ML20038A646

Revised Answers to Interrogatories on Contentions 8/9. Certificate of Svc Encl

ML20038A646
Person / Time
Site:	Waterford
Issue date:	11/02/1981
From:	Larry Jones GILLESPIE & JONES, JOINT INTERVENORS - WATERFORD
To:	LOUISIANA POWER & LIGHT CO.
References
NUDOCS 8111160093
Download: ML20038A646 (27)

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DOCKETED USHRC

'81 IT -5 N0 :27 UNITED STATES OF AMERICA NUCLEAR REGULATORY CGMMLSSION BEFORE TIIE ATOMIC SAFETY & LICENSING BOARD In the Matter of LOUISIAN A POWER & LIGHT COMPANY Docket No. 50-382 (Waterford Steam Electric Station e,4 Unit 3) -

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y;i (Ik(llij , t JOINT INTERVENORS REVISED ANSWERS TO P ll0V1 a ;M s -

INTERROGATORIES ON CONTENTION 8/9 Wa. ucca , o.

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Interropitory 8/9-7: ;I ' \)

The combined or synergistic effect of radiation and other agents has been shown to exist in various cell studies, animal studies, and human studies. The exhtence of this phenomenon has been amply documented by l

Joint In t ervenors. (See attached list of references prepared by Dr.

Mortimer Elkind. Also see references listed in Joint Petitioners' arguments Regarding Contested Contentions, pp. 8-11 dated June 1,1979. Also see l Joint Intcrsenors Answers to NRC Staff Inter-ogatories and Response to Request for Documents, pp. 7-18, filed January 18, 1980.)

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l lI 8111160093 811102 DR ADOCK 05000382 PDR

, r Joint Intervenors feel that the summary or recapitulation of Dr.

Elkind should appear in the record:

Recapitulation From the material reviewed, the questions raised in this Lssue Paper may be answered as follows.

It is clear from cell studies, and confirmed in a general way by animal studies, that radiation produces effects that are interactive with those due to other physical agents, chemicals of various types, and viruses. Our understanding is limited, however, in respect to the mechanisms of action in cells and, secordingly, even less penetrating in respect to our comprehension of effects in animals. In the first instance, the foregoing lack of knowledge reflects our incomplete under-standing of the complexities of the effects of radiation acting by itself in living systems. Since the other agents considered involve mechanisms of action which also may be subtle and involved, combined actions perforce must be even more complex.

Thus, the coryclusion follows at this time, that we are unable to predict responses in humans due to combined action because of our incomplete understanding of individual and combined reponses of radiation and other agents in experimental systems.

(Italies in original)

Our present inability to deal adequately with combined effects does not reflect deficiencies in laboratory-derived know-ledge alone. The connection between uranium mining and smoking makes clear that human epidemiological data are needed to help iden tify specific problems and specific interactants that warrant laboratory study. While it is highly unlikely that mechanisms can be discerned from epidemiological data alone, the foregoing example illustrates that without epidemiological data the experimentalists may miss important leads. Af ter all, it is not likely that an animal radiobiologist, who may have been studying the late effects of alpha-particle irradiation of the lung, will have been prescient enough to have used in his studies a colony of mice that smoke.

Thus, the study of possible public health hazards due to combined effects of radiation plus other agents is one that should be converged toon simultaneously by the laboratory investigator and the epidemiologist-public health specialist.

What is clear is the likelihood that agents biologically active in their own right will interact. Indeed, an important and signifi-cant guiding principle may already be extracted from current knowledge. Relative to induced cellular ch inges--e.g., cell killing, altered differentiation, mutation, and neoplastic transformation-agents that register lesions in the genetic sub t

e y stance of a cell are likely to produce interactive effects. Such effects may become expressed in individual cells, in tissues, or in whole organisms.

These observations correspond to the ' thoughts of Samuel S. Epstein, M.D. (The Polities of Cancer, Samuel S. Epstein, M.D., Anchor Books, Anchor Press /Doubleday, Garden City, New York,1979, p. 58).

