50 percent dissolved solids. The purified distillate from the VC-300 evaporator is continuously discharged to the VC-300 distillate tank. The C-30 distillate is first collected in the C-30 distillate tank and then pumped back to the VC-300 concentrate tank for reprocessing. VC-300 distillate is continuously recirculated by the main distillate pump, P-5, and the C-30 evaporator heating loop pump, P-4 Heating loop pump, P-4, circulates distillate from the VC-300 distillate tant as cooling water through the blender / dryer vapor condenser, then through che two 30 KW electric heaters to the C-30 evaporator as its heat source. From the C-30 evaporator heating section it returns to the VC-300 distillate tank. Distillate pump, P-5, pumps from the VC-300 distillate tank through a recirculation loop that supplies clean water to the desuperheater nozzles in the vapor recompressor suction, hot water as a heat source to the feed preheater, seal water to the VC-300 vacuum pump, P-6, and motive force to the VC-300 eductors E-1 and E-2. The water to the desuperheater, vacuum pump, and eductors is subsequently returned to the distillate tank. A side stream is discharged from this loop through letdown valves that operate automatically to provide level control for the distillate tank. When operating in the 4 coupled mode, which is expected to be the normal mode of operation, the letdown flow from the distillate loop will be discharged directly to the vaporizer. The distillate will pass through a radiation monitor and enter the vaporizer recirculation loop as described in Section 2.4 During operation, samples will be obtained periodically from the raw feed to the evaporator and from the distillate feed to the vaporizer. Later analyses of these samples in the site laboratory will confirm that the evaporator influent quality had been within the required specifications during the previous operating period and that the evaporator produced a , decontamination factor of at least 1000 If these two ! criteria are met, the environmental release from the system will have been within the limits discussed in Section 3.3 If either of these criteria have not been met, the system will be shutdown and corrective action will be taken. When tankage is available, an alternative to full system shutdown will be to terminate the release fran the vaporizer and return the evaporator distillate to an interim stsging tank. This will allow adjustments to the process to restore its operation to
- within the specifications without a full system shutdown.
j' System instrumentation will provide a continuous indication that the environmental releases are within the limits required by the THI-2 Technical Specifications. If sample analyses j show that the environmental release rates have been higher r 0225H/13H
TER 3232-019 Rev. O Page 15 of 38 than those stated in Section 3.3, influent limits will be adjusted for subsequent operating periods to ensure conformance to the average quarterly limits discussed is Section 3.3. Operation in the coupled mode will not occur until sufficient data has been obtained from system testing to verify that the design decontamination factor are achieved. 3.2.2 Decoupled Operation In the decoupled mode of operation, the evaporator and vaporizer are operated as separate units with the vaporizer feed independent of the evaporator distillate discharge. The source tank to be processed is isolated, recirculated, sampled, and analyzed for conformance to the criteria in Section 3.3 In decoupled operation, the evaporator influent criteria are based on assuring that the solid waste form produced meets the requirements for an LSA, Class A waste. In coupled mode operation, the evaporator influent criteria are based on assuring that the environmental releases from the system are within the established specifications and the solid waste produced meets the requirements for LSA, Class A waste. Slightly different influent criteria are imposed because in the decoupled mode, the evaporator does not discharge its distillate directly to the vaporizer for release to the environment. Tnis is discussed further in Section 3.3. Water from the source tank is fed to the system as in coupled operation. The evaporator operation is identical except that the distillate letdown is pumpred to a holding tank rather than being fed directly to the vaporizer. The water will be held until analysis shows it is acceptable for release. If the water meets the established effluent criteria, it may be later pumped directly to the vaporizer for vaporization and release to the atmosphere. If it does not meet the release limits it will be held and later reprocessed through the evaporator. This option allows using the evaporator as a preprocessing system for water sources that do not meet the criteria for discharge by direct coupled operation. Higher activity waters may be processed in batches through the evaporator until it is suitable for final vaporization. When processing higher activity water, care will be taken to avoid cross contamination of later lower activity batches. Sample analysis will confirm that cross contamination has not occurred. 0225H/13H
TER 3232-019 Rev. O Page 16 of 38 3.3 Influent Limits As previously stated, the primary method for control of the effluent from the eveporator or vaporizer is by establishing strict controls on the precess influent characteristics. The effluent liquid quality from the evaporator is dependent upon the decontamination factor, or DF, achieved by the process. The DF is defined as the concentration of contaminants in tie system influent divided by the concentration of contaminants in the effluent. The LICON evaporator has been designed to provide a decontamination factor of at least 1000 for particulates. In other words, less than one one-thousandth or 0.1 percent of the particulate radionuclides present in the evaporator influent will be carried over with the purified distillate. Further, 99.9 percent of the particulate radionuclides will be collected in the dry solid waste that will be packaged for disposal. This DF of 1000 for particulates will be verified by a series of tests performed by the vendor prior to delivery of the system to the TMI site. These tests will involve full flow ortration of the system using liquid solutions that are very close i.e composition to the THI-2 processed water but contain no radioactive material. Af ter demonstration of satisfactory evaporator performance, the system will be assembled at the THI site. It will again undergo a test run using a non-radioactive surrogde solution. The evaporator DF will be verified by chemical ana';ysis of the feed solutions and purified distillates. Once the system is placed in service, the DF will be periodically verified by laboratory analyses of the influent and ef fl uent. The system is also provided with instrumentation that will detect upset conditions that may affect the effluent Quality. This ir;strumentation is discussed in Section 3.4. The influent Quality must be controlled to assure achieving two effluent results. First, the purified distillate will be released to the environment via the vaporizer. Essentially all of the contaminants contained in the distillate will be vented into the atmosphere. The level of contaminants released must be kept low enough to assure minimal environmental impacts. Second, at least 99.9 percent of the contaminants contained in the evaporator influent will be collected as dry solid waste. This waste will be packaged , on-site and transported for burial in a comercially operated radioactive waste disposal facility. The waste form produced must be suitable for transportation and burial in accordance with the regulations of the U.S. Department of Transportation and the U. S. Nuclear Regulatory Comission. GPUN has chosen to process the watte to a form that meets the transportation requirements for Low Specific Activity (LSA) radioactive material. In addition it will conform to the burial requirements for Class A waste. In general, the criteria for LSA and Class A waste constitute the lowest level radioactive waste ma terial originating from comercial nuclear power plants that are reg d ated for purposes of transportation and disposal. 0225H/13H
i TER 3232-019 Rev. O Page 17 of 38 ih c , ster to be disposed is in storage in various tanks around the "ite, some of which is still in use for clean-up activities. Some of this water has already received final processing through the submerged Demineralizer System (SDS) and EPICOR !!. About 40 percent l of the 2.3 million gallon inventore will require some form of i l preprocessing before being processed for disposal by the evaporator , system in a coupled mode. Table 1 Columns 1 and 2 show the ;
; projected average activity levels for the total 2.3 million gallons !
