ML20154E406

Affidavit of H Behling (Contention 5d).* Supports Util Motion for Summary Disposition of Contention Re Effects of Tritium & Alpha Emitters/Transuranics.Certificate of Svc Encl

ML20154E406
Person / Time
Site:	Three Mile Island
Issue date:	05/13/1988
From:	Behling H GENERAL PUBLIC UTILITIES CORP.
To:
Shared Package
ML20154E212	List: ML20154E208 ML20154E230 ML20154E247 ML20154E268 ML20154E285 ML20154E293 ML20154E313 ML20154E325 ML20154E349 ML20154E368 ML20154E383 ML20154E406
References
OLA, NUDOCS 8805200205
Download: ML20154E406 (94)

Text

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UNITED STATES OF AMERICA NUCLEAR REGULATORY COMMISSION 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 Nuclear ) Generated Water)

Station, Unit 2) )

)

AFFIDAVIT OF DR. HANS BEHLING (CONTENTION Sd) hhk b h C

e:

e a TABLE OF CONTENTS I i

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e TRITIUM................................................ 2 j i

t A. Sources of Tritium............................... 3 B. Behavior of Tritium in the i EDViroD2ent....................................... 6 j i

C. Metabolism of Tritiated Water.................... 7 (

D. Physical and Radiological Characteristics t of Tritium....................................... 10

1. Physical Factors............................ 11 i

2. Effective Half-Life......................... 12 l

3. Quality Factor.............................. 13 .

E. Tritium Toxicity...........................'...... 16 i

1. Radiological Toxicity....................... 17 t

2. Non-radiological Toxicity................... 17 i r

HEALTH EFFECTS........................................ 20 A. Radiation and Cancer............................. 23 B. Genetic Effects.................................. 34 f i

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C. R diction Effcets on tho HumOn F3tus............. 36 III. RADIATION DOSES AND RISES TO THE PUBLIC FROM -

THE EVAPORATION OF TMI-2 WATER...................... 38 IV. AN ASSESSMENT FOR R2LEVANCY TO THE TMI-2 WATER DISPOSAL OF SCIENTIFIC DOCUMENTS CITED BY INTERVENORS................................ 46 A. Article 1: Dobson, R.L. and Cooper, M.F.

(1974), "Tritium Toxicity: Effect of Low-level HOH Exposure on Developing Female Germ Cells in the Mouse,"

Radiation Res., 58............................... 46

1. Dose........................................ 47

2. Specie Variations........................... 48 B. Article 2: Dobso., R.L., and Ewan, T.C.

(1976), The RBE of Tritium Radiation Measured in House Occytes: Increase at Low Exposure Levels. Radiation Res. 66.......... 51 C. Article 3: Zammenhof, S., and VanMarthens, E., (1979), The Effects of Chronic Ingestion of Tritiated Water on Prenatal Brain Development, Radiation Res. 77............. 52 D. Conclusion....................................... 53 V. TRANSURANICS.......................................... 54 A. Sources.......................................... 54

8. Chemical Properties.............................. 55

.e C. R-diological Prcpertics.......................... 56 D. Toxic Properties................................. 58 i

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E. Exposure Pathways and Distribution In the Body...................................... 59 I

F. Health Effects of Transuranics................... 62 G. Risk Estimates for Transuranics.................. 64 i H. Impact of Transuranics from TMI-2 r Evaporation...................................... 66 I. Comparison to Radon and Other Sources............ 71  ;

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.J. Summary.......................................... 74 L

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1 VI. CONCLUSION............................................ 76 4

REFERENCES............................................ 77 r

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UNITED STATES OF AMERICA NUCLEAR REGULATORY COMMISSION 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 Nuclear ) Generated Water)

Station, Unit 2) )

AFFIDAVIT OF DR. HANS BEHLING (CONTENTION Sd)

County of Dauphin )

) ss.

Commonwealth of Pennsylvania )

DR. HANS BEHLING, being duly sworn according to law, deposes and says as follows:

1. My name is Dr. Hans Behling. My business address is P.O.

Box 480, Middletown, Pennsylvania 17057. I am employed by GPU Nuclear Corporation as Manager of Radiological Health at Three Mile Island (TMI). In this position, my primary responsibilities are to provide technical and operational supervision of programs in radiation dosimetry and protection, and to provide technical expertisa and information in matters of health physics and radia-tion health effects. I have been employed in this position at TMI for four years, and have worked in the health physics and ra-A statement of diation health fields for approximately 20 years.

-- _ --------.------_ _------- - _ - - - - - l

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my professional qualifications and experience is attached hereto as Exhibit A.

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2. I make this Affidavit in support of GPU Nuclear Corpora-tion's Motion for Summary Disposition of Contention 5d, concern-ing the effects of tritium and alpha emitters /transuranics. I have personal knowledge of the matters stated herein and believe them to be true and correct. In my Affidavit, I discuss the im-portant aspects of tritium, particularly with respect to the pro-posed evaporation of accident generated water at TMI-2, and com-pare its risk to other sources of radiation exposure. Next, I discuss the effects and risks associated with alpha emitters and transuranics that might be present in the accident generated water. Based on the most current and authoritative studies, it is my opinion that the doses and risk of health effects attribut-able to tritium and alpha emitters /transuranics in t,he evaporator effluent will be insignificant.

I. TRITIUM

3. Tritium, owing to its ubiquitous presence in the environment and its properties, is perhaps the single most studied radionuclide. The environmental transport, metabolism, dosimetry and biological effects of tritium have been the subject of con-siderable research over the past three decades. Further, tritium has been extensively assessed by the National Council on Radia-tion Protection and Measurements (NORP) in NCRP Report No. 62, 2

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• "Tritium and the Environment," and NCRP Report No. 63, "Tritium  :

l and Other Radionuclide Labeled organic Compounds Incorporated i into Genetic Material." Tritium is also addressed in the Nation- .

al Academy of Science's Report on the Biological Effects of i Ionicing Radiation (1980), commonly referred to as the BEIR III Report.

1 J A. Sources of Tritium

4. There are numerous sources which independently contribute to the pool of tritium in the environment. The main sources of  ;

l tritium include the following (1) natural production by cosmic j rays, (2) nuclear weapons testing, (3) nuclear fuel cycle opera- f tien, (4) censumer products, and (5) tritium production facili- .

ties.  !

i l L i 5. Natural production of tritium occurs when cosmic rays frem )

outer space interact with atems of oxygen and nitrogen in the l 1 i

upper layers of our atmosphere. The total world inventory of i j 1

naturally produced tritium from cosmic ray production is estimat-ed at 70,000,000 curies (NCRP Report No. 62). Based on the loss of tritium threugh radioactive decay. it can readily be calculat-ed that the natural production rate is approximately 4,000,000

curies every year. Nearly all of this tritium is present as  !

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! tritiated water (HTC).  !

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6. Nuclear weapons testing produces tritium by both ternary fission and neutron activation. The tritium inventory of atmo- .

spheric weapons testing is not a constant but reached a maximum 5

in 1963 and in 1988 har been reduced to about 750,000,000 curias (NCRP Report No. 62).

7. Nuclear power stations also produce tritium by fission and neutron activution. Because of differences in water chemistry among various nuclear power plant designs, production rates vary.

Heavy water reactors which use deuterium as coolant and moderator produce hundreds to thousand times greater quantities of tritium than boiling water reactors (BWR) or pressurized water reactors (PWR). The TMI reactors are PWR design. Typical values of l tritium production are about 12 curies per billion watts of elec-tricity for BWR's and about 800 curies per billion vatts of elec-tricity produced for PWR's (Luykx, 1986). ,

8. Consumer products containing tritium include luminous dials  :

. t in watches and navigational instruments, and electronic devices filled with tritium gas. Tritium content of these devices may vary, but a standard wrist watch may contain 0.3 to 50 microcuries of tritium (Wehner, 1978). The total number of con-l sumer items is difficult to assess, but it is estimated that 1

about one percent of the processed activity in consumer items is j lost to the atmosphere during fabrication and ten percent is re-leased through waste disposal (incineration) of such consumer f

E items. Environmental releases from consumer items are estimated in the tins of thousands of curies per year. ,

9. Tritium production facilities produce tritium by activation of lithium in a reactor. Releases of tritium from production fa-cilities are-principally in gaseous form and quantities may reach several hundred thousand curies per year per facility.

10. Table 1 gives approximate estimates of tritium from dif-ferent existing sources. Of the total present-day world invento-ry, weapon testing remains the principal source of tritium.

Nearly ten percent of the total inventory of tritium is produced naturally.

Table 1 Total Inventory Source (curies) i Natural Production 70,000;000 Nuclear Explosion 750,000,000 Nuclear Fuel Cycle es1,080',000 Consumer Products ^/2,700,000

11. Most tritium exists in the form of water, and all things which contain water contain small concentrations of tritium including living tissues. Based on the yearly total volume of

( water in the Susquehanna River, it can be estimated that a total

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of 4650 curies flow past TMI annually. The total quantity of tritium which would Le relaased to the air from the evaporation of TMI-2 processed water is 1020 curies. This represents about 1/2000 of the tritium which is produced naturally every year.

B. Behavior of Tritium In The Environment

12. Tritium is an isotope of hydrogen and has one proton and two neutrons in its nucleus. It is most frequently symbolized as H-3 or T. Its chemical properties and therefore its distribution in nature are essentially the same as hydrogen. The dispersal of tritium as water (HTO) into the environment is governed by the same processes that control the transport and distribution of ordinary water. Thus, tritiated water follows the same pathways of natural water in the environment, and in plants, animals and humans. .

13. A small but biologically insignificant exception occurs when tritiated water passes across a liquid-gas phase boundary. Be-cause of the difference in mass between H O and HTO (18 vs. 20),

2 the vapor pressure of tritiated water is reduced to 90 to 92 per-cent that of normal water (Horton, 1971). This lower vapor pres-sure of HTO would slightly favor the surface evaporation of natu-ral water from . Avers, lakes, and ponds. Because animals and humans consume and excrete nearly all water across liquid-liquid boundaries, there is no significant bioaccumulation or concentra-tion of tritium in tissues.

14. In transpiring plants with leaves having large surface areas, tritium levels may exceed environmental levels through preferential transpiration of non-tritiated water from the sur-face of. leaves to the atmosphere. Under extreme conditions of low atmospheric humidity (as may occur in a desert), the tritium .

content in plants may be increased by as much as a factor of 3 over the specific activity of the environmental soil water. The potential for bioaccumulation in plants in temperate climates is small and has no significance for enhancing human exposure. In fact, in mammals, including man, the specific activities of tritium in body water and tissues are slightly lower than those in the environment, including drinking water and food (NCRP Report No. 62).

15. In summary, the distribution of tritiated water is nearly uniform in the environment and its concentration is governed pri-marily by the dilution with the large quantities of water which exist in the natural environment. Fully two-thirds.of the earth's surface is covered by water in the form of rivers, lakes, and oceans.

C. Metabolism Of Tritiated Water

16. Tritium in water, water vapor, and foods may enter the body through respiration, ingestion and skin absorption. A quantita-tive breakdown of the contribution by each of these pathways is highly variable among individuals and, depends on the choice and

'9 source of foods, the ratio of' local drinking water to liquids from other sources, etc. In assessing the theoretical upper limit of exposure to any one individual, however, conservative assumptions are made which grossly overestimate the exposure which one might actually receive. For the maximally exposed individual, it is assumed that all food is grown by the individ-ual at a location of maximum tritium concentration in air, water and soil, giving the individual maximal exposure from the combi-nation of all pathways. Exposure of the maximally exposed indi-vidual to tritium is primarily due to ingestion of food and water (65%) with lesser contributions from inhalation and skin absorp-tion (NCRP Report No. 62).

17. When tritium is released to the environment as water, it will, in time, become part of other molecules, including those of living tissues. Hydrogen or tritium which is incorporated into such molecules is referred to as organically bound. Thern are several ways by which tritium that is originally bound to a water molecule becomes part of an organic molecule.

18. The simplest and most prevalent way is through the exchange of hydrogen ions which occurs naturally among molecules containing hyd ogen. The tritium atom of a water molecule is ex-changed for a hydrogen atom formerly attached to an organic mole-l cule. In living tissues, about 80 percent of organically bound l

l hydrogen exists as exchangeable hydrogen which, under long-term t

exposure, readily assumes equilibrium with tritium. In this way, l I

tritium may enter organic compounds passively by exchange with I l

hydrogen bound to nicrogen, sulfur, phosphorus, and oxygen. At equilibrium condition, the total number of organically-bound tritium atoms is proportionate to the ratio of available tritium atoms to hydrogen atoms.

19. The remaining 20 percent of organically-bound hydrogen is non-exchangeable. Non-exchangeable hydrogen is primarily bound to carbon.

20. Tritium can become incorporated into an organic molecule as non-exchangeable hydrogen. The initial step is the photosynthetic conversion by plants of carbon dioxide (CO2) and water (H 2 O or HTO) in the presence of sunlight to the organic molecule hexose. The process by which tritium is subsequently incorporated as non-exchangeable hydrogen in animals and humans involves the ingestion of organically bound food products. Sub-sequent cellular synthesis (enzyme-regulated) of proteins, carbohydrates, fats, and constituents of the genetic molecules of DNA may introduce non-exchangeable tritium into human tissues.

The rate and degree of incorporation of tritium as non-exchange-able organic hydrogen is complex and is governed by the specific biological function, rate of metabolic activity of a cell, and whether or not a cell undergoes cell replication. In general, molecules which have a slow turn-over rate (or long biological

life span) will incorporate proportionately small amounts of tritium per unit time. During turn-over of these molecules, tritium bound to molecul,es of proteins, sugars, fats, and DNA are degraded and eliminated from the body as metabolic waste (water, carbon dioxide, urea, etc.).