A major deficiency in current carcinogenicity tests is their simplistic nature, dictated in part by practical considerations, such as testing the effects of one chemical at a time. Carcino-genicity tests thus do not adequately reflect the realities of multiple concurrent and sequential exposures to a wide range of carcinogens in the general environment and the workplace.

Because of the relatively small numbers of animals that can be tested and the impossibility of predicting human sensitivity from animal tests,,there is also substantive evidence of interactions between individual carcinogens making the carcinogens together much more potent than either separately. Also interactions between carcinogens and a wide range of non-carcinogenic chemicals may increase the potency of the carcinogens. . . The quantitative' response to a particular carcinogen can be substantially influenced by a wide range of factors, including interaction with other carcinogenic and non-carcinogenic che micals. Thus, these so-called synergistic effects further confound attempts to find safe levels of carcinogens. Such i

interaction studies clearly confirm that threshold levels of

} carcinogens cannot possibly 'be predicted by calculations based 2

on setting a dose arbitrarily lower than the lowest apparently carcinogenic animal dose in a particular experimental situation.

Epidemiology has given important clues on interactive effects between carcinogens, such as smoking and asbestos or uranium . .

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. There are now critical needs for large scale interactive tests designed to elucidate such additive and synergistic interactions as they occur in daily life, particularly when suggested by epidemiological observations.

The question becomes then "Is southeastern Louisiana excessively burdened with carcinogens presently?"

The National Cancer Institute listed ten counties (or parishes) in Louisiana in the top 18 in the country recording high incidences of the disea se. Eight of those counties are in the southeastern part of Louisiana.

They include Oricans, Jefferson, St. Bernard, Terrebonne, LaFourche, St.

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i Charles, Iberia and St. Martin. Let us assume that our " base area"is the 23 parishes in the southeastern part of Louisiana. Factually, there are 3,104 counties in the United States. Using hypergeometric probability, it .is a simple calculation to show that the probability of this cluster occurring by chance is 1.03 X 10 6 or a proximately one chance in a million.

This admittedly simplistic calculation is enough to establish that southeastern Louisiana is " burdened with cancer", at least vis-a-vis the rest of the United States. Excessive cancer implies the presence of execssive carcinogens, as reflected in the authorities quoted above. The 4

sources of these carcinogens (industrial, municipal, natural, self-induced) are outside the purview of the Atomic Safety and Licensing Board. The question this Safety and Licensing Board must answer is this: Should this "one in a million" cancer situation be handled with the same broad stroke

! radiation standards as the rest of the United States?

The following is a list o,f known human carcinogens, suspected carcinogens (from animal and tissue data) and toxic substances that occur in southeastern Louisiana:

Polycyclic armoatie hydrocarbons j

l Vinyl chloride i

Benzene Luschloromethylether Fuel oils i

Lubricating oils Cutting oils l Kerosene Nethylated napthalenes Asbestos i

r Coal tar Arcylonitriles

! Natural and synthetic hormones i

l Pitch Creosote Authrasene oil i

l beta-napthyla mine Benzidine 4-Anunodipher.yl DDT

Dieldrin

! Aramite ,

i l Carbon tetrachloride s

! Acetamide l

l Thioacetamide

• i f Thiouren i

j Thiouracil Aminotriazole Several urethane derivatives 1sopropyl chlorophenyl carbamate beta propriolactone Numerous types of chlorinated hydrocart,on?

Mercury l Arsenic Lead Copper i

%~rs e-_ - . - __.n,

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Chromium I

Cadmium j i

Zine j s

Phenols '

Cyanides Chloroform

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Zylene l l

Dimethyl Sulfoxide  !

Toluene diisocyanate  !

Nitrosamines Interrogatory 8/9-8(ah l

See all documents listed in 8/9-7. See all documents listed in  ;

Combined Effect, Ionizing Radiation Plus Other Agents, issue paper  !

, prepared by M. M. Elkind, Division of Biological and Medical Research, l' l

1 Argonne National Laboratory, Argonne, Illinois, 60439,1980.

Interrogatory 8/9-8(c)

See all d'acuments listed in The Environment and IIuman IIcalth in Louisiana, prepared by the O'ffice of Environmental Affairs, City of New f Orleans, by Velma M. Ca mpbell, M. D., January,1981. .