l of accident generated water assuming preprocessing of about forty ' percent of the total inventory. This data appears in the NRC staff's Programatic Environmental Impact Statement (PEIS) Supplement 2 j (NUREG-0683, Supp 2) in Table 2.2 and is identified as '8ase Case' water. These activity levels formed the basis for the NRC staff's analysis of the environmental impacts of evaporator discharges. The i activity releases occurring from evaporator discharges of "Base Case" water result in releases that are a small fraction of the releases j permissible by existing regulatory requirements. Even though higher f i releases are legally acceptable and of very minor environmental ! i consequence, the processed water disposal system will be operated in j such a manner that the PE!S projections of environmental impact are ! not exceeded. Since the PE!S analysis assumed processing "Base Case" i i water with a vaporizer discharge to the atmosphere containing 0.1 ! percent of the radioactive particulates f rom the influent, that value l will be used as the system operating limit. Therefore, when ' j operating the processed water disposal system in the coupled mode, l the volume of water being processed will be isolated from all sources j of contamination. The concentrations of the principal radionuclic'es J will be verified by on-site analysis to be within limits so that quarterly average concentrations of all water processed in this mode ! I will be no greater than the concentrations listed in Table 1 Column - j 2. When processing water through the vaporizer in the decoupled l l mode, the quarterly average vaporizer influent concentrations will be l j no greater than 0.1 percent of the values in Table 1, Column 2. .
- These limits equate to an atmospheric release rate for particulate '
I radionuclides of 8.2E-5 uti per second if processing water ' I containing the maximum limits at a rate of 5 gpm. These limits are , shown in Table 2. ~ i . l The evaporator influent limit for coupled mode operations assumes a ! J DF of 1000 for particulates. If system testing and operational . experience demonstrate with reasonable confidence that the system achieves a higher DF, the evaporator influent limit for coupled mode 3 operation will be increased accordingly. ; i When processing water in the decoupled mode, the evaporator will not l discharge the distillate directly to the environment since the ! } distillate is collected and stored in an on-site staging tank, it ! I will be held for future discharge directly through the vaporizer. l !' final processing through the evaporator and vaporizer in coupled mode, or further preprocessing through the evaporator in decoupled j j mode, depending upon its radionuclide content. Therefore, the l ! evaporator influent limits in the decoupled mode are based on , l assuring an acceptable final waste form. , l, i 0225H/13H l i j
TER 3232-019 Rev. 0 l Page 18 of 38 I The major constituent of the processed water that contributes to the final solid waste is ortho-boric acid (H 803)3 which has br.en used throughout the cleanup program for criticality control. The current processed water inventory of 2.15 million gallons contains an average concentration of boron from boric acid additions of about 3500 parts per million (ppm) but can range as high as 6000 ppm in some of the sources. Sodium hydroxide (NaOH) has been added to the water for control of pH and has an average concentration of about 700 ppm sodium ions in the 2.15 million gallons. As the water is evaporated, the NaOH and3H 803 will combine to yield sodium borate salts in the form of Nag 0 2B20 3 (Sodium Tetra-Borate) and Na20 82 03 (Sodium Meta-Borate). The remainder of the H3 803 will crystallize as ortho-boric acid. At the current averages of 3500 ppm Boron and 700 ppm Sodium, the 2.15 million gallons of processed water contain a>out 179 tons of boric acid and about 11 tons of sodium hydroxide. This material is non-radioactive. In contrast to this, Table 1, Columns 3 and 5 show the specific activity of the radionuclides present in the processed water and the resultant total quantity of each in 2.3 million gallons of "Base Case" water. It shows that the total weight of radioactive material present with the 190 tons of boric acid and sodium hydroxide is less than one pound. Therefore, the predominant material present in the solid waste is boric acid and its sodium salts. The projected weight of boric acf d and sodium hydroxide shown here are based, as previously stated, on the current inventory of 2.15 million gallons and average boron and sodiem concentations of 3500 ppm and 700 ppm respectively. The increase in the inventory to 2.3 million gallons projected between now and the end of the project is not expected to require any further boron additions. Therefore, the totd) projected weight of boric acid is not expected to change. Likewise, the weight of sodium hydroxide in the processed water is based on current inventories. The final amount in the projected 2.3 million gallons will depend upon processing requirements for pH adjustment and the amount of sodium removal that occurs in ion exchange preprocessing. These weights differ from the values given in the PEIS. The values used by the NRC in preparing the PE!S were based on data provided by GPU Nuclear in July 1986 (i.e. , 2.1 million gallons, 3000 ppm Boron, and 700 ppm Sodium.) Since submission of that data, additions of boric acid and inventory changes have increased the values to the current 2.15 million gallons, 3500 ppm Boron, and 700 pos Sodium. To determine the transportation category, each radionuclide present in the Naste is assigned an A-2 value which is the number of curies of that nuclide that may be shipped in a Type A container. The A-2 values are obtained from the applicable 00T and NRC regulations and are shown in Table 1. Column 4 From the A-2 values, a permissible LSA concentration is determined. The LSA concentrations are the maximum concentrations in mil 11 curies per gram that may be packaged in a strong tight container and shipped in an "exclusive use" vehicle as low Specific Activity (LSA) material. Calculations show that processed water containing 3000 ppm Boron and the radionuclide 0225H/13H
TER 3232-019 Reve O Page 19 of 38 concentrations of Table 1, Column 2, will yield an LSA waste when evaporated. The waste will be shipped in 00T Specification 17-C i containers. These containers exceed the minimum requirements for "strong tight containers". To determine the burial category of the waste, similar calculations are done to compare the waste to criteria in 10 CFR 61. Calculations show that processing of water with Table 1, Column 2 concentrations of radionuclides and 3000 ppm Boron will result in a Class A waste form. I i Boron concentrations higher than 3000 ppm will yield larger quantities of solids and resultant lower activity concentrations in j the final waste form. Similarly, higher activity concentrations in i the source water produce higher concentrations in the final waste form. Therefore, when processing water with activity levels higher
! than those shown in Table 1, Column 2, or Baron concentrations of less than 3000 ppm calculations will be performed and documented in accordence with a GPU Nuclear approved process control plan to determine the transportation and disposal categories of the final waste form. Only water that will yield an LSA, Class A waste form will be pro';essed through the evaporator, 3.4 System Instrumentation and Control , As previously discussed, the primary control on effluent quality from
- the evaporator is an operating program that places strict controls on the influent or raw feed quality. The system is designed to operate with minimal manual control by the operator even though an operator i' will be present during system operation. The automatic controls and instrumentation incorporated in the processed water disposal system are discussed in this section.
i 3.4.1 Liquid Level Controls
- Raw feed from the plant source tank is either purped or gravity flowed to the eviperator depending upon level in the l,
source tank. The feed enters the VC-300 concentrate tank .