21. In the average indiviudal, there are 7 kg of total hydrogen, of which 4.7 kg are in body water and 2.3 kg are in the organic constituents of tissue. In the case of chronic exposure to tritium, it is assumed that the specific activities of tritium in water and organic constituents are in equilibrium and the frac-tions of the radiation dose from body water and organic constitu-ents are 2/3 and 1/3, respectively (NCRP Report No. 63).

22. It is important to point out that the biological half-life of tritium under equilibrium conditions is a composite value which reflects the percent contribution of various tritium containing molecules and their respective biological life span.

The relevance of biological half-life to dose calculation is dis-cussed below.

D. Physical And Radiological Characteristics Of Tritium

23. Factors which affect the dosimetry of tritium include physi-cal and biological properties, assumptions made about the organic binding of tritium which affects specific activity, and the assignment of quality facter (Q).

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. 1. Physical Factors

24. Tritium has a physical half-life of 12.26 years. It decays to helium-3 by emitting a very low energy beta particle which has a maximum energy of 18.6 kev and an average energy of 5.7 kev.

In water or tissue, this beta particle has an extremely limited range. The mean range of a 5.7 kev electron in water is 0.68 micro-meter (um) and approaches 6.0 pm for maximum energy betas.

Although there is significant variation in cell size, an average cell diameter is 15 pm (or less than one-thousandth of one inch) .

The nucleus contained in a cell has an average diameter of 8 um.

25. It is the nucleus of a cell which contains the genetic mate-rial DNA; and it is DNA exclusively that is regarded as the tar- ,

get molecule responsible for the potential radiation injury which msy result from low dose exposure. From the physical relation-ships described above, it becomes app,arent that radi.ation injury to living cells can only result from the radioactive decay of tritium in close proximity to the DNA molecule. About 80 percent of the radiation absorbed by the cell nucleus originates from tritium in the cell nucleus and only 20 percent from the cytoplasm (Bond, 1966). For a chronic condition of tritium expo-sure, it can be assumed that tritium is in equilibrium with hy-i drogen in water as well as all organically bound hydrogen. Under this condition, the dose rate for a given specific activity with-in tissue is essentially constant. The dose rate to the nucleus

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can, therefore, be assumed to be equal to that of the rest of the cell.

26'. A specific activity of one microcurie (uC1) of tritium dis-tributed uniformly in one gram of tissue delivers a dose rate of 12.14 millirad per hour (NCRP Report No. 63).

2. Effective Half-Life

27. The time required for a biological system, such as that of a human, to eliminate half the amount of radioactivity that has been incorporated bodily is defined by the effective half-life for a given radionuclide. The effective half-life of a radionuclide is affected by the rate of radioactive decay as well as its natural biological elimination from the body. However, when one of these two routes of elimination greatly exceeds the ,

other, the effective nalf-life t.pproaches that of the higher route of elimination. The radioactive half-life of 12 years.for tritium is many times longer than the biological elimination through urine output and to a lesser extent perspiration, respi-ration and fecal water. The elimination of tritium as tritiated water and organically bound hydrogen in exchangeable and non-exchangeable positions is determined by the combined elimination rates of at least three compartments -- tritiated water, ex-changeable organically bound tritium, and non-exchangeable organ-ically bound tritium. Tritiated water, which represents the dom-inant compartment, has a relatively short biological half-life of a few days. Although non-exchangeable organically bound tritium may have a biological half-life of several to many months, its ,

relative size and :ontribution to d,ose commitment are small.

Since daily water consumption and excretion is highly variable among individuals and since this represents the primary route of elimination of tritium from the body, the biological half-life is equally variable among individuals. It is estimated that for the average individual, tritium has a biological (or effective) half-life of about ten days (NCRP Report No. 62).

3. Quality Factor

28. Biological effects of ionizing radiation on living cells are the result of energy deposited within cells. The probability of occurrence of an effect like cancer is proportional to the amount of energy deposited per unit cell, which is defined as radiation dose in rads. For a constant radiation dose, however, various types of radiation are more effective in producing such a biolog-ical effect It is the quality factor (Q) by which'the absorbed dose is multiplied to quantify biological damage for all ionizing radiation. The unit of radiation exposure which takes into account the Q value is the relative biological effectiveness (RBE) for a given form of radiation and is expressed in rem.

Although the terms RBE and Q are used interchangeably, the Inter-national Committee on Radiation Protection (ICRP) has recommended that RBE be a term confined to actual radiobiological i .

measurements and that in radiation protection it be replaced by quality factor, Q, to reflect the "judgment" that is' applied to .

RBE values for various types of irradiation and biological end-points under consideration. Judgment may include which biologi-cal end-points are of importance and how their RBE values should be weighted to establish Q. For x-rays, Q has a value of one (1); for alpha particles Q has a value of twenty (20). The rela-tionship of rad to rem is defined as follows:

Absorbed Dose (rad) x Q = Dose in rem

29. From this relationship, it can be seen that for alpha radia-tion, the same absorbed dose has a value that is twenty times that of x-rays when expressed in units of rem. This difference of relative biological effectiveness for various forms of radia-tion is largely determined by the rate with which energy is de-posited in tissue and is defined by the linent energy transfe"

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(LET) value of that radiation. For a beta particle with a mean energy of 5.7 kev (the average energy of a beta part'icle emitted from tritium), the energy when distributed over the full range of 0.68 um would have the LET value of about 8.2 kev /um. The RBE value increases linearly with increase in the LET value. Maximum Q values of 10 to 20 correspond to LET values which range from 53 to 175 kev /um (ICRU Report 40, 1986). The relative biological effectiveness for a particular form of radiation is the empiri-cally derived ratio of the dose of a "reference radiation" to the 3

dose of the particular form of radiation that produces the same biological effect, .

RBE = Dose of reference radiation Dose of investigative radiation

30. The radiation for which the RBE value is one (1.0) is termed the reference radiation. X-rays with an effective photon energy of 200 kev are :he recommended reference radiation against which other forms of radiation are compared. When radiation exposure to tritium is ccmpared to that of x-rays, a RBE of 1 is raost com-monly observed. However, some experimenters have used Co-60 as the reference radiation which emits high energy photons and has a RBE value of 0.5 when compared to x-rays. Consequently, the use of Co-60 as reference radiation in assessing tritium yields a RBE value of 2 for tritium. Thus, the reported RBE value for tritium as repo:ced in the literature can vary by a factor of approxi-mately 2 depending upon whether gamma rays or x-rays are used for the reference radiation. ,

31. The second ve.riable which affects the RBE value for a spe-cific type of radiation is the selection of the biological system and the specific biological end-point that is being investigated.

Biological systems may vary from cells cultured in a petri dish to human epidemiological studies. The biological end-point is equally variable. Common biological end-points include cell death, cyto-genetic changes, biochemical alterations in cell /

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tissue metabolism, morphological and functional cellular changes, changes in reproductive capacity at the cellular / organismal ,

level, neoplastic transformation or tumor induction, etc.

32. As a result, a variety of RBE values ranging from 1.to 3 for tritium have been reported by different investigators and can be attributed to differences in the biological end-points measured and the selection of reference radiation to which the effects of tritium are compared. Since the principal risk of low-level irradiation is the risk of cancer induction, it is this end-point which governs the selection of RBE value and, therefore, its quality factor.

33. The National Council of Radiation Protection and Measurement (NCRP Report No. 91) and the International Commission on Radiological Protection (ICRS Publication 26) both have adopted the Q value of 1 for tritium. -

E. Tritium Toxicity ,

34. The toxicity of any radioactive nuclide may have two compo-nents. A radionuclide as a potential source for internal expo-sure may be ranked on a scale relative to other radioactive nuclides with respect to its ability to produce biological harm.

Secondly, a radionuclide may have chemical and physical prop-erties which in themselves may produce biological harm.

1. Radiological Toxicity

35. The International Atomic Energy Agency (IAEA) has investi-gated the radiotoxicity of 236 radionuclides and established a relative ranking scale for each of them (Technical Report Series No. 15). This relative ranking scale incorporates all of the varlables which may have an adverse effect on human health. In-cluded are such variables as the type and energy of radioactive emission (s), the physical half-life of the isotope, and all of its chemical and biological properties. Chemical and biological properties determine how a nuclide enters the body and how it will be distributed, metabolized and excreted. Of the 236 radionucli, des thus ranked from high to low, tritium is number 225 and is classified as having a very low radiotoxicity. The low radiotoxicity ranking is due to the fact that tritium emits a very low energy beta, is not biologically concentrated in the ,

body, distributes itself nearly uniformly within the body, and has a short biological half-life. '

2. Non-radiological Toxicity

36. Tritium as an isotope of hydrogen is chemically non-toxic.

However, there has been some apprehension that tritium may con-stitute a hazard when it is metabolically incorporated into DNA.

A possible phenomenon, unique to some internal emitters, is the chemical transmutation effect and its potential for inducing mo-lecular disorientation.

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37. Chemical transmutation refers to the fact that when a radio-active isotope emits a beta particle, it also converts a' neutron to a proton and in the process becomes a new element. Tritium

('H), when it undergoes radioactive decay, becomes Helium-3 ('He) which is a chemically inert gas. The possible transmutational effects are obvious for instances where the radioactive atom' occupies a key location within a critical molecule.

38. Tritium has been extensively investigated for its transmuta-tion potential effects when it is organically bound to specific locations within the DNA molecule. Laboratory studies suggest that for some highly specific positions within the DNA molecule (i.e., 'H-5-cytosine, 'H-6-thymidine and 'H-2-adenine ) , cellular mutagenic effects may be produced by chemical transmutation.

When bacterial cells (Person, 1976), f ruit flies (Kaplan, 1965; Kieft, 1969) and mice (Carsten, 1976) were given these H-3 la-belled DNA precursor molecules, mutagenic effects were observed at levels in excess of what would have been expected from the ra-

,dioactive emissions alone. However, these laboratory conditions of exposures are extreme, if not unique, and may not represent transmutational effects under natural conditions to tritium expo-sure.

39. While DNA chromosomal breakage is not a genetic effect in the strict sense, it is closely related and may therefore serve l as an indicator of genetic damage. Sender (1962) studied the i

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e induction of chromosomal aberrations in human leukocytes in vitro following exposure to tritiated thymidine and found no correla-tion between the site.of labelling and the site of breakage.

40. It must be kept in mind that-the relative abundance of hy-drogen atoms having the potential for organic binding to the three positions within DNA for which transmutation effects have been demonstrated is extremely low. Moreover, these key posi-tions also represent organic hydrogen that is non-exchangeable.

As such, only cells which are actively dividing are potentially susceptible. In the adult human, only a v.sry small fraction of cells in the body are mit,otically active.

41. The National Committee on Radiation Protection and Measure-ment has stated that,

"...it is reasonably conservative to assume, for the purpose of practical hazards considerations',

that there is no significant transmutation effect for tritium incorporated in DNA, and that one may estimate hazards solely on the basis of absorbed beta dose.... There is, at present no reason to consider the RBE for chromosome aberration produc-tion by beta rays from incorporated tritium to be different from one." (NCRP Report No. 63)

42. In summary, the distribution of tritium within the nucleus

.seems to be relatively unimportant. Tritium as water or incorpo-rated into DNA or DNA associated proteins (histones) is not no-ticeably more detrimental than an equivalent dose of external body exposure from gamma or x-rays (Bond, 1966).

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II. HEALTH EFFECTS o

43. From the foregoing statements we can predict health eff.ects among a human population exposed to-tritium on the basis that the potential health effects for tritium are primarily confined to the radiation dose and that this radiation dose is identical to other radiation exposures for which human epidemiological data is L

abundant.

44. Medical scientists have been studying ionizing radiation and +

its effects on human health for more than eight decades. The General Accounting Office reported in 1981 that there were more than 80,000 separate scientific studies of the health effects of radiation. The estimated cost of this research is about

$2 billion. In fact, the National Academy of Sciences has stated l

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that, "...it is fair to say that we have mere scientific evidence  ;

on the hazards of ionizing radiation than most, if not all, other environmental agents that affect the general public" (BEIR III, l 1980).

45. Much of our current knowledge of the health effects of radi-a* ion comes from extensive laboratory animal experiments. Under l laboratory conditions many crucial variables can be accurately controlled. These include, for example, the total dose, time in-terval and quality of radiation, and the individual chacteristics such as age, sex and health status.

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46. While laboratory animal experiments serve as valuable models for human studies, there are limitations in drawing conclusions ,

from biological effects observed in irradiated animals to poten-tial health effects in humans. Thus, the most relevant studies are the epidemiological surveys that have focused on human popu-lations who received radiation under a variety of conditions of intentional or inadvertent exposure. Most of these epidemiological studies involved population groups ranging from several hundred to more than 100,000 individuals. The most im-portant surveys have involved the following groups:

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• Survivors of the Atomic Bomb and Nuclear Weacons Tests

- The most intensely studied human populations are the Japanese survivors of the atomic bombs in Hiroshima and

, Nagasaki. These people were exposed to radiation from the bombs and, subsequently, radioactive fallout.

Studies have also been made of natives of the Marshall Islands who were accidentially exposed to fallout from nuclear weapons testing in 1954.

• Medical Radiation - Large doses of radiation were given to treat various health problems, such as ankylosing spondylitis, thymus enlargement, ringworm of the scalp, and breast cancer. Children whose mothers were irradi-ated during pregnancy have also been studied.

Radium Dial Painters - Workers early in this century ingested radium-containing paint from luminous watches, . v clocks and aircraft instruments through a practice of "tipping" paint brushes with their lips.

Uranium Mine.rs - Early in this century, certain large i

mines in Europe were worked for pitchblende, a uranium ore. Lung cancer was highly prevalent among the miners t.

as a result of the inhalation of large quantities of airborne radioactive dust particles. Studies have shown that the risk of lung. cancer among these miners was at least 50 percent higher than that of the general population.