Interrogatory 8/9-10(a)

Joint Intervenors estimate the risk to the maxir l' exposed individual at between two times and fif ty times the present level Interrogatory 8/9-10(bh t Joint Intervenors arrived at these estimates by extrapolating from the literature. i l

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i Interrogatory 8/9-10(e):

i j Two times estimate: V. E. Archer, J. D. Gillom, and L. A. Jcmes. l l

Radiation, smoking, and height relatinoships to lung cancer in uranium i

miners. In Prevention and Detection of Cancer, Part :, Prevention (H. E. i I

Nieburgs, Ed. ), pp. 1689-1712, Marect Dekker, New York,1977.

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l Fifty times estimate: Radiation and Iluman IIcalth, John Gofman, M.

1 D., Ph.D., Sierra Club Press,1981. i l

Interrogatory 8/9  !

A 50 mile radius around Waterford 3 (100 mile diameter) includes the l entire southeastern portion of Louisiana. Joint intervenors believe the .

. i increasc in risk to a person living within 50 miles of Waterford 3 and the

" maximally exposed individual"is proportionately the same. Therefore, the answer to Interrogaory 8/9-12 is the same as the answer to 8/9-7.

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Interrogatory 8/9-13_:

See 8/9 8. .

Interrogatory 8/9-14:

See 8/9-9.

Interrogatory 8/9-15:

Sec 8/9-10.

Interrogatory 8/9-16:

Joint Intervenors have reconsidered the response to Interrogatory 8/9-16 (dated September 1,1981). We ace limiting our contention to three 4

types of individuals:

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1) niaximally exposed individual;

, 2) Individual witNn the exposure pathway (10 miles); and I 3) Individual within the ingestion pathway (50 miles). Therefore, risks to the general population are out of the scope of this proceeding.

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Joint Intervenors hope this oversight caused little inconvenience to the Applicant or the Staff.

Interrogatory 8/9-17:

Moot.

Interrogatory 8/9-18:

M oot.

Interrogatory 8/9-19:

Moot.

Interrogatory 8/9-20:

Moot.

Interrogatory 8/9-21:

All revised, answers to applicar.t's interrogatories to joint intervenors (second set) filed November 2,1981 were prepared by Gary L. Groesch, 2257 Bayou R oa d, New Orleans, Louisiana 70119. M r. Groesch is self-e mployed. Mr. Groesch is chief research associate for the Oystershell Alliance.

Respectfully submitted, GILLESP u- ON ES BY g c_

14 Y M A. /L. JON/S, Attort ay for Inferv ors 114 Richelake Dri .

Metairie, Louisiana 7000 (504)835-6458

I 1 Novt nibtr 2,1981 i

F SI' ATE OF 1,0UIST AN A

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P \RISil OF JEFFERSON

!!EFOR E M E, the undersigned, did appear G ARY 1,. GROESCII, a i

perm,n of the full .:;c of majority nnd a residcnt of the Parish of Orienns, who did d. elare on cath that the Revised Answers to Interrogatories on l C(. n t e nt i on 8/9 filed htrein are true nnd ccrrect to the best of his i

k lewled;e, inrortnation nnd belief.

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SY ISSUE FAPER NO. 5 i

Morticer M. Elkind, Ph.D.

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'Aar is Our Current Knculedge frc Anical and Cellular Systems About the Cc:bined Effects of Ienizing Radiation and Exposure to Other Agents (chemical, phar acciogic, physical, viral, etc.) and is This Knowledge l

Adequate to Fredict Human Respenses?

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COMBINED EFFECTS, IONIZING RADIATION PLUS OTHER AGENTS (a. ,nar ts <ncun, fr:m ce! uiar and ani gi gug:g g, cbcut the cor:bined effects of icnisin: r=bati:n

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and other c;cnre (phusical, che-ical, and bio cgical), nd is :his kncu:ed:e adep ate

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to Fredict responses in hu~ ns?)