! through a solenoid operated valve with a manual bypass valve.
l The manual bypass valve will be adjusted to maintain a nearly
- constant level in the VC-300 concentrate tank with the j solenoid valve open. The tank is provided with three sonic j level switches. If the level in the tank varies, the top j sonic switch closes the solenoid operated feed valve, the middle switch opens the valve, and the lower switch actuates a
! low level alarm and deenergizes the evaporator causing a ! system shutdown. In addition, a High-High level switch will l actuate an alarm and shut the main feed valve to the system j and the C-30 distillate tank discharge valve to prevent l overflow of the tank. Similarly the feed rate to the VC-300 l evaporator shell is set manually and the recycle rate back to l the concentrate tank is controlled by an electric motor l l 1 0225H/13H
TER 3232-019 Revo O Page 20 of 38 operated recycle valve in parallel with a manual valve. The solenoid valve is cycled open and closed by a sonic level detector on the evaporator shell. The C-30 concentrate tank is supplied by the concentrate drain from the YC-300 concentrate tank. The gravity flow line is provided with a similar arrangement of a anual valve and a solenoid valve in parallel, with the solenoid valve being controlled by level switches in the C-30 concentrate tank. The low level alars switch causes an alarm, deenergizes the evaporator system and trips the pump to the blender / dryer transfer tank. Discharge from the two distillate tanks is controlled in a similar Nnner. The level in the vaporizer flash tank is controlled by three sonic level switches. The top switch opens a solenoid valve in the blowdown line, tie middle switch closes the valve, and the bottom switch actuates an alars and trips the vaporizer circulation pump and electric heaters causing an automatic shutdown of the vaporizer. The VC-300 and C-30 evaporator vapor domes and the vaporizer flash tank have liquid level gauge glasses for visual indication of liquid level. The level gauges on the vapor domes are equipped with sonic level switches that actuate alarms to warn of excessive foaming or over feeding of the evaporator. They also deenergize the evaporator causing a system shutdown. The sonic level controls chosen for this system are widely used throughout the industry to control liquid levels in hostile environments. They have no moving parts, are unaffected by changes in dielectric constants, perform well in high density slurries, and work well throughout a large range of visccsities. 3.4.2 Flow Measurement A water flow meter is installed on the evaporator feed line to keep track of total volume of raw processed water sent to the evaporator. It is a turbine type flow meter with a totalizer. Similar flow meters are installed in the system distillate discharge lif.e and in the distillate line from the C-30 distillate tank. These will provide data for performance of the system m ss flow balances. Flowrate meters are installed in the desuperheat line. hoth evaporator recycle lines and the vaporizer blowdown line. These matcrs provide on-line indication of process conditions and provide no automatic control functions. 3.4.3 Conductivity Monitors An ef fective measure of the amount of dissolved sterial in water is its conductivitv. Four conductivity monitors are installed in the system to detect trends or upset conditions during processing. There is a monitor in the distillate lines from both the VC-300 evaporator and C-30 di:tt11 ate tant 0225H/13H
l TER 3232-019 Rev. 0 l Page 21 of 38 discharge. These monitors will give indication of excessive carryover f rom the evaporators or of unexpected tube leakage in the evaporator heat exchangers. Monitors are installed in both the vaporizer and evaporator feed lines. These will provide an indication of any unplanned upset that may degrade the influent water qbality. Each of these monitoring points is also equipped with a sample station for extraction of process fluids for chemical and radiochemical analysis. Operational experience and an accumulated data base accreed during actual evaporator operations will provide a sound '. asis for comparing these two methods of analysis, i.e., laboratory analysis and steady state conductivity monitoring. After adequate demonstration of comparable analytical results and conductivity data, operational procedures may be modified to rely more extensively on the steady state conductivity instrumentation. However, until a data base can be compiled based on actual system operations, the control method utilized in procedures and operating programs will be the physical sampling and laboratory analysis of process liquids in conjunction with conductivity monitoring. 3.4.4 Radiation Monitor A gamma radiation detector is installed in the vaporizer f eed line and is intended to detect gross upsets in the system operation. The primary means of monitoring and controlling the environmental releases of particulate radioactive material will be limiting the radionuclide concentrations in the system influents and by periodic sampling and radiochemical analyses. The radiation monitor will detect major deviations in the process and will cause a termination of the releases to the environment if upsets occur. It will alarm and cause an automatic shutdown before the environmental release rate exceeds the particulate rdlease limit of the THI-2 Technical Specifications. The detector is calibrated to the .661 MEV ' ganvna ray emitted by the Cesium-137/ Barium 137m decay chain. The alarm is set to a concentration in the liquid which corresponds to a particulate release rate of - 7.5[-2 pC1/sec. This represents 25 percent of the instantaneous particulate release rate limit of the THI-2 Technical Specifications. The alarm set point corresponds to a Cesium-137 release rate of 1.1E-2 uC1/see assuming the isotopic distribution of Table 1. Column 2. This correlates to a Cesium-137 concentation in the vaporizer feed of 3.5E-5 vC4/ml which is very nearly equal to the coupled trode evaporator influent limit. Thus, the detector alarm would also provide a warning that the evaporator had been inadvertently bypassed. The high level alarm signal on the radiation monitor will cause an audible alarm, trip the vaporizer recirculation purrp,
- and deenergize the vaporizer heaters. This will effectively 0225H/13H
TER 3232-019 Rev. O Page 22 of 38 terminate the release of radioactive material at a level below the Technical Specification instantaneous release limit. The monitor chosen for this system is a Nuclear Research Corporation Model 4PI-3 sampler. It uses a Sodium Iodide crystal as a gamma scintillation detector. It has a monitoring sensi:lvity of 1E-7 pCi/ml of Cesium-137 at a 99 percent confidence level. 