Radiolocists - Pioneer medical scientists and physi-cians using x-rays, unaware of the potential hazards, accumulated large radiation doses principally to their hands.

47. These and other populations, many of whom continue to be

studied today, add to our current understanding and provide reli- '

able data on health effects resulting from large doses of radia-i tion. Among radiation scientists, there is nearly complete agreement on the health effects and risks following such large radiation doses. What remains uncertain is the assessment of i

l potential health effects which may result from small doses of ra-l >

! diation. At issue is whether radiation health effects occur at >

! all for low dose exposure.

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. 48. Further, certain health effects may not appear'for years or E even decades after. exposure to radiation. Such effects result from specific changes that occur in some cells or a single cell.

Although these selective cellular changes occur rarely, when~they do there is a possibility that the altered cell may develop into cancer. If the altered cell is a reproductive cell, there is a possibility of transmitting genetic defects to the progeny of ir-

. radiated parents. Also, a developing embryo or fetus could .

possibly. suffer injury if a pregnant women is exposed to radia-tion.

9

49. For small doses of radiation, the likelihood that even a single cell will undergo such a selective alteration leading to cancer is extremely low. Furthermore, genetic effects, di s tu r-4 .

bances in growth and development of an embryo, and cancer can b3 caused by many chemical, physical and biological agents, many of which exist naturally in the environment. Thus, for even large doses of radiation, health effects can only be observed as small l increases above the spontaneous incidence.

I I A. Radiation and Cancer

50. Next to heart disease, cancer is the leading cause of death i

in the United States. The American Cancer Society estimated that l in 1986, about 930,000 people would be diagnosed as having can-cer. In 1985, an estimated 462,000 Americans died of cancer. It is estimated that one person in three (about 30 percent) will 1

develop cancer some time during their lives, of which slightly more than half w_.1 eventually die of the disease.

51. Cancer is considered to be a group of diseases, and more than 250 different forms have been identified so far in humans.

Taken together, they affect nearly every human cell type.

Studies indicate that the prevalence of cancer depends on many risk factors, including race, sex, diet, lifestyle, health, occu-pation and personal habits. However, among the most important risk factors is the age of the individual, particularly after the age of 40. Figure 1 illustrates the relationship of age and can-cer incidence in the general population. The risk increases sig-nificantly at about age 20 and increases approximately 100 fold by age 80.

Figure 1 Cancer incidence at Different Ages in the UnHed States 3500 i i s i i i i e

m - ~

8.

l, 2500 - MALES -

8 gm - "

a , .e

- ~

3 1500 ,

15 #

1000 -

, s, -#' FEMALES.

- 500 - * ~

l <

l i n  ; .1*

• _

I I I o

_ 1 O 10 20 30 40 50 60 70 80 85 i

AGE IN YEARS l I l

• 9

52. Contrary to common belief, cancer is not a new disease brought on by industrialization. In fact, researchers believe that the vast majority of cancer-causing agents arc of natural origin. Natural cancer-causing agents can be found in most foods which make up the human diet. A variety of mold, for example, which frequently contaminates food such as corn, grain, nuts, bread, cheese and fruits has been identified as a major cause of liver cancer. Microrganisms, such ~aus viruses, are also known to cause cancer.

53. In addition to an abundence of natural cancer causing agents, there are numerous man-made agents, including radiation, which can produce. cancer. Tobacco smoking is without a doubt a major and well-understood risk, causing about 30 percent of all cancer deaths, including lung, larynx, and possibly bladder and breast cancer, as well as 15 percent of the fatal heart attacks in the United Statea.

54. The evidence for radiation-induced human cancer comes largely from population studies of three groups of people: (1) persons exposed to atomic bomb radiation, .(2) persons exposed to medical radiation, and (3) persons exposed to radiation as part of their occupation. Collectively, these groups represent hun-dreds of thousands of individuals.

i e

• n,- . . , ,- - , - . , - , ~ , , , - . , ,-,-m -, --- -, - - - - - - , ,--..-p y ,

55. Interpreting epidemiological data requires an understanding of the disease process as it affects large populations, together ,

with the s.tatistical techniques used in the interpretation of data. Radiation-induced cancers may not appear for years or de-cades after exposure. This time delay between exposure to a cancer-causing agent and the clinical observation of a cancer is

~

called the latency period. Human leukemias,.for example, may not appear for two to five years after exposure; solid-tumor cancers, such as those of the lung or breast, may not be evident for 10 years or more. Long latency periods, therefore, make the inves-tigation of cancer-causing agents difficult. Many years of ob-servation are required for reliable conclusions.

56. A second difficulty in the analysis of human data arises from the fact that cancers induced by radiation are indistin-guishable from those arising spontaneously or those caused by -

other carcinogens. Physicians and pathologists cannot determine,

)

t based on tissue type, whether certain lung cancers, for example.

are caused by radiation or by cigarette smoking, air pollutants, t

chemicals or other cancer-causing agents. The ability to detect the common cancers caused by any specific agent is, therefore, limited to statistical analyses. These statistical methods rely on the fact that the incidence of various cancers in a given pop-i ulation can be predicted with reasonable accuracy. For a suffi- ,

ciently large group of people who have received radiation expo-sure, an incidence of cancers above the expected level would

suggest that radiation was a possible cause for the excess number of cancers, but it would not identify radiation as the cause of a cancer for any specific individual.

57. Epidemiological studies of people who were exposed to rela-tively high doses of radiation (greater than 50,000 millirems or r 50 rems) have shown a causal relationship between radiation and an increased cancer incidence. Studies of 82,000 Japanese survi-vors of the atomic bomb have provided valuable information on latency periods, the types of cancers associated with radiation and the dosos of radiation required to induce an excess incidence of cancer (Kato, 1982). Based on reported location at the time of the blast and other factors, dose estimates have been calcu-

, lated for 97 percent of these survivors.

o

58. Although radiation doses varied from thousands to hundreds of thousands of millirems (rems to hundreds of rems)*, the average whole-body dose has been estimated to be between 25,000 and 30,000 millirems (25 to 30 rems). Table 2 summarize's cancer mor- l tality among atomic bomb survivors.

l l

I r I

4 4

I

Table 2 Radiation-Induced Cancer Among Atomic Bomb Survivors Through 1978

• 82,000 Survivors (a group selected in 1950) 23,500 Total Number Deceased 4,800 Cancer Deaths From All Causes 250 Cancer Deaths Attributed to Radiation

59. Different cells and tissues of the body are affected by ra-diation in different ways. Thus, some cancers are more fre-quently linked to radistion than others. On a relative basis, breast cancer, thyroid cancer and leukemia occur at a higher rate among people exposed to whole body radiation then they do among the general population. A moderately increased incidence occurs for lung, pharynx, pancreas, digestive tract and lymph node can-Cers.

60. Other cancers have a low induction rate or correspond to tissues not known to be affected by radiation. Although these cancers occur frequently in the normal population, to date they have not been observed in excess of their normal ineidence among individuals exposed to radiation. This implies that the sensi-tivity to radiation induction of these cancers is either ex-tremely low or is absent.

61. Leukemia was the first type of cancer to appear in excess in the Japanese survivors of the atomic bombs. The first cases began to appear in the late 1940's and peaked about five to nine years after exposure. Initial increases in breast, thyroid, and

! _ m .-

.a. -

lung cancers were seen in the mid to late 1950's. A statistical.

excess increase for other cancers required even longer periods: ,

stomach (about 15 years), urinary tract (about 20 years), and ,

colon (more than 20 years). 'Some cancers, such as those of the-urinary tract, were not seen at increased rates execpt in survi-vers who received radiation doses of more than 100,000 millirems (100 rems). Other cancers, including Hodgkin's disease, have not been observed for even high doses of radiation.

62. Based on the epidemiological studies of large populations exposed to radiation, scientists can estimate how many people are likely to develop specific types of cancers. The probability of getting cancer from any cause is expressed in terms of risk coef-ficients (the number of cases expected per million people per unit of dose).

63. The earliest estimates of cancer risks were made by E. B.

Lewis in 1957 and were limitad to leukemia. Using data from the Japanese A-bomb survivors, patients treated with rad'iation for ankylosing spondylitis, children treated for thymic enlargement, and occupationally exposed radiologists, he arrived at life-time leukemia risk of about 0.5 x 10-4 per rem of exposure (i.e., one chance in twenty thousand per rem of exposure). Comprehensive numerical estimates for cancers including solid tumors were pub-lished independently in 1972 by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and by the

~

• Committee on Biological Effects of Ionizing Radiation of the Na-tional Academy of Sciences, known as BEIR.I. These were followed

• a few years later by a revised estimate. ICRP also published risk estimates in 1977.

64. Most estimates of the risk of cancers caused by radiation have relied on epidemiological studies where doses were generally more than 50,000 millirems (50 rems). In such studies, the long-term effects were observed as a higher incidence of cancer for a particular group of individuals than one would normally expect.

When individual radiation doses are less than 10,000 millirems (10 rems), the dose is too small to detect any statistical excess cancers in the presence of naturally occuring cancers. Realth i effects from such low doses occur so infrequently, if at all, that they cannot be observed directly or detected statistically above what would be expected to occur spontaneously or normally in an otherwise unirradiated population.

65. Estimates of health effects for low-level radia' tion are made by assuming that the frequency of risks obser"ed at high doses i can be proportionately related to corresponding low radiation i

doses. The estimates also assume that there is no threshold dose below which radiation will cause no cancers. This linear, no-I threshold hypothesis assumes that for any dose, no matter how i

i small, there is some correspondingly small risk, even if it can-1 not be measured. Most scientists believe that the linear, l

l 4

no-threshold relationship overestimates the health risk for small doses of low-LET radiation. . ,

66. Table 3 shows the current absolute radiation risk values for several types of cancer as estimated by the ICRP, the UNSCEAR and the BEIR III. For example, the ICRP estimates that for one mil-lion people, each exposed to 1,000 millirems (1 rem) of radia-tien, there could be 20 radiation-induced leukemia fatalities.

Risk values established independently by the three committees are in close agreement.

Table 3 Estimates of Lifetime Cancer Mortality by Anatomic Site Per Million People Exposed to 1,000 Millirems (1 Rem) Each Type of Cancer ICRP UNSCEAR BEIR III Leukemia 20 15-25 22 Lung 2C 25 28 Breast 13 30 11 Bone 5 2-5 0.5 GI Tract --

25 19 Thyroid 5 5-15 7 Other 50 25 31 Approximate Total 110 120 120

67. Since 1980 new information has accumulated which may impact current risk estimates. The most important study on which past risk estimates were based are those involving the Japanese A-bomb su rvivo rs . In recent years, two factors have been identified which may impact our current risk estimates for radiation induc-tion of cancer. For the most recent period, between 1975 and l

d

-4 1982, for which cancer data has been assessed, there was an unex-pected increase in the number of observed solid tumors among ,

A-bomb survivors (Sinclair, 1987).

68. Second, there has also been an awareness that the 1965 expo-sure doses assigned to the Japanese A-bomb survivors by Japanese-and American scientists (known as the T65D dosimetry data), were in error. The current reassessment of exposure doses (known as DS86) has significantly reducea the average dose to the A-bomb survivors. One difference between DS86 and T65D is the re-assignment of neutron doses to the Hiroshima population where the ratio of neutron to gamma ray dose component was initially over-estimated.

69. The combined impact on risk estimates is still not known.

Dale Preston and Donald Pierce of the Radiation Effects Research Foundation have compared the risk estimates for the two i dosimetries. Risk estimates for leukemia may increase by a fac-t ter of two while those for solid tumors may increase by only 50 l percent (Roberts, 1987).

70. In con. ext with the possibility that current risk estimates

) may, in the future, be increased by possibly a factor of 2, it l must also be pointed out that many scientists believe that cur-I

rent estimates tend to overestimate the risk of cancer by a fac-

! tor of 3-5 (Sinclair, 1981). The reason for assuming that cur-I rent risk estimates overestimate the real risk is based on the following scientific observations.

=.

71. In laboratory experiments it can be demonstrated that the likelihood of observing a biological effect not only increases ,

with the dose of radiation but also with the rate with which the dose is delivered. For a fixed dose of low-LET radiation, the faster it is delivered the more probable an effect may occur.

The NCRP (Report No. 64) has reviewed animal systems in which the effect of dose rates was studied. These studies showed that for a constant total dose of low-LET radiation, high dose rates were 2 to 10 times more effective in producing a particular biological effect than protracted exposure. Han (1980) showed that normal cells in tissue culture when exposed to Co-60 radiation delivered at a dose rate of 100 rad / min were eight times more likely to un-dergo neoplastic transformation than cells exposed to the same total does but delivered at a rate of 0.1 rad / min.

72. From these observations, it can be assumed that the current risk values may, in spite of other errors, still overestimate the real risk since the current risk estimates frem the, Japanese data were based on radiation exposure which was delivered nearly in-l stantaneously (high dose rate). These risk estimates, when epplied to low-level exposure conditions for other human popula-tions, would equally tend to overestimate the health risks sever-l al fold.

B. Genetic Effects

73. Genetic changes in the sperm or egg cells can result in ill health appearing in future generations. The fertilized egg contains all of the genetic information necessary to produce the organs and tissues of a new individual. This information is car-ried in the cell's nucleus in small chromosomes, of which equal numbers are contributed by both parents. The chromosomes trans-mit the genetic information from one generation to the next.

74. The genetic material contained in thn cell nucleus can be altered by a large variety of toxic agent:3, including heat, chem-icals, and both natural and man-made radiation. Genetic muta-tions occur randomly in all plant, animal and human populations and are considered to be the primary mechanism for evolutionary changes in all species. Geneticists generally agree that most such mutations are harmful. Epidemiological studies'have shown that about 11 percent of all people are affected by a genetic disease at some time in their lives.