Issue Paper prepared by M. M. f1 kind j

Division of Siological and Medical Research Argonne Naticnal Laboratcry Argonne, Illinois 60439 -

Today's world is shrinking in the sense that the vaste products of expanding, industrialized societies have been increasing in concentration and diversity. These products are frequently liberated into the environ-cent and many have the potential for biological activity. Enyirennental biological activity also ccres fro: natural scurces, for example, from sunlight and frc the ionizing radiatica due to ces:1c rays and earth-beund radica:tivity. In addition, current-day diagnostic and therapeutic medicine frequently invcives the use of one or =cre agents, each of which may be potentially able to produce untevard ancillary reactions. In sc=e cases, the end effects prcduced by envirennental and medical agents are biologically similar to these produced by radiation. Consequently, the possibility cust be censidered that ene or more of these agents may produce in humans cc:bined effects not readily predictable frc: a knew-ledge of their indiridual actions.

In this Issue Paper we censider: what is kncvn of the cc bined effects of varicus kinds of agents when acting together with ionizing radiation; whether or not ccabined effects suggestive of unexpected interacticns have been detected in humans; and to what degree responses in humans can be predicted from available laboratory data.

End Points Radiation can prcduce a variety of short- and long,-tem chaages in animals and humans. The short ter changes--which in the extreme may result in tissue ulceration or death--generally are a result of the killing of relatively rapidly dividing cells related to essential cell renewal syste s of the bcdy (e.g. , skin, intestinal mucosa, and blood ferring crransi. The cc prenising of cell renewal systems occurs particularly wN n whole-body expcsures are received. After only partial body or nonlethal whoic-body enpesures, a variety of long-ter: sequelac 4

=ay result. The latter may reflect degenerative changes in tissues and

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i organs in which, because cell turnover is slow, cell death is slow.

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However, cells that survive radiation exposure may give rise to late {

effects that reflect their altered =etabolis=, altered genetic con- '

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stitution, or altered properties of growth. Late-appearing degenerative and other changes are quite effectively integrated by acasuring reduc-tiens in life span and censiderable data exist on the dose-dependent i reductions in lengevity in mice due to y-rays and fission-spectrum j neutrons (2,2).

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i Relative to public health, concern centers cq small acute deses, I on small fractionated deses, or on small total doses protracted over tong periods (i.e., low dose rate exposures). In such cases, the principal cause of life shortening is usually cancer induction. A cause-e ffect connection between somatic cutation and cancer is a popular hypothesis although secatic mutation by itself is not sufficient to account for other factors that influence the grcwth of transfortn. l cells like horronal status, compensatory repopulation, and '

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, perturbations in the i==une co:petence of the host. This latter group l of ancillary factors *may reflect changes, in varying d egrees, in the l viability of the cells relevant to them. Thus, in addition to somatic  !

l rutation in target cells, survival of target cells as well as the  !

I suriival of cells that can interact with target cells, eay be important l in oncogenecis. In the instance of fetal irradiation, developmental changes may also be registered. Lastly, the mutation of germ cells may lead to teratagenic effect2 as well as to less severely altered offspring.

. i Thus, the end points of interest due to radiation alene, or radiaticn in combinatien with other agents, include developmental, l genetic, and transformational changes--in relation to teratogenesis, '

f mutagenesis, and oncogenesis, re sp e c t ively. Since each end point j

depends upon viability for expression, cell killine cust also be .

censidered. The foregoing end points are of principal concern in I respect to Icw deses; they are also of 1 portance in respect to mid-te-high deses but for these dese ranges, ard particularly in regard  ;

to late-appearing lesions, the bases fer the syndreres observed are l not fully werked out. r

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.r Modes of Cctbined Effect if two or scre agents can preduce by themselves the same H biological effect, this knowledge is usually not adequate to predict j

the quantitative aspects of their conbined action. In some instances, even the qualitative nature cf their cc binntion may not be predict- l able. The essential reason for this uncertcinty is that different {

agents may induce a particular end effect in part cla ditierent colecular, cellular, and/or pessibly pFysioicgical changes and ccnsequently, a large variety rf codes of interaction are pcssible.  ;

As will be illustrated further in the discussica to foll w, assessments r of acdes of interaction require a knculedge of the mechanisms whereby particular enc points are prcduced by particular agents. Mcwever, it {

is also inportant to knew in the first instance if the changes due to I the agents interact.