3.4.5 Other instrumentation In addition to the instrumentation and cortrols discussed above, additional features support the system and enhance the ease of operation and system reliability. Full view sight windows on the evaporator shells and viewing windows on the vapor domes allow the operator to see the process as concentration progresses. They provide easy assessment of too much or too little foaming in the evaporator and provide a means of immediate confirmation of any carry-over f rom the separators if indicated by the conductivity monitors. The distillate pumps, P-3 and P-5, are equipped with discharge pressure switches tnat provide assurance of sufficient pressure for operation of the condensate eductors. Low pressure would cause the eductors to back-fire and the system would operate erratically. If pressure falls below 35 psig, the pressure switches actuate a system shutdown by deenergizing the electrical system. Pressure switches are provided in the vaporizer heating loop and in the C-30 evaporator heating loop to deenergize the heaters in the event of insufficient water flow through the heaters. These loops are also equipped with high temperature shut-off switches. The transfer skid holding tank which receives concentrated liquid from the C-30 concentrate tank for feed to the - blender / dryer is equipped with a conductance type level control. A high level will shut-eff the transfer pump and a low level will deenergize the tank heater. The blender / dryer discharge hopper has an RF capacitance level control which will automatically close the blender / dryer discharge valve on high level. The pellet mill feed hopper has an ultra:onic type level control to prevent overfilling of the hopper. It will automatically trip the transfer conveyor. The drum filling enclosure is equipped with a thru-scan LEO photocell that will monitor the drum filling operation. If the drum overflows, the photocell circuit will shutdown the pellet mill. 0225H/13H
TER 3232-019 Rev. O Page 23 of 38
4.0 TECHNICAL EVALUATION
The purpose of this section is to describe the engineering specifications to which the processed water disposal system has been built, and to discuss the applicable codes, standards, and regulatory requirements imposed on its design, fabrication, and assembly. This section will further discuss the technical features of the system that make failures unlikely and that mitigate the safety impacts of postulated system failures. 4.1 Codes, Standards, and Engineering Specifications The vendor supplied evaporator components are classified as Important To Safety (ITS) per the GPU Nuclear Recovery Quality Assurance Plan for TMI-2. Equipment and hardware procured and installed on-site which is required to maintain the pressure boundary for radioactive fluids are also classified as ITS. Process instrumentation, including the power and signal cabling, which is required to ensure that releases from the system are maintained within the design specification are ITS. All remaining components are classified as Not Important To Safety (NITS). The system design and its intended operations have been classified under the standards of Quality Group D per the recommendations of NRC Regulatory Guide 1.26, "Quality Group Classifications and Standards for Water, Steam, and Radioactive Waste Containing Components of Nuclear Power Plants", conformance to these standards is shown in the discussions that follow. The system was reviewed for conformance to the guidance of NRC Regulatory Guide 1.143, "Design Guidance for Radioactive Waste Management Systems, Structure, and Components Installed in Light-Water-Cooled Nuclear Power Plants". Although this guide is applicable to permanently installed radwaste treatment systems rather than temporary removable systems, we have determined that the evaporator system does in general conform to Regulatory Guide 1.143 with the following exceptions: 1) The piping system and the building foundation and walls are not designed to the specified seismic response criteria. The seismic design criteria, however, were specifically exempted for recovery systems in the NRC approved Recovery Quality Assurance Plan; 2) The requirement to have a dike or retention pond around outside tanks as stated by regulatory position 1.2.5 is not met. The only outside tanks associated with the system are the Processed Water Storage Tanks. These tanks are atmospheric storage tanks built to the standards of API-650. They are fabricated of ASME !A T85 grade C carbon steel with an epoxy-phenolic type interior lining. The tanks were built and are operated under the provisioet of an NRC approved plan for storage of processed water. The VC-3Go and C-30 evaporators are engineered in conformance with the ASME Code, Section VI!!, for unfired pressure vessels and to TEMA (Tubular Exchanger Manufacturers Association) standards where applicable. The shells are made of 316 stainless steel. The VC-300 0225H/13H ,
TER 3232-019 Rev. O Page 24 of 38 heat exchanger is a Bayonet Augumented Tube (BAT) type with both the tubes and bayonets built of titanium. The C-30 is also a BAT type heat exchanger with titanium tubes and chlorinsted polyvinyl chloride bayonets. The C-30 condenser is similar in construction 4th a 316 stainless steel shell, titanium tubes, and polyvinyl chlor ide bayonets. The support building foundation and floor sleb are built to ACI Standard 318-83, "Building Code Requirements for Reinforced Concrete". The floor is sealed with an epoxy based coating and the structure is curbed to provide sufficient retention volume to contain the entire liquid contents of the system in the event of catastrophic system failure. The support building is a prefabricated structure that conforms to the Uniform Build'ng Code of the International Council of Building Officials. All four atmospheric tanks in the system are fabricated of stainless steel and conform to ASME Code Section IX and V. The tanks have tne following capacities: VC-300 Concentrate Tank, 75 gallons; C-30 Concentrate Tank, 60 gallons; VC-300 Distillate Tank, 90 ga'lons; and C-30 Distillate Tank, 34 gallons. The tanks are provided with sealed lids equipped with an atmospheric vent that discharges to the building atmosphere through a HEPA filter. The electrical system is protected by suitably sized wiring, hardware, and circuit breakers per NEC 1987. All electrical junction boxes and enclosures are NEMA 4 or equivalent and all motors are l TEFC. All equipment is grounded through the switchgear ground bus which is connected to the GPUN grounding system. All process piping in the system i.e 304 stainless stect and conforms to the requirements of the ASME Code for Pressure Pipir , ANSI B31.1, "Power Piping". Tank overflow lines and system drains are routed to the building sump using flexible hose. These are non-pressure retaining components and conform to ANSI B31.1, Sectic- 105.3(C). The following is a list of the engineering specifications on major ~ system components not previously discussed.
- Vapor Compressor: Roots rotary lobe model 1039 compressor, 4100 CFM at 1400 RPM, driven by a 125 HP TEFC motor.
- Vaporizer Recirculation Pump, P-7: Goulds Model 3196 MT, Size 4X6-10, 500GPM at 40f t TDH, driven by a 7-1/2 HP TEFC motor,1150 PPM.
0225H/13H
TER 3232-019 Rev. O Page 25 of 38 VC-300 Concentrate Pump, P-1: Corcoran Series 2000 OH, with double mechanical seals, 10 GPM at 50 ft TOH, driven by a 3.4 HP TEFC motor, 3500 RPM. C-30 Concentrate Pump, P-2: Same as P-1 except with a cut down impeller to give 3 GPM at 60 ft TOH.
- VC-300 Distillate Pump, P-5: Grundfos Model CR4-50N, multi stage, 35 GPM at 110 f t TOH, driven by a 2 HP TEFC motor at 3500 RPM.
C-30 Distillate Pump, P-3: Grundfos Model CR2-30N, multi stage, 10 GPM at 110 f t TOH, driven by a 3/4 HP TEFC motor at 3500 RPM.
- Vacuum Pump, P-6: Atlantic Fluidic Model A-10, rotary liquid ring pump / compressor, driven by a 1.5 HP TEFC motor at 3500 RPM. The pump will evacuate 14 CFM at 25 inches Hg Vacuum.
- Conductivity Monitors: Series 800, MK 817 Wet Tap assemblies. Stainless steel housing, 2.0 cell constant, range 0 to 25,000 yS/Cm.
- Sonic Level Sensors: SONARSWITCH Model 700, 316 Stainless steel NEMA 7 enclosure, .03 inch repeatability.