75. Laboratory studies of mice exposed to large doses of radia-tion for many generations have shown genetic effects. Studies of humans, however, have not yet produced reliable evidence for in-heritable effects, such as development mal formations, still births or neonatal deaths. It is difficult to measure most muta-tions because they are difficult to observe and are randomly dis-tributed within a population group. of the 35,000 children bcrn I

to parents irradiated at Hiroshima and Nagasaki, - the averige parental dose being 25,000 to 30,000 millirems (25 to 30 rems) there has been no observable increase in genetic defects. Using all the information available, scientists have estimated that 100,000 to 200,000 millirems (100 to 200 rems) to each person in a large popluation would be required to produce genetic mutations equal in number to those occurring naturally in a non-irradiated population.

76. Using a number of extremely conservative assumptions, it is possible to arrive at an estimate of the risk of genetic damage per rem While no genetic effects are observable at low doses, such risk estimations are useful in establishing radiation pro-tection standards and bounding possible effects of radiation.

The most current risk estimates are those contained in the BEIR III Report, using the linear no thresP.,ld hypothesis. These es-timates are shown in Table 4.

e

1 Table 4 Risk Coefficients Effect per Million Current Incidence, Genetic Liveborn offspring, per Million Liveborn Abnormalities

• Rem per Generation Offspring Geometric Mean Range First Generation 19 (5-75) 107,100 All Future Generations 257 (60-1100) ---

• BEIR III p. 85 (based on average population exposure of 1 rem per 30 year generation). See U.S. EPA "Radionuclides,"

Vol. 1 pp. 8-49 (1984).

C. Radiation Effects on the uman Fetus

77. Studies of the embryo-fetus exposed in-utero have demon-strated that the human fetus is sensitive to radiation. Radia-tion injury to the human fetus may be expressed as congenital de-fects, mental retardation and leukemia.

78. Childhood cancer studies among the ' ',panese exposed to radi-ation in-utero showed no significant excess of mortality from ju-venile leukemia or other cancers. Other studies predict that the risk of leukemia and other childhood cancers in children in-creases if the mother is exposed to diagnostic radiation to the abdomen during pregnancy. However, these surveys remain contro-versial. There has been some criticism that the original surveys may be flawed by certain selection factors, particularly since l ,

many of the radiological procedures were requested by physicians for medical reasons, and the data depended almost exclusively on recall of past events by affected mothers.

79. BEIR III data suggest that the incidence of leukemia among children from birth to 10 years of age in the United States could -

rise by 0.6 cases in 1,00^ children if each child were exposed to 1,000 millirems (1 rem) of radiation before birth.

80. As regards the induction of mental retardation, the fetus is most likely to be affected during the 8th to the 15th week of pregnancy, an initial period when specific cells, including those of the brain, are undergoing crucial development. Although ani-mal experiments have shown developmental health effects with the embryo-fetus for radiation doses as low as 5,000 to 10,000 millirems (5 to 10 rems), it is not possible to demonstrate with certainty that injury to a human fetus can be induced by such low doses. The evidence is based on the epidemiological studies of <

children born to women of Hiroshima and Nagasaki who'were exposed to radiation in-utero.

81. According to the medical evidence available today, the in-

, creased risk from doses less than 10,000 millirems (10 rems) for any individual is very small compared with the normal risk of de-velopmental abnormalities in the newborn. BEIR III concludes that with respect to teratologic effects, threshold doses proba-bly do exist below which such effects are not induced in man by exposures at sensitive stages in development. Further, these thresholds may be higher for protracted or fractionated radiation than for acute single exposures.

III. RADIATION DOSES AND RISKS TO THE PUBLIC FROM THE EVAPORATION OF TMI-2 WATER

82. The impact on the envir?nment and human population living within the vicinity of Three Mile Island from the disposal of TMI-2 accident generated water was initially assessed by the NRC in the 1981 Programmatic Environmental Impact Statement (PEIS) on the cleanup of the TMI-2 accident (NUREG-0683). A final supple-ment to the PEIS was prepared and released by the NRC in June of 1987 (NUREG-0683, Supplement No. 2, Final Report). This Supple-ment includes new information obtained from the GPUN and a host of scientific experts including scientists from the Pacifia Northwest Laboratory of the U.S. Department of Energy. The Sup-plement reassesses potential environmental impacts which might result from the disposal of accident generated water,.

83. In addition, the National Council on Radiation Protection and Measurement (NCRP), at the request of the NRC, established a Task Group to indepen'dently review the potential environmental impacts of these proposals (NCRP Commentary No. 4, 1987). The request for the NCRP to independently investigate potential envi-ronmental impact at the TMI facility was considered appropriate in view of their previous work and expertise on this subject. In 1979, the NCRP had published NCRP Report No. 62, Tritium in the Environment, which reviewed all pertinent scientific studies up ,

to that time and provided useful models for assessing the envi-ronmental impact of tritium.

84. Finally, in 1986, GPU, Nuclear Corporation issued its own report. This report specified three technically feasible and en-vironmentally safe rathods for disposing of the water and also assessed the environmental impact.

85. In any situation involving the potential radiation exposure by a member of the public as a result of environmentally release radioactivity, it is desirable not only to calculate average individual exposures but also to establish a theoretical upper limit for individual exposure. Assumptions which are highly im-probable, but nevertheless theoretically possible, are made to calculate the dose of this maximally exposed individual. Includ-ed among these conservative assumptions is the continuous breath-ing of air and exclusive consumption of locally obta'ined food and drinking water each at their highest levels in the environment.

86. For the entire two year period of evaporation, the NRC has calculated that the total doses from all radionuclides to the maximally exposed individual are 0.7 mrem to the total body, 0.8 mrem to the bones, and 4 mrem to the thyroid. These three doses can be added to establish a single dose which is termed the "effective dose equivalent." The effective dose equivalent represents the sum of the weighted dose equivalents for irradi-ated tissues and takes into account the relative susceptibility ,

and contribution to stochastic risks (cancer / hereditary) of any one tissue relative to the irradiation of the whole body. Rela-tive susceptibility is quantitatively expressed by weighting fac-tors (WT ) which were established by the ICRP (Publication 26) in 1977. The WT values for bone and thyroid are 0.15 and 0.03 re-spectively. For example this implies that a dose of 1,000 mrem to the thyroid has the same health risk (cancer) as a dose of 30 mrem to the whole body (i.e. 0.03 W x 1,000 mremthyroid

• T 30 mrem effective dose equivalent). Using the NRC's calculated doses for evaporation, the effective dose equivalent is 0.94 mrem to the maximally exposed individual. The population which may be potentially affected by the evaporation of processed water is de-fined by a 50 mile radius around TMI and includes 2.2 million individuals. The average exposure for this populatibn yields a dose value of 0.00146 mrem per individual. The total population or collective dose is calculated by summing up each individual dose for the 2.2 million people living within a 50 mile radius of Three Mile Island, yielding a collective dose of 3.21 person-rem (effective dose equivalent).

87. The doses as calculated by GPUN are slightly higher. GPUN calculates that the hypothetical maximally exposed individual will receive 3.6 mrem to the bone and 2.0 mrem total body, which when combined produces an effective dose equivalent of 2.54 mrem.

- The average exposure for the population within a 50 mile radius is 0.01 mram/ individual and the total population dose is rounded F

up to 25 person-rem (effective dose equivalent).

b

88. Applying current risk estimates (1 to 2 x lO'4/ rem) to GPUN's and the NRC's estimates of population dose, the total num- j ber of fatal cancers among the 2.2 million people living within

50 miles of the plant ranges from 0.0003 to 0.005. Since "frac- ,

tional" cancers do not exist, this risk can be redefined as having an upper-limit of less than one chance in two hundred for the possible occurrence of a single fatal cancer among the 2.2 million people. The upper limit probability of a fatal cancer i

for the maximally 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 GPUN's calculated dose. [

89. Even when very small risks can objectively be defined in 4

quantitative terms by scientists, public attitudes may frequently be at variance. This is especially true when such r'isks are per-i ceived as involuntary. For most individuals, statistical numbers ,

alone are insufficient to evaluate the acceptability of a given risk, no matter how small. A better understanding of risk can be obtained when a risk is viewed in context with other risks, such j as risks associated with the exposures all of us receive in our i daily lives from natural sources of radiation. -

4 i

1 ,

L i

P

90. Mankind has lived with radiation and always will; there is no choice. Radioactivity has been a part of our planet since its ,

creation. Even some of the atoms that constitute our bodies are radioactive; more than 7,000 atoms give off radiation in our

bodies every second. Within that same second, about 300 cosmic

. rays from outer space pass through the body.

91. Life on earth has evolved amid the constant exposure to nat-j ural radiation. In fact, the single major source of radiation to which the general population is exposed comes from natural i .

sources.- Although everyone on the planet is exposed to natural i

radiation, some people receive more than others. Radiation expo-4-

sure from natural background has three components (i.e., cosmic, l terrestrial, and internal) and varies with altitude and geograph-4 ic location, as well as with living habits.

92. For example, cosmic radiation originating from deep in-terstellar space and the sun increases with altitude, since there

! is less air which acts as a shield. Similarly, terr'estrial radi-j stion resulting from the presence of naturally occuring

radionuclides in the soil varies and may be significantly highcr

)

l in some areas of the country than in others. Even the use of i

particular building materials for houses, cooking with gas, and home insulation affect exposure to natural radiation.

[ 93. The presence of radioactivity in the human body results from i

I the inhalation and ingestion of air, food, and water containing i

a

(

a ,

naturally occurring radionuclides. For example, drinking water

.contains trace amounts of uranium and radium and milk contains ,

(

t radioactive potassium. Table 5 summarizes the common sources of l radiation-and their average annual doses.

Table 5 i Sources and Doses of Radiation

• Natural (82%) Man-made (18%)

i Radiation Dose Radiation Dose Source (millirems / year) Source (millirems / year)

Radon 200 (55%) Medical x-rays 39 (11%)

Cosmic rays 27 ( 8%) Nuclear medicine 14 ( 4%)

Terrestrial 28 ( 8%) Consume; products 10 ( 3%)

Internal 40 (11%) Other (Releases Less-than 1 (1%)

from natural gas, phosphate mining, burning of coal, weapons fallout, &

nuclear fuel cycle)

Approximate Approximate Total 300 63

• Percentage contribution of the total dose is shown in parentheses.

94. The average person in the United States receives about 300 millirems per year from natural background radiation sources.

This estimate was recently raised from about 100 to 300 millirems beacuse of the inclusion of radon gas which has always been present but has not previously figured in the calculations. In some regions of the country, the amount of natural radiation is significantly higher. Residents of Colorado, for example, re-ceive an additional 60 millirems per year due to the increase in

<,6'

.~_

cosm'ic and terrestrial radiation levels.. In fact, for every 100 l'

feet-above sea level, a person will receive an additional 1 .

millirem per year from cosmic radiation. In several regions of

[

the world, high concentrations of uranium and radium deposits re-sult in doses of several thousand millirems each year to their residents (NCRP Report No. 93).

95. Recently, public attention has focused on radon, a naturally occurring radioactive gas' produced from uranium and radium decay.

These elements are widely distributed in trace amounts in the 1.

~

earth's crust. Unusually high concentrations have been found in certain parts of eastern Pennsylvania and northern New Jersey.

] Radon levels in some homes in these areas are hundreds of times l- greater than levels found elsewhere in the United States. While additional surveys are needed to determine the full extent of the problem nationwide, radon is the largest component o,f natural l background radiation. The National Council on Radiation Protec-tion and Measurements estimates that the average individual in i the United States receives an annual dose of about 2,400 millirems (2.4 rems) to the lung from natural radon. This lung dose is considered to be equivalent to a whole body dose of 200-millirems (0.2 rem).

I j 96. In addition to natural radiation, we are exposed to radia-l tion from a number of man-made sources. The single largest of i

{ these sources comes from diagnostic medical x-rays and nuclear l

l l l

{

l t

medicine. Some 180 million Americans receive x-rays each year.

The annual dose to an individual from such radiation averages ,

about 53 millirems (0.053 rem). Much smaller doses come from consumer products such as television, smoke detectors, and fer-tilizers, and from nuclear weapons fallout. Production of nuclear power and its associated fuel cycle contributes less than 1 millirem (0.001 rem) to the. annual dose of about 360 millirems (0.36 rem) for the average individual living in the United States.

97. In review, the maximally exposed individual for the full duration of water evaporation would theoretically receive 1 to 2 mrem of whole body radiation exposure. For the same two year period, this individual or any individual in the United States will receive approximately 600 mrems of equivalent whole body dose from natural radiation sources alone. Even less significant is the corresponding population dose of from 3 to 25 person-rems for the 2.2 million individuals who, for the same period of time, would be expected to receive a total of about 1,320,000 person-rems from natural background radiation.

E l

• IV. AN ASSESSMENT FOR RELEVANCY TO THE TMI-2' WATER  !

DISPOSAL OF SCIENTIFIC DOCUMENTS CITED BY INTERVENORS r f

98. In responses to interrogatories, Intervenors have cited three studies concerning the effects of tritium. Each of these f

studies is discussed below, and none of the studies is inconsis-f tent with GPUN's or the NRC's evaluations. i A. Article 1: Dobson, R.L. and Cooper, M.F. (1974),

"Tritium Toxicity: Effect of Low-level HOH }

Exposure on Developing Female Germ Cells in the Mouse," Radiation Res., 58.

99. In this study, female mice-were continuously exposed to- '

3 tritiated water from the time of conception to 14 days of age.