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Some insight into the nature, and the rede, of the interaction of two agents may be obtained from :easurecents of the influence each has on the dese response of the other. This is illustrated schematically in Fig. I where two kinds of dose responses are shown; on the left, the reduction in surviving fraction with dose (as illustrated, surviving fraction is usually plotted on a logarithmic scale and dose on a linear scale); and on the right, the increase in the frecuency with dose of cell end points like mutation and neoplastic transformation, or anical end points like turorigenesis (induced frequencies are usually plotted on linear-linear coordinates). What is shown in Fig. 1 is the effect that a dose B of agent B (left part), or a dose B' of agent B' (night part), has on the dose-response curve for agent A,or for agent A',

respectively. Four conditions tay be identified and are characterized in respect to cell survival as follows. If graded doses of A following dose B result in a survival curve of the same shape as when treatment with B is critted, then the effect of B is independent of that due to -

A. If after B, the survival curve 'is the same as the portion of curve A correspcnding to doses gre ater than the dose of A survival-equivalent to dcse B (2 units of A in Fig. 1), then the effect of A is additive to that of B. And if followins dose B, graded doses of A result in a curve lying above that marked " independent," or below that marked

" additive," then antagonistic (or protective), or synergistic action, respectively, is indicated. The applicatien of these terms to the dose dependence of the frequency of induced events is readily apparent from the curves in the right part of Fig. 1.,

Some qualifications need to be applied to the foregoing definitions.

In respect to cells, for example , it is kncwn that dose-responses may depend on grcwth phase at the time cf exposure. If such a dependence is not the same for two different agents, questions of population selection

=ay have to be resolved before a mode of interaction may be identified with cenfidence. Although not likely, the terms in Fig. 1 may be appli-cable caly within certain dose ranges and different terms may apply in different dose ran;es. Further, the terms used may have different

=canings to a cell biologist, to a physiologist, or to an epideriolcgist as the raterial to follew will illustrate. Lastly, when survival varies expenentially with dose, or induced frequencies vary linearly with dose, it should also be noted that additive and independent actions are not distinguishable. Ncnetheless, these terms will suffice to identify, if only provisionally in sc:e cases, the nature of the interaction of radiation with another agent.

Cerbined Effects in Exterimental Svstems l

With the nemenclature set dcun in the preceding section, we are now in a position to review what is known fro: laboratory studies. For present l purperos, it suf fices to draw examples from cell and animal experiments.

Cell Studies. Bv far the lar est a: cunt of data derives fron studies of anical and human cells grown in culture primarily because of the facility with which such data cay be obtained. Also, as concerns cc bined effects, cell killing is the principal end point that has been pursued this tco reflecting relative ease of reasurerent. A series of exanples follcw.

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e X-rays _plus physical agents. Studies have been performed demenstrating that the damage due to X-rays interacts with that due to nenieni:ing radiation, heat, or other types of ionizing radiation.

X-r pa p::.s :d tra;-i.?:ct GT' ~ f:t . .. Survival stodles with Chinese hamster cells have shewn that damage due to far-HV Iight interacts with X-rav damage additively tace 5 and citations therein). A qualitatively similar result la obt ained when near-L*V li >;h t simulating the short wavelength part of the sun'o spectrum on earth is used although quantitatisely the degree of additivity is less.

X-ra,.J 7::is I:yr. PS:c2--f a. Raising the temperature of cells before, during, and/or af ter irradiation results in enhanced cell killing because of synergistic int e ract ions (5. rO . Qualitatively similar results have been reported for normal and tumor tissue in rodents, and preliminary trials of heat and radiation are beine introduced in the treatre,nt of cancer t').

X-r :,.s p::.s ;'aa t *:c:<t era:J. In contrast t o X-- and 7-rays , which produce damage in biological material by setting electrons into mation, fast neutrons prcduce damage mainly by energizing protons.