- Blender Dryer Transfer Skid Level Control: B/W control, Series 1, Model 1E1C4.
l - Blender Dryer Discharge Hopper Level: Penberthy Model 801132-1, RF capacitance level control. Pellet Mill Feed Hopper Level: Bindicator Breakdata 2200, ultrasonic level control.
- Drum Enclosure Filling Monitor: Microswitch Model FE-LP, thru scan LED photocell.
I 0225H/13H
TER 3232-019 Rev. O Page 26 of 38 4,2 System Response to Upset Conditions As shown in the previous section, the processed water disposal system is designed and built to sufficient industrial codes and standards to assure a high standard of quality. The system is designed and built to su:h quality standards to minimize system failures. However unlikely, the system design has been evaluated to assure safe and environmentally sound response to a number of abnormal conditions. 4.2.1 Loss of Electrical Power All electrically operated valves in the system are energized to open and are spring loaded tc close when deenergized. Upon loss of electrical power, feed water to the vaporator building will be automatically secured by closure of the feed valves. All heaters will shutdown securing the heat source to the vaporizer and the C-30 evaporator. The vapor compressor will shut down securing the heat source to the main evaporator. The blender / dryer wl11 shutdc.vn and all electrically driven pumps will trip. Thus, all evaporator and drying processes terminate and the system becomes stagnant. The only adverse consequence of this event is possible precipitation of dissolved solids from the concentrate as the systera cools. If plugging of piping or heat exchanger tubes occurs, the precipitate can be redissolved by dilution of the liquid with clean water. If necessary, the system is designed for relatively easy removal of the tube bundles for cleaning. 4.2.2 Loss of Service Air Service air is supplied to the processed water disposal system from the plant instrument air system. It is used to power the air driven pump in the building sump, the air driven diaphragm pump on the blender / dryer transfer tank, and the air operated discharge valve on the blender / dryer. Loss of service air pressure will result in the blender / dryer discharge valve failing closed and shutdown of the transfer pump. Thus, material will not be able to be transferred into or out of the blender / dryer. The heaters can be secured if necessary and the material allowed to remain in the vessel until service air can be restored. Thus, loss of service air supply will not result in a major upset condition for the overall process and will not hinder an orderly system shutdown if necessary. 4.2.3 Tank or Pipe Rupture l Tank or pipe ruptures are considered to be of extremely small probability because of the system design and fabrication and pressure conditions to which the system will be exposed. But in the very unlikely event of such an occurrence, low level sensors on the tanks will cause a system shutdown by ceenergizing the electrical system. The building is designed ( i 0225H/13H i I
l I l TER 3232-019 Rev. O I Page 27 of 38 ! l l to contain the entire volume of liquid that could be present in the system if completely flooded, so spillage of I radioactive liquids to the environment will not occur. Minor spills occurring during system sampling or as a result of small leaks are similarly of little consequence. Standard radiological control practices will assure mininal spread of contamination. In addition, the building floor is sloped to channel water to the building sump and it is sealed with an epoxy coating for easy cleanup and decontamination. If a spill of dry solid waste occurs outside of the ventilated drum enclosure, the area will be controlled to prevent the spread of contamination until cleanup is complete. This will prevent unplanned environmental release of airborne radioactive material. 4.2.4 Severe Weather Conditions The evaporator building is designed to the Uniform Building Code and will provide a secure protective enclosure around the system under all normally expected conditions. If severe weather or environmental conditions exist that would result in declaration of an Unusual Event as specified in the GPU Nuclear Emergency Plan, the processed water disposal system will be shutdown. Therefore, severe natural phenomenon that may result in damage or destruction of the building will not cause uncontrolled release of radioactive naterial f rom evaporator operation. 5.0 Environmental and Radiological Assessment The purpose of this section is to present an evaluation of the environmental and radiological ef fects of processing 2.3 million gallons of water meeting the influent and effluent criteria discussed in Section 3.3, and discharging the effluent directly to the atmosphere. 5.1 Environmental Assessment The processed water disposal system will produce environmental releases of tritium, particulate radionuclides, and boric acid and sodium borate salts. The 2.3 million gallons of processed water contains about 1020 curies of tritium as reported in the PEIS. All of this tritium will be released to the environment through the vaporizer since the evaporator system will not remove it. Tritium has a specific activity of 9.7E+3 curies per gram which corresponds to a total quantity 0.105 grams of tritium in the 2.3 million gallons of water. If all of the tritium in the processed water is in the fonn of tritiated water (H-T-0), this equates to 0.7 milliliters of H-T-0 in the 2.3 million gallons. This tritium will be released at an averane rate of 37 9C1 per second during evaporator operation. Since no 0225H/13H
TER 3232-019 Rev. O ! Page 28 of 38 i conventional waste treatment processes will affect the tritium j content of the water, the release rate of tritium to the environment will vary depending upon the water source being processed and the vaporizer processing rate. Tritium concentrations in the source tanks range f rom as low as 1.4E-5 uCi/ml to as high as 0.31 uCi/ml. This corresponds to environmental release rates ranging f rom 4E-3 to 98 pCi per second at a 5 GPM processing rate. The continuous tritium release rate is limited by the current Environmental Technical Specifications, Section 2.1.2 C. The release rate limit for a ground level release that is derived from that specification is 570 pCi/sec. Thus, the average and maximum releases that will result f rom evaporator operation are a small fraction of the releases permitted by the facility license. The processed water disposal system will cause small environmental releases of particulate radionuclides. The release rate is dependent upon the particulate concentrations in the influent and upon the DF achieved by the evaporator. The minimum 0F that the evaporator