I The three levels of exposure corresponded tc 8.5 uCi/ml, 0.85 pCi/ml, and 0.085 uC1/ml. These tissue concentrations resulted in dose rates of 2400, 240, and 24 mrads/ day, respectively. Fe-male offsprings from these three exposure groups were sacrificed at day 14 post-partum, and the number of primary occytes per

'r ovary were counted and compared to non-irradiated controls. The percent reduction in primary oocytes for the three experimental l

groups were 93%, 44%, and 13% relative to the control animals. '

From the nearly linear dose-response curve, Dobson estimates 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 of unirradiated controls.

r f

r

3 100. There are two factors which must be considered in assessing the relevancy of this study: 1) corresponding dose values in hu-mans, and 2) variations in specie sensitivity to radiation.

1. Dose 101. If this animal model can be assumed to have relevancy to human exposure, one would first want to establish an equivalent dose for humans. In spite of what appears to be small doses in mice for corresponding reductions in primary occytes, certain ad-justments are necessary to account for differences in gestational periods between mice and humans. For the mouse, the gestational period is 19 days; for humans, the normal gestational period is 280 days.

Comparable Dose Requirements:

Mouse: For a 50% reduction in primary cocytes, a total in-utero dose of 10,640 mrads is required (i.e., 19 days x 560 mrad / day = 10,640 mrad).

Human: For a corresponding 50% reduction in human occytes, a total dose in-utero of 156,800 mrad would be re-quired.

102. With respect to the evaporation of accident-generated water at TMI-2, the maximally exposed individual over the two year period of evaporation would receive a 50-year committed dose on the order of 1 mrem from tritium. Ignoring the protracted expo-sure over a 50 year period and for simplicity (and conserva-tively) assuming that the 1 mrem exposure occurs over only two years, the maximally exposed person (female) would, over any 280 day period, receive 38% of the 1 mrem dose or 0.38 mrem. Due to maternal and fetal differences in cellular kinetics which enhance organic metabolic binding of tritium, it may conservatively be assumed that the female offspring of a maximally exposed individ-ual would receive twice the maternal dose for an in-utero dose of 0.76 mrem (NCRP Report No. 63). Assuming the linear dose re-sponse established in mice applies to the human fetus, the maxi-mally exposed human female offspring would be expected to have a reduction in the number of primary cocytes of 0.001% (i.e., if a dose of 156,800 mrem reduces cocytes by a factor of 2, then 0.76 mrem would reduce it by a factor of about 1 x 10-5). This is an insignificant effect. -

2. Specie variations ,

103. Laboratory studies which attempt to determine the effect of a given agent on humans, for ethical (and sometimes practical) reasons, turn to various biological models including mice for in-formation. This is most notably the case for testing experimen-tal drugs. Among researchers, it is well known that in animal models, although they may parallel the human response, their sen-sitivity (or lack thereof) may, for certain agents, dirier by

-. E

.- j

= i t

. several orders of magnitude. Any extrapolation from animal j i

studies to humans must therefore be done with extreme caution. -

104. Within the discipline of radiation biology, it has been ~

firmly. established that particular reproductive cells in the fe-male tissues of the ovary exhibit radiation sensitivity which is .

l considerably higher than other cells of the body, Reduction in l l

oocyte survival following radiation exposure is the result of i mitotic inhibition of_ oocyte precursor cells. Among radiation  !

biologists, it is also well known that extreme _ specie variations l j

l exist and that the relatively high radiosensitivity of oocytes in mico does not apply to humans.

105. Dobson, the very author of the article under review, states that: i i

"Great caution must be exercised in extrapolating from the results reported here on mice to possible effects )

on human beings. Available experimental evidence, l though limited, suggests that occytes of primates are i i

very much more resistant to radiation than are those of [

mice and rats."  !

i i

t l

49 '

l I

,f,l4 106. In a more recent article (Dobson, et. al. 1982), Dobson fur-ther states that, .

... human cocytes are probably not highly sensitive to radiation..."

107. The National Academy of Sciencies (BEIR III, 1980) also has stated that,

...the radiation doses required to kill a given frac-tion of primary follicles are also specie-deplendent:

in the mouse, a single acute dose of 10R of x-rays reduced the number of primary cocytes to half; in the rat, the comparable dose was 100R; and in the monkey, perhaps as high as 900R." (Note: a dose of 1R of x-rays is approximately equal to 1 rem or 1000 millirems). ,

108. :n addition to tht above comments which identify both the insignificance and irrelevance of the article in question with regard to the TMI-2 water disposal doses, it must also be pointed out that even for the condition in which significant reduction of primary occytes does occur, the impact on female fertility (the ability to bear offsprings) is not significantly impaired. At the time of birth, the female has a total pool of about two mil-lion oocytes, of which only one mature occyte is produced per month during ovulation. During the period of 35 years, a total 9

O of about 360 to 400 mature occytes are produced during her entire reproductive life (BEIR III, 1980). From this relationship, it j

. can be seen that even when extremely high doses do result in sig-f nificant reduction of primary cocytes, fema 3.e fertility is not  ;

significantly impaired. [

B. Article 2: Dobson, R.L., and Kwan, T.C. (1976),

The RBE of Tritium Radiation Measured in Mouse  ;

Oocytes: Increase at Low Exposure Lovels.

Radiation Res. 66.

109. The protocol of this study was similar to that of Article

1. 1. Developing mice (in-utero) were exposed to tritium in body  !

water continuously from conception to 14 days post-partum. Tis-sue concentrations of tritium were maintained at 1, 3, 6, and 9 ,

uCi/ml, respectively, in each of four groups of mice. When the offsprings were 14 days old, primary occytes in their ovaries were counted microscopically and compared to non-irradiated con-trols. In parallel groups of animals, exposure dose rates of 1, l 2.1, and 3.2 rads / day were delivered by external bedy Co-60 ,

! irradiation. The relative biological effectivenass (RBE) of tritium (relative Co-60 irradiated animals) was shown to vary j

]

i l from 1.6 to 3. )

]

i i 1 110. As was discussed previously on this Affidavit, RSE values ,

ranging from 1 to 3 have been reported in the literature. This

. l 4

difference is primarily due to the selection of the "reference  !

radiation." When Co-60 is chosen (as opposed to the recommended t

i

i f

i l

9.

..l(

M

.. use of 200 kev.x-rays), an RBE of 2 must be anticipated. In ad-dition, the. biological model as well as the section of a biologi-cal end-point can produce significant variations in defining the RBE value of any form of radiation. Dobson's reported RBE value of 1.6 to 3 for tritium is expected in view of his selection of Co-60 as his reference radiation. Furthermore,.his selection of the mouse cocyte model as a biological end-point has limited sig-nificance for consideration in context with the proposed TMI-2 water evaporation process for reasons cited above.

C, Article 3: Zammenhof, S., and VanMarthens, E.,

(1979), The Effects of Chronic Ingestion of Tritiated Water on Prenatal Brain Development, Radiation Res. 77.

111. In this study, five generations of rats were sequentially maintained at body tritium levels of 3 uCi/g of tissue. This corresponds to a continuous dose rate of 780 mrad per day. From each generation, newborns were analyzed for cerebral DNA, cere-bral protein, and cerebral protein /DNA ratios. When compared to non-irradiated controls, there were statistically significant re-ductions in cerebral DNA for the five generations which varied from 2% to 13%. Comparable reductions in cerebral proteins were also observed. Since the DNA and protein content for a single cell is thought to be constant, the observed reduction in total cerebral DNA and protein is interpreted as a corresponding reduc-tion of the number of brain cells.

f l

i

=

112. The maximum reduction of DNA content in cerebral tissues  !

corresponded to a continuous exposure dose rate of 780 mrads/ day

• e i

throughout gestation. If one were to apply this exposure to the  !

I human condition for which gestation extends to 280 days, then a i

j comparable dose of 218,400 mrads would be required for the ex-

pected 13% reduction in cerebral DNA. With the tentative assump- [

tion that this relationship may, in fact, apply, we can assess its relevance to the TMI-2 evaporation plan.

1 113. As was calculated previously assuming the maximally exposed individual to be a pregnant female, a dose of 0 76 mrad was cal-  !

4 culated for the maximally exposed fetus. If, as was calculated ,

above, a dose of 218,400 mrad corresponds to a 13% reduction in

cerebral DNA and assuming a linear dose-response, it follows that a dose of 0.76 mrad would result in a 0.00036% reduction of cere- t bral DNA. '

k D. Conclusion I l

! 114. Based on human studies, there is no scientific evidence that l -

) would suggest a potential harm to any pregnant female and her i j offspring from the evaporation of accident generated water at  !

i i

TMI-2 over a two year period. There is a fair amount of data t

l concerning the radiosensitivity of the embryo and fetus to expo- l sure in-utero. When deletereous effects have been observed, the [

t dose of radiation has generally been thousands of times greater i 1 f than the upper limit of exposure (0.76 mrad) as previously l l

1 i

[

i i

?

r- - -

Q o  !

defined for the maximally in-utero exposed embryo / fetus. More-over, in instances of human exposures resulting in observable of- l j

facts, the exposure to radiation was not only delivered at ex-l tremely high doce rates (nearly instantaneously), but in part  ;

consisted of high-LET radiation and most frequently coincided with the most sensitive period of gestation.

V. TRANSURANICS A. Sources 115. Transuranics (TRUs) sonstitute a group of elements which have an atomic number groater than uranium (atomic no. 92). Atom-ic number refers to the number of protons within the nucleus of an atom. It is the number of protons which identifies each ele-ment of the periodic table. Transuranic elements as a group are members of the actinide series beginning with neptunium (atomic no. 93) and ending with lawrencium (atomic no. 103). For each transuranic element, there may be several isotopes (having the same atomic number but different numbers of neutrons).

Transuranic elements are principally produced in nuclear reac-tors, accelerators, or in nuclear weapons explosions. In the en-vironment, their presence is lmost exclusively the result of weapons testing of the 1950's and 1960's (BEIR IV). More than 500 tons of transuranics have been released to the atmosphere from weapon tests.

116. Production of TRUs results from the successive neutron cap-ture of unfissioned material and their radioactive decay. These interactions of neutron capture and radioactive decay are quite complex. Production of transuranic nuclides begins by neutron 238 capture of U which is the primary constituent of commercial reactor-grade fuel. 239 239 The resultant U decays to Np and finally to 239 Pu, which by sequential neutron capture produces several isotopes of plutonium. Flutonium-241 undergoes beta decay to form americium-241. Although there are a large number of transuranic elements which can be formed, most transuranics, because of their very short half-lives or the short half-lives of precursor nuclides, are either not produced in significant quan-tities or rapidly decay after being formed. The principal 1

transuranic elements for consideration relative to human health are limited to plutonium-238, -239, -240, -241; americium-241; and curium-242. .

B. Chemical Properties ,

117. The chemistry of plutonium and other transuranic elements has been extensively researched. A comprehensive review of actinide chemistry is provided by Duffield and Taylor (1986). In spite of all that is kncvn about the chemistry of transuranics, only two aspects are relevant to the discussion of the proposed evaporation plan and potential health effects. The first is the degree of solubility of TRUs and the second is the particle size in which they may exist.

55

118. Plutonium and other transuranic elenents exhibit multiple oxidation states which vary from +3 to +7. The chemical exida-tion state is very important inasmuch as it affects the solubili-ty of transuranic compounds. It is the temperature in which the oxidqs are formed which determines the oxidation state. It has been well established that transuranic oxides formed at high tem-peratures are highly insoluble in water. Conversely, oxides formed at low temperatures are relatively soluble in water (ICRP, 1986).

119. Related to solubility are the physical characteristics of  !

transuranics. Oxides formed at temperatures above 350 C are

. t known to form molecular aggregates resulting in particles having diameters ranging in size from nanomete'rs (nm) to micrometers (um).

t 120. Plutonium and other transuranic elements suspected to be l

present in accident generated water can be assumed to have been l

produced at high temperatures during the brief operational period

of the TMI-2 reactor. As such, their residual presence in AGW i,

would be as insoluble micro-particulates.

C. Radiological Properties 121. The common aspect of the transuranic elements under conside-ration in this Affidavit is that they all emit an alpha particle  :

in the process of radioactive decay. The corresponding energies

[

a

3 of these alpha particles range between 5 and 6 MeV and are, therefore, relatively constant. However, there is considerable variation with respect to their physical half-lives (Table 7).

TABLE 7 Transuranics Nuclides of Potential Biological Significance Alpha-Energy Element Isotope Half-Life (yr) (MeV)

Plutonium 238 86 5.6 Pu 239 Pu 24,400 5.2 240 Pu 6,580 5.3 241 p 13 5.1*

Americum 241g , 433 5.6 Curium 242 Cm 0.45 6.0

• Pu-241 principally decays by beta emission.

122. The size, electrical charge, and energy of alpha particles when absorbed in tissue produce a spatial distributi'on of depos-ited energy per unit distance traversed that is about twenty times higher than that of x-rays or beta particles. For a con-stant radi ation dese, various types of radiation are more effec-tive in producing a biological effect. As discussed earlier, this difference of relative biological effectivenuss for various forms of radiation is largely determined by the rate with which energy is deposited in tissue and is defined by the linear energy transfer (LET) value of that radiation. It is the quality factor (Q) by which the absorbed dose is multiplied to quantify biologi-cal damage for all forms of ionizing radiation. For alpha

O radiation, the quality factor of twenty (20) is generally assumed to apply when the radiation of reference is x-radiation of 200 ,

kev energy.