The proton, being some 1800-times more massive than the electron, is characterized bv a greater rate of linear enernv transfer (LET) when they recoil from neutrons of average energy of one to a few tens of .MeV. Thus, by carparison, X- and 3-radiations are low LET in quality compared to fast neutrons or charged particle beams made from atemic nuclei. Fast neutron beams are biologically more effective than X- or Y-rays (5). Hewever, although the survival dependence on dose follcwing r.eutron exposure is qualitatively and quantitatively different from that for lev LET radiations, the damage registered by X-rays is partly additive to that due to neutrens ( .' ) .

• X-ravs plus chemical agents. A variety of data exist indicating that radiation and certain checicals, including pharmaceuticals and some dru;s used in cancer therapy, prcduce interactive effects. r.xamples fo11cw.

T-?~y: ;*u3 ::;.;e", ::j;in- ikt m:~cculas, ami su:P.y.ir,1~ x =cu'.it.

The presence of molecular oxygen in solution at the time of irradia-tien is well known to enhance the effectiveness of radiation in respect to essentially all end points. Since crygen at sensitizing ccncentraticas is usually without effect by itself, this acticn is clear 1" synergistic. Similarly, a cicss of cc pounds that have sirilar electron affinic prcperties to oxygen produce similar l

effects at both cellular, tissue, and whole animal levels (see ~T).

Metrenidc:cle, a well-established antiparasatic drug, has electron affinie prcperties and is an effective sensiticer of hypoxic cells.

In ccr.trcst, ccapcunds containing SH-groups, are typical of a class that 2:e able to yrctect cells, tissues, and animals under ccnditicas where the capounds alene have minimal effect. As with electron affinic agents, radiepratectors of the SH type act, in part, at a i

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physical-chemical level by altering the effective magnitude of the dose that is available to produce biological lesions. Most of the information about physical-chetical sensitizers and '

protectors comes free studies in which cell killing is primarily responsible for the effect. however, because of the radiochemical nature of the mechanism of action of these molecules, it is quite reasonable to expect qualitatively similar char.ges in respect to '

other end points.

X-rays pins phar =:ceutic Is. A pharmaceutical like cetronidazole

, is effective when present during radiation exposure since, because it is electron affinic, it acts like oxygen. Other drugs may be given before and/or after irradiation with considerable effective-ness. For example, the cancer treatment drug actinomycin D is of this type (5) as is the anti =alarial quinacrine. In both cases, the mode of interaction relative to cell killing is largely additive.

In contrast, the cancer therapy drug nitrogen mustard--a compound that has come to be characterized as radic=1:etric because it produces effects similar'to radiation--nevertheless, was found to act independently of X-rays in cell killing (11). Additional insights of the cc:bined effects in cells and anicals of radiation and chemicals which are in use in cancer therapy are emerging from a progrce of the National Cancer Institute directed at devising i proved strategies for the treat:ent of cancer (22).

X-rays p!as carcinocer.s. An important class of carcinegens are the polycyclic aromatic hydrocarbens produced by, or. derived froz,the ince:plete cc:bustion of varicus natural substances (e.g., coal, oil, tebacco, etc.). In respect to the transfor ation of cultured ra==alian cells to tumorigenic properties, it has been reported that X-rays significantly ' enhance the transformation of Syrian hamster e:bryo cells treated with benzo (a);yrene even though the concentratiens of the carcinogen used had negligible effect upon the X-ray surv val of nontransforced cells (~J).

X-rays pD.s przearers. Various 'cinds of -'a 3-al carcinogens have been shcwn te be promoted (i.e., incressed in effectiveness) by other chemicals which are by the selves withcut effect.

Similarly, it has been reported that X-ray-induced transfor ation

. can be enhanced by a che ical pro =oter (!!).

i l eX-ravs plus viruses. Scte bacterial viruses are temperate in that they may infect a sc-called lysegenic host, he integrated into its genome, and be propagated  :: generation to generati:n. yet they may not cultiply or affect the hest. A variety cf agents, including ionizing

radiation, are able to indu a tral replication and a lytic response in

the hest. While the detail are very likely different, and the =echanis

(s) yet to be fully elucidated, radiation can induce viral expression or enhance viral production in mammalian cells (2E, see also discussion in !?).

F;riher, in rodents this may lead to the cell transformation of newly I

1 infected cells and cancer.