will achieve is 1000. The maximum influent concentrations that will be fed to the evaporator in coupled mode are as shown in Table 1, Column 2. Included in the table is lodina-129. It is expected that Iodine is present in the chemical form of Cesium Iodide or other alkali-metal iodide. In this form, the iodine will be removed by the evaporator in the same proportions as the other particulates. However, in the very unlikely event that it is present in the elemental form, it will volatilize and be carried over with the distillate. For conservatism in projection of environmental releases, it will be assumed that all of the I-129 is released to the atmosphere. (Note that in calculating the nuclide content of the solid waste, it is assumed that all of the I-129 is present also in the evaporator bottoms.) This yields a concentration of particulates and I-129 in the distillate of 8.6E-7 uti/ml and an atmospheric release rate of 2.7E-4 pCi/sec. This is comprised of 8.2E-5 uti/sec of particulates, predominantly Cs-137, Sr-90, and C-14; plus 1.89E-4 pCi/sec of I-129. This is a small fraction of the continuous particulate release rate of 2.4E-2 pCi/sec permitted by the current Technical Specifications. The radiation exposure to the public from releases of this magnitude were analyzed and evaluated by the NRC Staff in NUREG-0683, Supplement No. 2, and found to have no significant affect on the human environment. In addition to the radionuclides released, the processed water disposal system will also release small quantities of boric acid and sodium borate salts to the atmosphere. Based on a DF of 1000, no more than 0.1 percent of the chemical constituents of the processed water will be released. For conservatism, a total released quantity of 0.2 tons was used in the following environmental analysis. If the release is averaged over the 2-year projected time span for the evaporator project, it gives an average release rate of 0.0028 g/sec of particulates. Applying the annual average dispersion 0225H/13H
TER 3232-013 Rev. O Page 29 of 38 factor of 2x10-6 sec/m3 cited in the TMI Of f-site Dose Calculation Manual (ODCM), the average concentration of the chemical constituents off-site will be approximately 6x10-3 pg/m3 , Applying the worst case dispersion factor of 6x10-4 sec/m3 (based on the TMI-2 FSAR accident dispersion f actor), the worst case of f-site concentration of particulates will be approximately 2 vg/m3 Neither of these concentrations is a threat to the public, plant nor animal communities as shown in the following comparisons. o The threshold limit value, or TLV, (i.e., eight-hour time weighted average concentration) for nuisance particulates, including boron oxide, recommended for the human environment is lx104 ug/m3 The calculated average particulate concentration of 6x10-3 pg/m3 and the calculated worst case particulate concentration of 2 pg/m3 resulting from the proposed evaporation process are more than 1.5 million and 5000 times smaller, respectively, than the recommended TLV. o According to studies documented by the NRC in NUREG/CR-3585, the typical nuisance dust concentration in the Central l Atlantic States is 258 ug/m3 This is over 40,000 times i greater than the projected average concentration resulting l from the evaporator. It is also more than 125 time greater than the concentration which would result from the evaporator during the worst case atmospheric conditions which are not common and of only very short duration, o The NRC advises, in Regulatory Guide 4.11, Revision 1, 1977, that chemical studies of cooling tower drif t are usually not needed when all of the following apply: 1) the dominant salts are harmless mixtures of biological nutrients, 2) the expected peak deposition beyond the site boundary is less than 20 kg/ hectare - year of mixed salts, and 3) the drif t does not contain toxic elements or compounds in amounts that could be hazardous to plants or animals either by direct or indirect exposure over the expected lifetime of the facility. Comparing the first guideline, the evaporator emissions will deposit sodium borate. Sodium and calcium borate salts are typically found in nature. The element boron is a micro nutrient which is essential to the nutrition of higher plants. It is comon practice to add boron to agricultural fields as a supplemental nutrient. The highest annual deposition factor of 6.5x10-8 m2, / cited in the TMI ODCM, can be applied to compare the second NRC guideline to the evaporator emissions. The resultant total solids deposition would be less than 6x10-2 kg/ hectare - year. This concentration is approximately 300 times lower than the NRC guideline. The third guideline regards toxic elements or compounds. The evaporator emission would not contain toxic substance. Boron compounds are typically found in soils at an 0225H/13H b
TER 3232-019 Rev. O Page 30 of 38 average concentration of 50 ppm and ranging up to 150 ppm. The total solids from the evaporator are conservatively l estimated to be 0.25 ppm if they accumulated in the first inch of soil over the two year period. Boron exists in river and lake waters at concentrations averaging 0.1 mg/L but ranging as high as 5 mg/L. A conservative estimate of the concentration of total solids from the evaporator would be below 0.5 mg/L if they accumulated in shallow depths of water. The EPA limits boron concentrations to 0.75 mg/L for long-tern irrigation on sensitive crops (Quality Criteria for Water,1986 EPA 440/5-86-001) . The example of sensitive crops given by the EPA is citrus plants and those plants are not produced in the TMI vicinity. Regarding animal life, in the dairy cow,16 to 20 g/ day of boric acid for 40 days produce no ill effects (EPA 440/5-86-001). Also, the minimum lethal dose for minnows exposed to boric acid was reported to be 18,000 mg/L (EPA 440/5-86-001). Thus, the emissions from the evaporator process fall well below the guideline advised by the NRC requiring a chemical study. o With regard to impact on plant species, the Air Pollution Control Association (1970) documents the following:
"Particulate emissions are not generally considered harmful to vegetation unless they are highly caustic or heavy deposits occur". As shown in the previous comparisons, the depositions resulting from the proposed evaporation process are neither "highly caustic" nor will they result in "heavy" deposition.