D. Toxic Properties 123. Some radioactive elements in addition to their radiological properties may exhibit chemical properties which are regarded as toxic for biological systems. Radioisotopes with extremely long half-lives have a low specific activity. A low specific activity implies that per unit weight of material, there are few atoms which undergo radioactive decay per unit time. If the radioac-tive element has an associated chemical toxicity, it is the chem-ical toxicity which may become the limiting factor for re-stricting human exposure. For the transuranic elements identified in this report, however, it is their radiological properties on which human exposure limits are based.-

124. The toxicity of non-radioactive materials is fr,equently as-sessed for short-term effects which may be observed for periods ranging in minutes to weeks. When toxic substances as lead, mer-cury, carbon monoxide, hydrogen cyanide, chlorinated hydrocar-bons, bacterial toxins, animal vanoms, etc. are compared to even the most restrictive radioisotopes (transuranics) in terms of acute effects, many of these toxins are relatively far more toxic. A comparison of the acute toxicity for some agents in terms of lethal dose to 50% of the animals over a period of 30 days are provided ir, Table 8.

.e -

i a i

t

• J TABLE 8 i Comparison of Acute Toxicity (LD 50/30)*

, f r

Substance Species Quantity ** }

t Botulinus toxin Mouse 0.000000003 mg/kg l Tetanus toxin Mouse 0.0000001 mg/kg  !

Diptheria toxin Mouse 0.00003 mg/kg  ;

curare Mouse 0.5 mg/kg  ;

Strychnine Mous'e 0.5 mg/kg i Plutonium-239 Dog 1.3 mg/kg  ;

Plutonium-239 Rat 2.0 mg/kg j

Reference:

Stannard, 1976 l

E

• • Quantity is expressed in milligram weight of toxin  !

administered per kilogram body weight of animal. j i

125. The often-heard statement that plutonium is "the most toxic substance known to man" is f ar from true. For acute toxicity,' l r

certain agents are thousands to millions of times more toxic. l E. Exposure Pathways And Distribution In The Body I

126. With a total range in tissue of about 40 um (NCRP Report l No. 46), a 239 Pu alpha particle would not penetrate 'the exterior I

t surface layer of skin. For any alpha emitting nuclide to be of >

concern, it must first be internal to the body. This may occur in two ways. Plutonium and other transuranics may enter the body through ingestion of food or water containing TRUs, or they may

= i k

enter the body through direct inhalationc The International Com- I mission on Radiological Protection (ICRP Publication 31) has con-cluded that the absorption of transuranic elements from the  !

i gastrointestinal tract is minor and insignificant in relation- .

1 >

ships to the inhalation pathway. For plutonium oxide, the ICRP l 1

(ICRP Publication 48) has adopted an absorption coefficient of j i

1x10-5 . This is equal to the absorption of 1 part in 100,000 from the digestive tract.  ;

I 127. The inhalation of TRUs and their distribution and elimina- .

tion from the body is largely governed by the size of the parti- f E

! cles and their degree of solubility in body fluids. The ICRP r P

Task Group on Lung Dynamics . (ICRP, 1966) has developed a model  ;

for the distribution and kinetics of respired micro-part:culates, i i~

This original lung model has been modified over the years with l

, e the most recent revisions described in ICRP Publication 30. The l,

a ICRP Task Group Lung Model predicts particle deposition in vari- l 1  :

ous regions of the respiratory tract and their subsequent clear-  !

{ ance rate from the nasal passage, the trachea and bronchial-tree, j 2

I the pulmonary parenchyma, and the thoracic lymph nodes.  ;

v >

i 128. Large-size particles (10 um) when inhaled almost exclusively  !

i

] deposit in the upper regions of the respiratory tract. In the i 1

upper regions, various mechanisms exist for the rapid renoval of i

l particulates and thstr elimination from the body through the di-i i gestive tract. Radiation exposure from these particulates is not ,

1 I l 1  !

l

)

only of short duration but.of _imited significance since the l l

I short range of alpha particles does not allow penetration of the mucus which normally covers the cells of the digestive tract.

l 129. Only smaller particles (1 um) are likely to' reach the deeper region,of the respiratory tract where clearance mechanisms of the upper regions are not operating. For inhaled small particles, about 25% may reach the pulmonary parenchyma or deep lung. The

. retention of particles deposited in the deep lung is determined by their degree of solubility in lung fluids.

130. If the particles are readily soluble, the dissolved material enters the blood stream where it is subjected to two competing mechanisms of removal. The first mechanism is the removal of ma-terial from the blood by the kidney and subsequent elimination e through urine. The material (i.e., transuranics) in the blood that is not removed by the kidney may be deposited in other organ (s). Radioactive elements, like their non-radioactive coun-terparts, behave in the body according to their biol'ogical sig-nificance. Transuranies have chemical properties which are simi-lar to calcium and can, therefore, metabolically be assimilated into bone tissue.

131. For insoluble particles reaching the pulmonary parenchyma, their retention in the lung may be for longer perieds of time.

For insoluble particulates deposited in the pulmonary parenchyma, the lung becomes the organ of highest radiation exposure. Slow

9' removal of insoluble micro-particulates from the lung-has been ooserved in both animals.and humans (ICRP Publication 48). It is-thought that the transfer of insoluble micro-particles from the lung to regional lymph ncdes occurs through the action of immune cells (alveolar macrophages) in the lung (BEIR IV).

132. Exposure to airborne transuranics may therefore result in radiation exposure of- several tissues. For insoluble particulates, the lung is considered the primary organ for expo-sure. For solubilized transuranics which enter the blood stream, about 50% may deposit in the skeleton and 30% in the liver (ICRP Publication 48).

F. Health Effects of Transuranics 133. For low-dose radiation exposure to the whole body, health concerns are confined primarily to the potential induction of cancer, and secondarily genetic effects. Radiation exposure from internal emitters, in most instancas only expose selectivo tis-sues. Plutonium and other transuranics do not significantly de-posit in reproductive tissues and, because their radiation is limited to alpha particles, reproductive tissues are not exposed.

I . Potential genetic effects are, therefere, not associated with human exposure to transuranics (NCRP Report No. 89).

134. Tissues of interest for potential cancer induction by I

transuranics are the lungs, bone, liver, and lymph nodes. Animal

l I

studies have shown that the predominant cancer sites are the lung I and bone. The National Academy of Sciences has recently pub-lished a report which specifically reviews health effects associ-ated with internally deposited alpha-emitters (BEIR IV). This report includes an extensive review of scientific studies of health effects associated with plutonium and other transuranic elements. Most of the scientific data for assessing the carcinogenic potential of inhaled transuranics comes from various animal studies. Cancer risk estimates from these studies, how-ever, must be treated with caution when applied to humans, in as so much as they may overestimate human risks. The National Acad-emy of Sciences (BEIR IV) states:

"Available published data do not indicate that inhaled transuranic elements are associated with as high an inci-dence of respiratory carcinoma in non-human primates as that seen in rats and dogs."

135. Workers in nuclear fuel production with occupat'ional expo-sure to transuranics have been studied for health effects. The most systematic study of occupationally exposed individuals to date are employees of Rocky Flats Nuclear Weapons Plant (Wilkinson, 1987). Workers with more than 2 nci of plutonium ex-posures were evaluated for overall mortality for all causes, as well as cancer mortality rates. The plutonium exposed groups showed a standardized mortality ratio of 62 for all causes of 4 .

death, and 71 for all cancer mortality when compared to the age and sex adjusted mortality values of the U.S. population. A standardized mortality ratio of 100 would have implied that there were no differences between the plutonium workers and the general population of the United States. A standardized mortality ratio of less than 100 indicates reduced mortality rates among the plu-tonium workers. When compared to the general population, pluto-nium workers lived longer and had fewer cancers. In summary, the National Academy of Sciences in their recent report (BEIR IV) states: 1

"...no significant lung , bone , or liver-cancer risk has been found in plutonium workers exposed 30 yr ago or more."

136. In spite of such observations, human health studies involv-ing exposures to transuranics elements are too few to make accurate assessment of health risks. For this reason, cancer risk estimates for exposure to transuranic elements are currently calculated by assessing the cancer risks to other alpha emitting radionuclides for which more reliable human data does exist.

G. Risk Estimates for Transuranics 137. Lung Cancer. For the estimates of lung cancer risks for plutonium and other transuranic alpha-emitters, risk estimates are obtained from various human populations exposed to high lev-els of radon and radon daughters which also emit alpha radiation.

Among populations studied are uranium miners who were exposed to large concentrations of radon and its daughters. Based on radon studies, a risk estimate for exposure to transuranics has been established at 700 lung-cancer mortalities per million person-rad (BEIR IV).

138. If the exposure is expressed in units of rem by applying the quality factor (Q) of 20 to alpha radiation, the risk of lung cancer is reduced to 35 lung cancers per million person-rem.

This risk implies that a single person receiving 1000 mrem (1 rem) to the lung from exposure to transuranics would have a life-time risk of approximately 1 chance in 30,000 of dying of lung cancer. If the lung dose is reduced to 1 mrem, the risk is reduced to 1 chance in 30,000,000.

139. These radiation exposure induced lung-cancer risks can be evaluated more realistically when compared to the normal inci-dences of lung cancer in the United States. For all males, near-ly 4% will die of lung cancer (ACS, 1986); and since'85% of lung cancers are the result of cigarette smoking, the risk of lung cancer among smokers is, therefore, several times greater than for non-smokers.

140. Bone-Cancer. There have been several human studies in which individuals were occupationally exposed to radium used in lumi-nous paints for watches and navigational instruments. Radium when ingested behaves like calcium and is assimilated in bone I

a-

' tissue. There are several isotopes of radium which emit alpha particles. As such, cancer risks in bone tissue established for radium can be assumed to apply to transuranic elements. For bone cancer, the estimates of risk vary from.4 to 55 bone-cancer deaths per million person-rem (BEIR IV).

141. Liver Cancer. In the late 1920's through 1955, thorium-232 was commercially prepared in colloidal solution as thorium dioxide (Thorotrast). Its use was primarily in medical radiogra-phy as an intravenous contrast medium. The insolubility and col-loidal nature of Thorotrast caused much of it to concentrate in the liver where it remained for long periods of time. Thousands of patients who had received Thorotrast have been studied for health effects. Based on human Thorotrast data, it is estimated that the risk of liver-cancer for transuranics is 15 cancer deaths per million person-rem (BEIR IV).

H. Imoact of Transuranics From TMI-2 Evaporation 142. The proposal to dispose 2.3 million gallons of TMI-2 acci-dent generated water (AGW) involves evaportion of water over a two year period at a rate of 5 gallons per. minute. The evaporator system is described in detail elsewhere and, there-fore, only relevant aspects of this system to environmental re-lease of radionuclides will be mentioned. A key aspect in the design of the evaporator is its two-stage design.

l l l l

143. AGW entering the first stage is heated to form steam leaving nearly all material including radioactive material that is either dissolved or suspended behind. The highly purified steam is sub-sequently cooled back to water and collected in a tank as a water distillate. This water distillate is monitored for residual radioactivity before it is pumped to the second stage which re-heats the water to steam before it is released to the environ-ment. With exception of tritiated water which cannot be removed, this two-stage evaporation reduces all other radioactivity which may be released to the environment by at least a factor of one-thousand. The reduction factor of one-thousand primarily applies to highly soluble material which exist as simple ions in water.

It is most probable that any material which is not dissolved but merely suspended in water as particles will be reduced many times more.

144. Oxides of plutonium formed at high temperatures, as are e those in a reactor, are very insoluble in water and most likely exist in particles of varying sizes. As particulates, their re-moval is likely to exce~.d values which are significantly greater than one-thousand, i

145. Quantities of Transuranics. Analysis of AGW has shown that transuranic elements do not exist at concentration levels where they can be measured by GPUN's normal alpha spectroscopy. Their presence in AGW may, therefore, vary from zero (0) to just below the level of concentration where they could be detected.

l t l

l i.

146. In assessing possible releases of transuranics to the envi-ronment, the very_ conservative and highly improbable assumption will be made that each of the transuranic elements exists in con-centrations which are at their threshold levels of detection.

The_second conservative assumption in estimating environmental releases of transuranics is the evaportion reduction factor of one-thousand. Table 9 identifies each of the nuclides and their upper limit content in AGW and in environmentally released water vapor.

TABLE _9 Upper-Limit Quantities of Transuranics (Ci)

Nuclide AGW Water Vapor Pu-238 1.0E-4 1.0E-7 Pu-239 1.2E-4 1.2E-7 Pu-240 1.2E-4 1.2E-7 Pu-241 5.7E-3 5.7E-6 Am-241 1.0E-4 1.0E-7 Cm-242* 8.7E-4* 8.7E-7*.

• Curium-242 has a half-life of 165 days (0.45 yrs) and in 1988 after more than 18 half-lives can be assumed not to be presenc. '

The upper-limit of total transuranics which could be released to the environment is 7 microcuries.

147. Maximum Exposure. The potential for human exposure is fre-quently calculated for the maximally exposed individual which represents an upper-limit dose values. Since the exposure to l transuranics is limited to the inhalation pathway, the maximally l l l

l t

e exposed individual is assumed to be "reference man" who for the entire two year period of evaporation lives at the location of highest radionuclide concentrations ~for inhalation.

148. Using the above conditions of exposure and further assuming the redioactive release to be at ground-level, inhalation quan-

.tities can be calculated for maximum exposed individual (Table 10).

TABLE 10 Maximum Quantities Inhaled

• Nuclide Inhalation (pC1)**

Pu-238 0.0003 Pu-239 0.0003 Pu-240 0.0003 Pu-241 0.0156 Am-241 0.0003

• Quantitative values were obtain~ed by the MIDAS (Meteorological Information and Dose Assessment System) computer dispersion model.

• • pCi (pico-curie) is one-trillionth of 1 curie (C1).