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Animal Studies. Data of varying degrees of ec:pleteness exist for both short- and 1cng-ter: end points. Partly because of practical con-strain ts : hat li=it the arount of data and therefore the resolution of~

in vivc reasurements when two kinds of treatments are being cerpared, and partly because of inherent limitaticns in such comparisons, it is frequently not possible to be confiden: about che code of interactica at a cellular level. To begin with, to identify such interactions fro:

tissue or whole snical ef fects, a source of uncertainty may develop f rca cell-specific differences in action as already noted. An additional cerclexity comes fro: the possibility that in an anical tissue systens say in:eract. To illustrate, the expression of ture-igenesis by a chemical treatment added to a radiation treatment say be less than that due to radiation alene, for exa:ple, if the radiaticn transfor:ed cells in questien require for tumor developnent a greath factor (e.g., a hor:cne) the availability of which is reduce by :he chemical treatment.

Ccnsiderations,of the foregoing type take evident that the ecdes of in:eraction of two agents at a tissue or whole anical level may reflect differen: sechanists than at a cellular level. Furtherrore, the two cgen c cay have--or at least may appear to have--different codes of in:eracticn depending on the end point.

Te illustrate, radiatian plus a chemical may act syn +r31 stically in killing ani:21s due to the sterilicarica of stem cells of the blood f>: ming systes even thcugh these.tvo agents may act independently in lethally affecting the relevant target cells, i.e., hematopoetic ste=

cells. Since the end point in this case reflects the proportion of stem cells surviving :he ccebined treatrent (as explained belev), independent ecdes of cell killing may act synergistically in animal killing as long as scre degree cf cell lethality results frcs each agent. The foregoing is : rue even if :he respective s:c: cell survival curves have thresholds.

In ::ntrast, le: us assure that in the animal sublethal deses of radiation or a che:ical cay induce leukemia linactly with dese. Now, the existence -

cf independent action at a cellular level could lead to the cenclusion of inde;enden: actica at an animal level. The reason for the apparent difference in the cdes of action in these two cases is that anical death due to failure af the biced forming systen requires that hematepcetic l ste cell survival be reduced tc a certain critical level. Hecatepcetic ster cells are crdinarily present in ccasiderable excess of that level.

.nus, :ne survival curve of anicals has a bread threshold regardless of the lethal agent or the shape of the survival curve of individual stem cells treated with that agent. Ccasequently, scre degree of cell killing by cne agen: vill reduce the width of the thresheid fer the second agent thus pr:ducing synergist. ?he induction of leukemia, hcuever, may be 3 tnearly proporticnal to the nu ber of cells transfer =ed with dese.

Eence, :h'e lack of a shoulder takes it p;ssible in this case to cbserve actice that is independent although the resul: nay be referred to as additivity because the net frequency is the su: cf the individual frecuencies.

$1 S

'41th the foregoing cautiens in mind, a series of examples are presented that de enstrate enhanced as well as independent action between radiation and ancther agent.

e X-rays plus physical acents. Interactions, at least additive in nature, have been obser.ed in respect to X-radiation plus heat in regard to acreal as well as to tumor tissues responses (?). Because these studies were related to cancer therapy, shor:-ter: end points mainly reflecting cell survival were used but in sc e instances, late tissue-degenerative changes were also scored. Additive action has also been reported in ecuse intestinal mucosa when neutron and electron exposures (i.e., a high LET radiaticn and a low LET X-ray-like radiation, respectively) were applied in quick successien (17).

e X-rays plus c h e mi c a ls_. The extensive literature that is develeping frc both anical and cell studies as a result of the progra of the "aticnal Cancer Institute to imp' rove cancer therapy pertains mainly to short-ter: end points reflecting cell-killing (20). In a number of instances, conclusiens abcut cie of interaction in ncrtal or turer tissues have been reached censistent with si ilar conclusicas derived frem studies with cells in culture. In instances where apparent discrcpancies exist, it has not been always clear te:her or not inheren: differences in cell respenses, or inherent differences in the end points (as noted earlier) are res;cnsible.