Further, the element boron, as discussed in NUREG/CR-3332, is relatively imobile in plants. 5.2 Radiological Assessment 5.2.1 Off-site Ooses were calculated using the Meteorological Information and Dose Assessment System (MIDAS) which is used by TMI Environmental Controls for quarterly and semi-annual dose - assessments which are submitted to the NRC with THI-1 and THI-2 effluent reports. MIDAS uses hourly averages of on-site meteorological data to calculate an integrated dispersion for the period of interest. It integrates the dispersion over each hour into each of sixteen sectors at ten distances. The location of the five nearest vegetable gardens larger than 500 square feet, and the location of the nearest milk cow, milk goat, meat animal, and residence in each of the sixteen sectors, is used to evaluate seven airborne pathways: plume exposure, direct dose from gre,nd deposition, inhalation, and the consumption of meat, cow .nilk, goat milk, and vegetables. The maximally exposed hypot.1etical individual is conservatively taken to U that person in the maximum inhalation location and is assumed to consume meat. 0225H/13H
TER 3232-019 Rev. O Page 31 of 38 vegetables, and milk from each of the other maximum locations. These calculations are performed in accordance with Regulatory Guide 1.109 and are identical to those used for semi-annual and quarterly effluent / dose reports. The meteorological data from 1985 was used to calculate annual dispersion into the atmosphere. There is good confidence that the dispersion resulting from the 1985 data is similar to annual dispersion in recent years. Using the releases projected in Section 5.1, the dose estimate for the maximally exposed individual for the duration of the project is 2.0 mrem total body and 3.6 mrem to the bone. Since the expected duration of the project is two years, the annual exposure to the maximally exposed individual is one-half of this. To estimate the population dose MIDAS was again utilized. The affected population is considered to be the population surrounding TMI-2 out to a distance of 50 miles. The population affected by the atmospheric release associated with the evaporation of the processed water is estimated to be 2.2 million people. The dose pathways include inhalation; milk, meat, and vegetable consumption; plume exposure; and direct dose from ground deposition. This yields a total population l dose of 18 person-rem total body and 25 person-rem to the bone i and an average exposure to a mermer of the population of 0.008 i mrem total body and 0.011 mrem to the bone. 5.2.2 On-site Occupational Exposure Personnel exposure resulting from evaporator operation will be primarily due to ambient radiation in the vicinity of the evaporator and from packaging of the dry solids. Since the proposed influent criteria are such that only water that will produce an LSA, Class A waste will be processed, the radionuclide concentrations even in the concentrated evaporator bottoms, will be relatively low. The maximum dose is conse vatively estimated to be 23 person-rem. This is - based on 16,000 person-hours for the evaporation process in a radiation field of 0.6 mrem /hr, about 3500 person hours for packaging of the dry solids in a radiation field of 2.5 mrem /hr, and preprocessing operations for about 40 percent of the total inventory. In the unlikely event of an on-site accident involving the rupture and spill of a drum full of dry solid waste, the dose to the on-site worker would be from a spilled quantity of LSA material. The dose from such an accident is bounded by previous analysis of on-site spills of radioactive materials. The Jose to the on-site worker would be no more than the permissable dose to a member of the oublic from a 0225H/13H
TER 3232-019 Rev. O Page 32 of 38 transportation accident involving LSA material as used in IAEA Safety Series 37 in the development of A-2 quantities for radioactive waste shipments. 6.0 SAFETY EVALUATION 10 CFR, Paragraph 50.59, permits the holder of an operating license to make changes to the facility or perform a test or experiment, without prior Commission approval, provided the change, test, or experiment does not involve a change in the Technical Specifications incorporated in the license, and it does not involve an unreviewed safety question. Disposal of processed water does not require a Technical Specification change. NRC approval of the disposal option selected by GPU Nuclear is required by Technical Specification 3.9.13; accordingly, this evaluation is submitted to obtain that approval. In addition, at the request of the NRC staff and to clarify the current license conditions, Technical Specification Change Request number 56 has been submitted to delete the prohibitions on disposal of the AGW as presently stated in Specification 3.9.13. Further, the effluent release analyses performed in support of this evaluation demonstrate that the effluents from the proposed process water disposal system are well within the limits imposed by Appendix B to the TMI-2 Technical Specifications. Therefore, no changes to the THI-2 Technical Specifications are required. 10 CFR 50, Paragraph 50.59, states a proposed change involves an unreviewed safety question if:
- a. The probability of occurrence or the consequence of an accident or malfunction of equipment Important To Safety previously evaluated in the safety analysis report may be increased; or
- b. The possibility for an accident or malfunction of a different type than any evaluated previously in the safety analysis report may be created; or
- c. The margin of safety, as defined in the basis for any technical specification, is reduced.
Although the disposal system outlined in this report is different from the disposal options for liquid waste outlined in the FSAR, the consequences of these activities are bounded by analyses provided in the FSAR. The disposal system proposed does not increase the probability of an accident or malfunction of equipment important to safety. The operation and control of the system will be governed by procedures prepared and approved pursuant to Section 6.8.1, 6.8.2 and 3.9.13 of the TMI 2 Technical specifications and will be designed to minimize the potential for an inadvertent release and, therefore, reduce the probability of an accident. Additionally, the consequences of any accident associated with the disposal system would be bounded by the evaluations given in the TM!-2 FSAR for a postulated f ailure of the Borated Water Storage Tank (BWST). 0225H/13H