! 149. Maximum Dose. For most internal emitters, radi'ation expo-j sure is specific to those organs in which the radionuclide is de-l posited and retained. Following inhalation of transuranics, ex-i posure to certain organs is dictated by solubility. Because of I

the long retention times, all doses are calculated as 50 year committed doses and represent the total dose to the organ over the life-time of the maximally exposed individual. Table 11 lists organ dosos for each transuranic element suspected to be present in AGW.

l l

. l

e

'h TABLE 11 Organ Doses ( Mre:a )

• Nuclide Lung Bone Surface Liver

~4 ~4 ~4 Pu-238 (insol) 3.3 x 10 8.7 x 10 1.9 x 10

~4 -3 ~4 Pu-239 (insol) 3.6 x 10 1.1 x 10 1.9 x.10 Pu-240 (insol) 3.6 x 10 ~4 1.1 x 10-3 1.9 x-10

~4

-3 -2 -3 Pu-241 (insol) 3.6 x 10 2.6 x 10 5.1 x 10

-3 ~4 Am-241 (sol) ----------

2.6 x 10 5.7 x 10 TOTAL: 0.005 mrem 0.03 mrem 0.006 mrem

• Organ doses were calculated using dose conversion factors listed in UNSCEAR, 1982.

150. Acute Toxicity. Based on the total activity (pCi) inhaled for each nuclide by the maximum exposed individual, the physical weights of each nuclide can be calculated from their specific activity constants. The quantities are shown in Table 12.

TABLE 12 ,

Nuclide Quantity (Milligrams)

Pu-238 1.7 x 10-14 ,

Pu-239 5.1 x 10 -12

-12 Pu-240 1.4 x 10 Pu-241 1.5 x 10

-13 Am-241 8.1 x 10 ~14 Total: 6.6 x 10

-12 mg l

I I

l

.s ,

, 151. Since~the maximally exposed individual' who would'have a total body burden of 6.6 x 10

-12 mg (i.e.,

less than one-hundredth of a billionth of one milligram) of transuranic ele-ments is considered to be the "Reference Man" who weights 70 Kg, this body burden of transuranics translates to 9.4 x 10 -14 mg/Kg.

Table 8 of this Affidavit depicts acute toxic levels for plutoni-um at about 1 mg per Kg of body weight level. The. average tissue level of the maximum exposed individual is approximately 10 tril-lion times below this toxic level.

152. In reality, it must also be recognized that individuals liv-ing in the TMI area would be exposed to yet smaller fractions of quantities established for the maximum exposed individual.-

I. Comparison to Radon and Other Sources 153. Radiation doses and their associated risks to the public from potential exposure to transuranic elements assuhed te be present in TMI-2 accident generated water can best be viewed in context with other radiation exposures from sources which are l very similar.

154. There are a host of natural radioactiva elements which have and always will be present inside and outside the human body.

j The National Council on Radiation Protection and Measurement has

! recently issued a report (NCRP Report Ne. 93) entitled, "Ionizing Radiation Exposure of The Population of The United States."

}

J

a

.- Average annual doses to tissues from various natural radionuclides contained within human tissues are given in Table

13. The majority of these nuclides emit alpha radiation.

TABLE 13 Average Doses From Natural Nuclides Contained in Body (NCRP, 1987)

(mrem /yr)

All Soft Radionuclide Tissue Bone Surfaces Bone Marrow C-14 1 0.8 3.0 K-40 18 14 27 Rb-87 1 1.4 0.7 U-234*/238* 0.5 0.3 0.04 Th-230* 0.01 0.6 0.1 Ra-226* 0.3 9 1.5 Ru-227* 0.7 1.4 1.4 Pb-210*/Po-210* 14 70 14.0 Th-232* 0.01 0.2 0.04 Ra-224*/228 0.2 12 2.2 '

Rn-220* 0.1 ---- -----

Rounded Total 36 mrem 110 mrem 50 mrem

• Radionuclide emits alpha particle.

155. The largest tissue dose from natural radionuclides, however, comes from the inhalation exposure to various alpha emitting nuclides. This inhalation exposure is different from that of in-ternal radionuclides inasmuch as these radioactive elements are not within the tissue (s) . Inhalation exposure is principally the result of radioactive daughters of radon which are deposited as dust on cells which line the respiratory airways Alpha radia-tion from these particles irradiate the bronchial epithelium of the respiratory system.

9

o l

l 1

4 6 l TABLE 14 Average Inhalation Doses From Naturally Occurring Radionuclides (NCRP, 1987)

Radionuclide Annual Tissue Dose Epithelium Whole Lung Bronchial Epithelium Ru-222* 20 Po-218*/Po-214* 2400 Po-210* 0.8 Th-232*/Ra-224* 0.02 Ru-220* 0.01 Pb-212/Po-212* 40 Rounded Total 20 mrem 2400 mrem

• Radionuclide emits alpha particle 156. As can be seen from Table 14, the, single highest tissue dose resulting from natural radionuclide exposure is about 2400 mrem per year to the bronchial epithelium which results from alpha ra-diation emitted from polonium-218 and polonium-214. These two nuclides are the radioactive daughter products of naturally oc-curring raden. Most of this exposure is due to radon seepage into homes and buildings where radioactive radon dau'ghter prod-ucts are able to concentrate.

157. In certain geographical areas within the United States, the natural concentration of uranium and radium are considerably higher. Some areas within Pennsylvania are known to have unusu-ally high levels of radium in the soil resulting in proportion-ally higher indoor radon levels. Based on preliminary data of indoor radon levels in Dauphin County, PA (Personal

. Communication), the average dose to the-bronchial epithelium for an individual living in Dauphin County can be approximated at 22,500 mrem per year.

158. In addition to the involuntary tissue doses all of us re-ceive from naturally o'c curring radionuclides, there are a number

. of radiation exposures that are the result of choice. For some of these, like medical radiation and radiation from a host of consumer products, the benefits far exceed any concern of radia-tion associated risks. For others, the weighing of risk is a matter of personal choice. For example, it is known that tobacco products, in addition to known carcinogens, also contain alpha emitting radionuclides. The National Council on Radiation Pro-tection and Measurement (NCRP Report No. 93) has estimat5d that the average smoker receives a dose of about 16,000 mrem yearly to the bronchial epithelium from cigarettes.

J. Summary 159. This Affidavit has reviewed the proposed evaporation of TMI-2 accident generated water, relative to concerns about human exposure to transuranic elements. In an attempt to assess the risk to any one member of the public, tissue doses to the lung, liver, and bone were calculated for conditions of maximum expo-sure. The tissue doses of 0.005, 0.006, and 0.03 mrem for lung, liver, and bone (surface) reflect upper-limit values which are in reality many times higher than doses which might actually be received by individuals.

4

, =

, 160~.'The insignificance of these one-time tissue doses resulting from TMI-2 water evaporation becomes apparent when compared to tissue doses from naturally occurring radionuclides. For a sin-gle yevt, naturally occurring'nuclides produce tissue doses which are hundreds to many thousands of time greater.

161. Finally, the concern for the release of transuranic elements into the environment from the TMI-2 evaporation process can be assessed from another point of view.

162. The useful application of transuranic elements in a variety of commercial and consumer application has been realized for many years. There are dozens of consumer items containing long-lived alpha emitting nuclides. Perhaps the item most common to the av-erage household is the smoke detector. This device uses alpha radiation to cause ionization in air between two electrodes, thereby allowing a small electric current to flow ac,ross the air gap under the influence of a small electric potential. This cur-rent, if interrupted by smoke particles, triggers the alarm.

163. The National Council on Radiation Protection and Measure-ments (NCRP Report No. 56) estimated that in 1976 a total of 4 million of these devices were in use in the United States. The source of alpha radiation in these devices is generally americium-241 which has a half-life of 433 years. The amount of americium-241 for a single smoke detector may vary from 5 up to 100 pCi (NCRP Report No. 56).

a 164. The total upper-limit of release of transuranic elements for the entire evaporation of TMI-2 accident generated water was identified in Table 9 of this report as 7 pC1. A simple compari-son of values would indicate that the disposal and incineration of.just one smoke detector would result in an airborne release of the transuranic element Am-241 that is greater than the total transuranic elements which may potentially be released during the evaporation process.

VI. CONCLUSION 165. As shown above, the effects of tritium and' alpha emitters /

transuranics are being fully considered with respect.to the pro-posed evaporation of accident generated water at TMI-2. The ef-fects are insignificant.

MY[ D Hans Behling St.bscribed and sworn to before me this \3A day of May, 1988 b ld b Notary Pubile me utC11E1LE Lito, NOTARY Puttic My commission expires: mm m.ma counn gy M IIME3 $EM.11.1989 Guder. Peauptuosts Assedstes of Botenes x

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Bender, M.A., Gooch, P.C., and Prescott, D.M. (1962). "Aberra-tions induced in human leukocyte chromosomes by 'H-labeled nucleosides," Cytogentics, 1.

Bond, V.P. and Feinendegen, L.E. (1966). "Intranuclear

H-thymidine

Dosiemetric rdiobiological and radiation pro-tection aspects," Health Physics, 12.

Carsten,' A.L. and Commerford, S.L. (1976). "Dominant lethal mu-tations in mice resulting from chronic tritiated water (HTC) ingestion," Radiation Res., 66.

dobson, R.L., Kwan, T.C., and Straume, T. (1982). "Tritium Ef-facts on Germ Cells and Fertility," in: European Seminar on the Risks from Tritium Exposure, Report Eur 9065 EN.

Duffield, J.R., and Taylor, D.M. (1986). "The biochemistry of actinides," in: Handbook on Physics and Chemistry of Actinides (eds. A.J. Freeman and C. Keller), Vol. 4.

GPU Nuclear (1986). "Disposal of TMI-2 Water."

Han, A., Hill, C.K., Elkind, M.M. (1980). "Repair of cell kill-ing and neoplastic transformation at reduced do'se rates of 60 Co x-rays." Cancer Res., 40.

Hill, C.K., Han, A., and Elkind, M.M. (1984). "Fission spectrum neutrons at a low-dose rate enhance neoplastic transforma-tion in the linear dose region (0-10cGy)." Int. J. Radia-tion Biology, 46.

Horton, J.H., Carey, J.C., and Wallace, R.M. (1971). "Tritium loss from water exposed to the atmosphere." Environmental Sci. Technology, 5.

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No. 15, Vienna.

International Commission on Radiation Units and Measurements (1986). "The Quality Factor In Radiation Protection." ICRU Report 40.

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, International Commission on Radiological Protection Task Grouplon Lung Dynamics (1966) . "Deposition and retention models for internal dosimetry of the human respiratory tract." Health Physics 12 (2). .

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Kato, H. and Schull, W.J. (1982). Studies of the Mortality of A-bomb Survivors." Radiation Res., 90.

Kieft, P. (1968). "Induction of recessive lethals by 'H-uridine and 8H-thymidine in Drosophila," in: Biological Effects of Transmutation and Decay of Incorporated Radioisotopes. IAEA Public No. STI/ PUB /183. ,

Lewis, E.B. (1957). Leukemia and ionizing radiation." Science, 125.

Luykx F., and Fraser, G. (1986). Radiation Protection Desimetry, Vol. 16, No. 1-2, pp. 31-36, Nuclear Technology Publishing.

Miller, R.W. and Mulvihill, J.J. (1976). "Small head size after atomic radiation." Teratology, 14.

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National Academy of Sciences (1988). Report of Biological Ef-fects of Ionizing Radiation, "Health Risks of Radon and other Internally Deposited Alpha-Emitters." BEIR IV Report.

l l

g-re-- m r-----.-e--,. -e--,,p -t,----+- ------,-mm- --c.-:---ee,. + -e-- ---,---, rov.,-w v.,- -,--+-------,~----m--, - . - , , - >

a.

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(1977).

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Stannnard, J.N. (1976). The Health Effects of Plutonium and Pt dium. J.W. Press, Salt Lake City.

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Watts, L. (1974). "Clearance rates of insoluble plutonium-239 compounds from the lung." Health Physics 29.

Wehner, G. (1978). Conference: "Behavior of Tritium in the En-vironment," San Francisco, IAEA, STI/ PUB /498.

Wilkinse'n, G.S., Tietjen, G.L., Wiggs, L.D., Galke, W.A.,

Acquavella, J.F., Reyes, M., Volez, G.L., and Waxweiler, R.J. (1987). "Mortality among plutonium and other radiation workers at a plutonium weapons facility." American Journal of Epidemiology. 125.

Exhibit A Curriculum Vitae Hans Behling GPU Nuclear Corporation 6 Fox Chase Drive Three Mile Island Hershey, PA 17033

, P.O. Box 480 (717) 533-6502 Middletown, PA 17057 (117) 948-8582 Academic Trainina:

1965 Bachelor of Science Rutgers University Major: Chemistry 1966 Master of Science Temple University Major: Health Physics 1967 Master of Public Health University of Pittsburgh Major: Radiation Biology .

1975 Doctor of Philosophy Temple University Major: Health Physics ,

Honors:

• Recipient of PHS Fellowship (3 years)

• Recipient of AEC Fellowship (2 years)

• External Reviewer for the journal Infection and Immunity

• Adjunct Professor.' University of Pennsylvania (1982 - 1984)

Professional Affiliations:

• Health Physics Society e American Society for Microbiology

• Curriculum Vitae '

Hans Behling Page Two Professional Experience: .

• Date: 3/84 - Present: Manager, Radiological Health TMI Employer: GPU Nuclear Corporation Three Mile Island Nuclear Station, Middletown, PA 17057 Princioal Accountabilitlei:

Responsible for the technical and operational supervision of programs in radiation dosimetry and records; instrumentation and calibration; whole body counting and bioassay; and respiratory protection. All areas involve support to both TMI-1 and TMI-2.

Dosimetry activities ir.clude managing the GPU Nuclear Corporate Dosimetry Laboratory that processes personnel TL0s for THI-1, TMI-2, and Oyster Creek Nuclear Generating Stations. While in this position, major achievements occurred in the development, testing

- and implementation of a state-of-the-art Panasonic TLD system which included development of algorithms and an on-line computerized 4 radiation exposure management system (REM System). The GPUNC personnel dosimetry program has been accredited by National Voluntary Laboratory Accreditation Program (NVLAP).

In addition, this position provides technical expertise and information in matters of health physics and radiation health ef fects to a variety of GPUN departments and outside groups which include: 1) legal staf f, 2) Communications and Public Af f airs, 3)

Radiological Engineering, 4) Medical Health & Safety, 5) Training, and 6) Environmental Centrols.

This position supervises a staff of 9 professionals, 20 technicians and 3 clerks, with an .innual budget of $2.2 million.

• Date: 2/82 - 3/84: Supervisor of Technical Training Programs i

Employer: 6PU Nuclear Corporation, Oyster Creek Nuclear Generating Station, Forked River, NJ i PrinciDai Accountabilities: F Supervisory responsibility for development and presentation of all technical training peograms in areas of 1) radiological controls,

2) chemistry, 3) instrument repair and calibration, 4) maintenance (electrical, I&C, and mechanical), and 5) dosimetry and bioassay.

Major achievements include the establishment of laboratory facilities for all the above training programs for hands-on experience; college accreditation (12 college credits - Rutgers University) for the radiological controls program; and standardizing training programs. Several of these training programs have since received INPO accreditation.

N.-

7 Curriculum Vitae

- Hans Behling Page Three Professional Exoerience: (continued)

• Date: 2/77 - 2/82: Assistant Professor Employer: University of Pennsylvania School of Dental Medicine Philadelphia, PA Princioal Accountabilities:

Conduct research and supervise the research of assistants, graduate students, and post-doctoral fellows; lecture and conduct laboratory training sessions; and administrative duties.

• Ohte: 8/75 - 3/77: Post-doctoral fellow and instructor Employer: Temple University, School of Medicine Philadelphia, PA Princioal Accountabilities:

Conduct research; lecture; supervise laboratory exercises for graduate medical students.

• Date: 9/69 - 9/71: Application Engineer Employer: EG&G and Oak Ridge Technical Enterprise Corporation Princioal Accountabilities:

Provide consultation to users in the high/ low energy physics research in the design and application of NIM modular electronics and solid state detection systems.

Military Service:

Date: 9/67 - 9/69: Senior Assistant Health Services Officer (Rank 03/ Full Lt - Navy)

Employer: U.S. Public Health Service, Bureau of Radiological Health Rockville, MD Principal Accountabilities:

Provide radiation dosimetry for biological research; investigate potential use of radio-sensitive organic dyes f or application in 3-dimensional dosimetry.

l t

o curriculum Vitae .

Hans Behling Page Four Past Research Interest:

• Radiation induced genetic notation and chromosomal aberrations in mammalian cells e Kinetics and interactions of various immunological cell lines following exposure to radiation

• Immunopotentiation and modulation by natural ar.d synthetic products

• Immuno-pathogenic mechanisms in oral pathology Consultant Research (1980 - 1981)

Research under contract with LESCARDEN Ltd., Goshen, New York, was conducted for the development of a natural substance derived from bovine cartilage which preliminary investigations have shown to exhibit immuno-stimulatory and anti-inflammatory properties.

Publications:

• Thesis - 1975, Doctor of Philosophy "Alterations of humoral and cellular immunity in normal and lethally ,

irradiated mice treated with bacterial endotoxin and its derivatives". .

• Thesis - 1967, Master of Science "Radiation induced endoreduplication and polyploidy in peripheral blood leucocytes'. ,

e Report - Behling, U.H. and Hildebrand, J.E., ' Radiation and Health Effects: A Report on the THI-2 Accident and Related Health Studies",

issued by GPU Nuclear Corporation, June 1986.

• Journal Articles:

Behling, U.H., ' Radon: Answers to Common Questions', GPU Nuclear Today, Vol .1, No.1,1986 Behling, U.H., ' Medical Radiation and the Nuclear Employee', GPU Nuclear Today, Vol. 1, No. 3, 1985 Behling, U.H., ' Skin Contaminations: An Overstated Radiological Health Concern', GPU Nuclear Today, Vol. 1, No. 2, 1985 l

_ - - - - _ _ _ _ _ - . _ _ . _ _ , _ _ . . . _ . . . . _ _ _ - - _ - - - ~

e Curriculum Vitae Hans Behling Page Five

• Journal Articles (continued)

Behling, U.H., "Radiation Exposure in Perspective", GPU Nuclear Today, Vol .1, No.1,1985.

Behling, U.H., 'VDTs: Are They Safe?", GPU Nuclear Today, Vol. 1.

No. 3, 1984.

A. Nowotny and U.H. Behling, ' Studies on Host Defenses Enhanced by Endotoxins: A Brief Review', Klin. Wochenschr,12:735, 1982.

A. Nowotny, U.H. Behling, B. Hammond, C.-H. Lai, M. Listgarten, P.H.

Pham ar.d F. Sanavi, ' Release of Toxic Micro-vesicles by Actinobacillus actinomycetemcomitans', Infect. & Immun., 14:312, 1981.

U.H. Behling, C. Sallay, F. Sanavi, P.H. Pham and A. Nowotny, ' Humoral and Reduced Periodontal Bone Loss in Eikenella corrodens -

Mono-associated Rats', Infect. & Immun., 11:001, 1981.

U. H. Behling and A. Nowotny, ' Biological Activity of the Slime and Endotoxin of the Periodontopathic Organism Eikenella corrodens" Infect.

& Immun., 11: 580, 1979.

D.A. Johnson, U.H. Behling, M. Listgarten and A. Nowotny, "Role of Bacterial Products in Periodontitis: Humoral Immune Response to Eikenella corrodens' Infect. & Immun., 11:382, 1978.

0.A. Johnson, U.H. Behling, C.-H. Lai, M. Listgarten S.S. Socransky and A. Nowotny, ' Role of Bacterial Products in Periodontitis. II. Immune Response in Gnotobiotic Rats Monoinfected with Eiken 611a corrodens",

Inf ect. & Imun., 11:246, 1978.

U.H. Behling and A. Nowotny, 'Long-term Adjuvant Effect of Bacterial Endotoxin in Prevention and Restoration of Radiation-Caused Immunosuppression', Proc. Soc. Exp. Bio. Med. 157:348, 1978.

U.H. Behling, B. Campbell, C.M. Change, C. Rumpf and A. Nowotny,

' Synthetic Glycolipid Adjuvants', J. Immunol., 117:847, 1976.

U.H. Behling and A. Nowotny, ' Immune Adjuvancy of Lipopolysaccharide and a Nontoxic Hydrolytic Product Demonstrating Oscillating Effects with J

Time", J. Immunol., 118:1905, 1977.

A. Nowotny, U.H. Behling and H.L. Change, ' Relation of Structure to Function in Bacterial Endotoxins. VIII. Biological Activities in a ~

Polysaccharide-rich Fraction', J. Immunol. 115:199, 1975.

a Curriculum Vitae

• Hans Behling Page Six

• A29.b.

U.H. Behling, 'The Radioprotective Effect of Bacterial Endotoxin'. In Beneficial Effects of Endotoxins. A. Nowotny, ed. Plenum Press, N.Y.

and London, 1983.

U.H. Behling and A. Nowotny, "Bacterial Endotoxins as Modulators of Specific and Nonspecific Immunity'. In Oscillatory Ovnamics in the Immune Resoonse. C. Delisi and A. Hiernaux eds., CRC Press, Boca Radon, F L, 1982.

U.H. Behling and A. Nowotny, ' Cyclic Changes of Positive and Negative Effects of Single Endotoxin Injections'. In Bacterial Endotoxin and Host Response. M.K. Agarwal ed., Elsevier/ North Holland Biomedical Press, N.Y., 1980.

A. Nowotny, A. Nowotny and U.H. Behling, 'The Neglected Problem of Endotoxin Heterogeneity'. In Bacterial Endotoxin and Host Resoonse, M.K. Agarwal ed., Elsevier/ North Holland Biomedical Press, N.Y.,1980.

U.H. Behling and A. Nowotny, ' Immunostimulation by LPS and its Derivatives'. In Immunomodulation by Bacteria and Their Products.

H. Friedman ed., University Press, Baltimore, 1980.

U.H. Behling, P.H. Pham and A. Nowotny, ' Components of LPS Which Induce In Microbioloov, Colony Stimulation, Adjuvancy, and Radio-Protection';

ASM Publication, 1980.

• Abstracts .

A. Nowotny, U.H.' Behling, G. Nejman, H. Hayatghab, R.W. Beideman and F.

Sanavi, Cffect of Tolerance to Endotoxin on the Alveolar Bone Resorption of Ligature Treated Rats IADR Conference, New Orleans, 1982.

F. Sanavi U.H. Behling, G. Nejman, E. Kovats and A. Nowotny, In vitro 3one Resorption by Endotoxic and Non-toxic Lipopolysaccharide (LPS)

Preparations IADR Conference, New Orleans, 1982.

K. Sallay F. Sanavi, I. Ring, P. Pham, U.H. Behling, and A. Nowotny, Acute Alveolar Bone Destruction in Immunosuppressed Rats, IADR Abstract

1. 701, 1981. <

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O o Curriculum Vitae Hans Behling Page Seven

• Abstracts (continued)

A. Nowotny, U.H. Behling, B. Hannond, C.-H. Lai, M. Listgarten, P.H.

Pham and F. Sanavi, Biological Effacts of Membrane Vesicles of Actinobacillus actinomycetemcomitans (Y4). IADR Abstract #851,1981.

0. A. Johnson, A. Nowotny and U.H. Behling, Imune Response to Eikenella corrodens in Gnotobiotic Rats During the Development of Periodontitis.

IAOR Abstract #963, 1977.

A. Nowotny, U.H. Behling, and H.L. Chang, Relation of Structure to Function in Bacterial Endotoxin. 1975. European Imunclogy Meeting, 16th Workshop ' Bacterial Endotoxins' Amsterdam, Holland, p. 171-172, 1977.

4 8

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4 D0LMETED May 16, 1988 USNRC

'88 MAY 18 P2 :01 UNITED STATES OF AMERICA ,

~, NUCLEAR. REGULATORY CO> MISSION OFFICE OF EuitlAd f 00CKEitNG A 3Eevicf.

SRANCH L 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 Nuclear ) Generated Water)

Station, Unit 2) )

CERTIFICATE OF SERVICE I hereby certify that copies of the documents identified on r

the attached document list were served this 16th day of May, 1988, by U.S. mail, first class, postage prepaid, except as indi- ,

r cated by astericks, upon the parties identified on the attached j Service List.  ;

L 4. h Thomas A. Baxter, P.C.

't i

5 t

t i

i r

9 i

_ , _ - ....,,_y .

G DOCUMENT LIST

1. Licensee's Motion for Summary Dispositiori on Alternatives (Contentions 1, 2, 3 and 8).

2. Licensee's Statement of Material Facts as to Which There is No Genuine Issue to be Heard (Contentions 1, 2, 3 and 8).

3. Joint Affidavit of Dr. Gary G. Baker, David R. Suchanan, James J. Byrne, Thomas A. Grace, James E. Tarpinian, Charles S. Urland, Jr., and William W. Weaver (Contentions 1, 2, 3 and 8).

4. Licensee's Motion for Summary Disposition of Contentions 4b In Part and 6 (Chemicals).

5. Licensee's Statement of Material Fact" to Which There is No Genuine Issue to be Hear- ' ..tentions 4b In Part and 6 On Chemicals).

6. Affidavit of Kerry L. Harner (Contentions 4b In Part and 6 On Chemicals);

7. Affidavit of David R. Buchanan (Contentions 4b In Part and 6 On Chemicals).

8. Affidavit of Dr. Gary G. Baker (Contentions 4b In Part and 6 On Chemicals).

9. Licensee's Motion for Summary Disposition of Contention 5d.

10. Licensee's Statement of Material Facts as to Which There is No Genuine Issue to be Heard (Contention 5d).

11. Affidavit of Kerry L. Harner (Contention 5d).

12. Affidavit of Dr. Gary G. Baker (Contention 5d).

13. Affidavit of Dr. Kans Behling (Contention 5d).

o UNITED STATES OF AMERICA NUCLEAR REGULATORY COMMISS, TON 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 Nuclear ) Generated Water)

Station, Unit 2) )

SERVICE LIST Sheldon J. Wolfe, Esquire Richard P. Mather, Esquire Atomic Safety and Licensing Department of Environmental Board Panel Resources U.S. Nuclear Regulatory Commonwealth of Pennsylvania Commission 505 Executive House Washington, D.C. 20555 Harrisburg, Pennsylvania 17120 Mr. Glenn O. Bright ** Ms. Frances Skolnick Atomic Safety and Licensing 2079 New Danville Pike Board Panel Lancaster, Pennsylvania 17603 U.S. Nuclear Regulatory Commission Ms. Vera L. Stuchinski Washington, D.C. 20555 315 Peffer Street Harrisburg, Pennsylvania 17102 Dr. Oscar H. Paris Atomic Safety and Licensing Dr. William D. Travers Board Panel Director, Three Mile Island U.S. Nuclear Regulatory Cleanup Project Directorate Commission P.O. Box 311 Washington, D.C. 20555 Middletown, Pennsylvania 17057

• Stephen H. Lewis, Esquire Adjudicatory File Colleen P. Woodhead, Esquire Atomic Safety and Licensing Board '

Office of the General Counsel Panel Docket U.S. Nuclear Regulatory U.S. Nuclear Regulatory Commission Commission Washington, D.C. 20555 Washington, D.C. 20555 Docketing and Services Branch Secretary of the Commission U.S. Nuclear Regulatory Commission r Washington, D.C. 20555 l

By hand delivery on May 17

• • By Federal Express

. - - _