TER 3232-019 Rev. O Page 33 of 38 Supplement 2 of the THI-2 FSAR evaluated the postulated failure of the BWST. The evaluation assumed that the BWST contained "design basis" radioisotopic concentration. The mix of radioisotopes, in the FSAR evaluation, is vastly different from the mix of radioisotopes in the processed water. However, the resulting doses from tha release of the BWST contents into the Susquehanna River can be compared to the expected doses resulting f rom a hypothetical release to the river of all of the processed l water. The doses calculated below are for illustrative purposes cnly and ' show that the hypothetcal release of all cf the processed water is bounded l by a previously reviewed accident evaluation. Table 1 in Supplement 2 i (page S2-13C) of the FSAR, presents the resulting concentrations in the river from the postulated failure of the BWST. For this mix of radioisotopes, the radiologically significant radioisotopes are Cs-134 Cs-136, and Cs-137. Using the concentrations given in Table 1 of Supplement 2 for the east side of the island and the dose methodology given in Regulatory Guide 1.109, an adult is estimated to receive a dose of 7.8 rem to the liver from the consumption of one kilogram of fish residing in the east side of the island. The liver is the limiting organ for exposure to cesium. For comparative purposes, Section 7.2.4 of the NRC's PEIS (NUREG-0683 of March 1981) presents analyses of various accidents involving rupture of a processed water storage tank (PWST). The resulting doses evaluated in the PEIS for these accidents are significantly less and bounded by the dose consequences for the postulated failure of the BWST presented in the FSAR. The disposal system being proposed would not create an accident or malfunction of a different type. Postulated accidents associated with processed water disposal would consist of line breaks or tank ruptures for which the bounding accident has been evaluated above. The disposal of the processed water does not reduce any margin of safety as defined in the basis for any technical specification. The disposal system has been evaluated to determine the controls necessary to ensure, by compliance with governing procedures, that the operation of the system will comply with applicable technical specifications. Compliance with the applicable technical specifications ensures that public exposure from the planned gaseous or liquid discharges is well within the objectives of 10 CFR 50 Appendix 1. In conclusion, the disposal of the processed water does not involve an unreviewed safety questien. i I 4 0225H/13H
TER 3232-019 Rev. O Page 34 of 38 TABLE 1 IDENTIFICATION OF RADIONUCLIOES IN PROCESSEO WATER i Column 1 Column 2 Column 3 Column 4 Column 5 ' Curies Concentration Specific Total Grams Present in in pCi/ml Activity in A-2 Present in Nuclides 2.3 MGAL in 2.3 MGAL Ci/aram Value 2.3 MGAL l l l l l Cesium-137 l 3.2E-1 l 3.7E-5 l 9.8E+1 l 10 l 3.7E-3 Cesium-134 l 7.66E-3 l 8.8E-7 l 1.2E+3 l 10 l 6.38E-6 Strontium-90 l 9.6E-1 l 1.1E-4 l 1.5E+2 l 0.4 l 6.4E-3 Antimony-125/ l 2.0E-2 l 2.3E-6 l 1.4E+3 l 25 l 1.43E-5 Tellurium-125m l l l 1.8E+4 l 100 l Carbon-14 l 8.7E-1 l 1.0E-4 l 4.6 l 60 l 1.89E-2 Technetium-99 l 8.7E-3 l 1.0E-6 l 1.7E-2 l 25 l 5.12E-1 Iron-55 l 4.2E-3 l 4.8E-7 l 2.2E+3 l 1000 l 1.91E-6 Cobalt-60 1 4.2E-3 l 4.8E-7 l 1.1E+3 l 7 l 3.82E-6 Iodine-129 l <5.2E-3 l <6.0E-7 l 1.6E-4 l 2 l <3.25E+1 Cerium-144 l <1.4E-2 l <1.8E-6 l 3.2E+3 l 7 l <4.38E-6 Manganese-54 l <3.5E-4 l <4.0E-8 l 8.3E+3 l 20 l <4.2E-8 Cobalt-58 l <3.5E-4 l <4.0E-8 l 3.1E+4 l 20 l <1.13E-8 Nickel-63 l <5.2E-3 l <6.0E-7 l 4. 6 E +1 l 100 l <1.1 E -4 I Zinc-65 l <8.5E-4 l <9.8E-8 l 8.0E+3 l 30 l <1.06E-7 l Ruthenium-106/ l <2.9E-3 l <3.3E-7 l 3.4E+3 1 7 l <8.53E-7 l Rhodium-106 l l l l l Silver-110m l <4.9E-4 l <5.6E-8 l 4.7E+3 l 7 l <1.04E-7 Promethium-147 l <4.2E 2 l <4.8E-6 l 9.4E+2 l 25 l <4.47E-5 Europium-152 l <3.3E-6 l <3.8E-10 l 1.9E+2 l 10 l <1.74E-8 . Europium-154 l <3.8E-4 l <4.4E-8 l 1.5E+2 l 5 l <2.53E-6 Europium-155 l <9.6E-4 l <1.1E-7 l 1.4E+3 l 60 l <6.86E-7 Uranium-234 l <8.7E-5 l <1.0E-8 l 6.2E-3 l 0.1 l <1.40E-2 Uranium-235 l <1.0E-4 l <1.2E-8 l 2.1E-6 l 0.2 l <4. 7 6 E +1 Uranium-238 l <1.0E-4 l <1.2E-8 l 3.3E-7 Unlimited l <3.03E+2 l Plutonium-238 l <1.0E-4 l <1.2E-8 l 1. 7 E +1 l .003 l <5.88E-6 ! Plutonium-239 l <1.2E-4 l <1.4E-8 l 6.2E-2 l .002 l <1.94E-3 Plutonium-240 l <1.2E-4 l <1.4E-8 l 2.3E-1 l .002 l <5.22E-4 Plutonium-241 l <5.7E-3 l <6.5E-7 l 1.1E+2 l 0.1 l <5.18E-5 Americium-241 l <1.0E-4 l <1.2E-8 l 3.2 l .008 l <3.13E-5 Curium-242 l <8.7E-4 l <1.0E-7 l 3.3E+3 l 0.2 l <2.64E-7 I I I l l 7otal l <2.27 Ci l <2.6E-4 pC1/ml l l<384.66 grams l l l l l l s 0225H/13H __ _ _ _ . . _ _ _ _.)
TER 3232-019 Rev. O Page 35 of 38 TABLE 2 PROCESSEO WATER DISPOSAL SYSTEM INFLUENT LIMITS IN uC1/ml AND THE RESULTING ENVIRONMENTAL RELEASE RATES IN uCi/mi CouDied Mode Decoupled Mode Environmental Evaporator Resulting Vaporizer Release Rate Constituent Influent limit VaDorizer Limit influent Limit Limit l l l l Cesium-137 l 3.7E-5 l 3.7E-8 l 3.7E-8 l 3.7E-8 Cesium-134 l 8.8E-7 l 8.8E-10 l 8.8E-10 l 8.8E-10 Strontium-90 l 1.1 E-4 l 1.1E-7 l 1.1E-7 l 1.1E-7 Antimony-125/ l 2.3E-6 l 2.3E-9 l 2.3E-9 l 2.3E-9 Tellurium-125m l l l l Carbon-14 l 1.0E-4 l 1.0E-7 l 1.0E-7 l 1.0E-7 Technetium-99 l 1.0E-6 l 1.0E-9 l 1.0E-9 l 1.0E-9 Iron-55 l 4.8E-7 l 4.8E-10 l 4.8E-10 l 4.8E-10 Cobalt-60 l 4.8E-7 l 4.8E-10 l 4.8E-10 l 4.8E-10 lodine-129 l <6.0E-7 l <6.0E-10 l <6.0E-10 l <6.0E-10 Cerium-144 l <1.8E-6 l <1.8E-9 l <1.8E-9 l <1.8E-9 Manganese-54 l <4.0E-8 l <4.0E-11 l <4.0E-11 l <4.0E-11 Cobalt-58 l <4.0E-8 l <4.0E-11 l <4.0E-11 l <4.0E-11 Nickel-63 l <6.0E-7 l <6.0E-10 l <6.0E-10 l <6.0E-10 Zinc-65 l <9.8E-8 l <9.8E-11 l <9.8E-11 l <9.8E-11 Ruthenium-106/ l <3.3E-7 l <3.3E-10 l <3.3E-10 l <3.3E-10 Rhodium-106 l l l l Silver-110m l <5.6E-8 l <5.6E-11 l <5.6E-11 l <5.6E-11 Promethium-147 l <4.8E-6 l <4.8E-9 l <4.8E-9 l <4.8E-9 Europium-152 l <3.8E-10 l <3.8E-13 l <3.8E-13 l <3.8E-13 Europium-154 l <4.4E-8 l <4.4E-11 l <4.4E-11 l <4.4E-11 Europium-155 l <1.1E-7 l <1.1E-10 l <1.1 E-10 l <1.1E-10 Uranium-234 l <1.0E-8 l <1.0E-11 l <1.0E-11 l <1.0E-11 Uranium-235 l <1.2E-8 l <1.2E-11 l <1.2E-11 l <1.2E-11 Uranium-238 l <1.2E-8 l <1.2E-11 l <1.2E-11 l <1.2E-11 Plutonium-238 l <1.2E-8 l <1.2E-11 l <1.2E-11 l <1.2E-11 - Plutonium-239 l <1.4E-8 l <1.4E-11 l <1.4E-11 l < 1. 4 E -11 Plutonium-240 l <1.4E-8 l <1.4E-11 l <1.4E-11 l <1.4E-11 Plutonium-241 l <6.5E-7 l <6.5E-10 l <6. 5 E-10 l <6.5E-10 Americium-241 l <1.2E-8 l <1.2E-11 l <1.2E-11 l <1.2E-11 l Curium-242 l <1.0E-7 l <1.0E-10 l <1.0E-10 l < 1. 0 E -10 l l l l , Limits as specified are averaged over a calendar quarter. I 1 l 0225H/13H [
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TER 3232-019 Rev. O Page 38 of 38 LIST OF SPECIALITY SYMBOLS Figure 4a LAH level Alarm High LSH Level Switch High LAL Level Alarm Low LSL Level Switch Low LC Level Control LG Level kuge TI Temperature Indicator PI Pressure Indicator TW Themal Well DP Differential Pressure Gauge M Flow Meter C Compound Gauge PS Pressure Switch COND Conductivity Meter TS Temperature Switch TM or Thermostat Sight Flow Gauge Flow Indicator Terminal Connection _ C Eductor S Flow Strainer "1 - s , se Heat Exchange?, n y_}}