Tumor indue:icn due to ccabined action has been studied althcugh the acde of tSe cc-bined effect is not always cicar because of limited data having limited resolatien. A nutber of observaticas have involved Icw LET radiations--e.g., X-rays, v-rays, er f-rays, the latter frc: isotopic sources--plus chemical carrinegens. For o.xcnple, skin papillccas in rice are reported to be prcduced synergistically by topic 4lly applied 2-tethylchelanthrcne plus i-irradiation although skin cancers were reported in the same study to be induced caly additively (25). Additivity was also reper:ed in the inducti:n cf _m_ o s. adenc s in rats for the same polycyclic arcratic hydrccarbon plus X-rays (:. ) . Repeated small exposures (20 R) of-the head, plus the topical applicarica of 7,12-dimethylbenc(a) anthracene to the tongue of Syrian narsters, prcduced an excess of papilloras and of nenlingual eral tuncrs (ff). X-radiation plus the carcinogen urethan l were reported to act additively in producing lung tuncrs in mice while the immune suppressant ccr:iscne also increased the induction due to radiatica with:ut urethan (22).

A fcw cbservatiens hcVe been rade using high LET radiations. Fissicn- -

spectru neutrens -lus 2-:ethylchelanthrene act additively (IS), whereas the es:r: gen-like synthetic her cne, diethylstilbesterol and 0.43 MeV neutrens act syner_cisticalle (22), in producing :strary cancers in rats.

Felonie: :-particles plus ben:c(a) pyrene administered tcgether into the trachse of Syrian harsters are also reeorted to act synergistically in inducing lung cancer ( f ') .

Ia many of the studies acted abcVe, specific schedules of administra-l tien of the :wo agents were used and f requently this was f ound to make a 1

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difference. For practical reascas, only limited information exists in a given case about the 1 portance of the sequence of administration, or the use of single, repeated, or continuous ad inistration of one agent or the other. The persistence of interactive damage can also be relevant as illustrated by the observatien that the topical application to the skin of rice of the carcinogen 1-nitroquinoline 1-oxide at intervals after f-irradiation of the skin from.11 to 408 days, resulted in about the sane level of malignant skin cancers whereas no effect was observed due ta the radiation or to the carcinogen alone (25).

Designations of todes of interaction in animal experitents cay be ambiguous in sone instances. As noted in reference to Fig. 1, when dese-responsec are lineat (or expcnential in the case of survival), a distinction cannot'be made between additive Jersas independent action.

Thus, if the total incidence due to two agents is the sum of their individual incidences, the ter: " additive" =ay be correct if the dose dependencies are linear. If they are not linear, then in terms of the dt:2ge produced--riot the incidences produced--the agents may act independently.

X-rays ple_s .*irases. A nurber of examples exist in which ionizing radiatica can in:uce the erpressica of viral prcperties frequently culninating in tracrigencais. The induction of thysic.ly phc as (26), .

1One tumors (27), a-d n2=: .ry turers (0S) in mice are exa:ples. In each case, synergistic c: tion res"Its from the radiation-induced expression of apparently endogences encogenic viruses.

Furan Stydies. In respect to data resulting fro: studies of humans, there are a few examples that indicate the likelihood that co:bined effects may he greater than expected f c independent action. .

Urzniu: rininc and lune cancer. Craniu is usually found in the carth at near equilibrit: with its daughter products one of which is the chemically nert, but radioactive gas radan. Epidemiclogical studies have been conducted of the relationship between lung cancer (of various histological types) to the arount of exposure to raden, to scoking habits, and to other characteristics of =iners in the United States (ES). The relaticnship of these factcrs to ncncalignant respiratory diseases was also enacined. The results of the studv cake clear that the excess .

tortality due to caligrant and to non:211gnant lung disease is related to both e:cpescre to radon and its daughter products, which are largely

-particle aritters, and to e: cessive srcking.

3

^

P.adiat_ijn treatrent of tinea espitis. 3etween about 1910 and 1959, it vts not unc;n=on to treat children with advanced cases of tinea capitis (ringwarni cf the scalp) uith large doses of radiation (from 500-cC0 rcds), dsen11y scne five different exposures were administered furing cne treat:<nt session. Shielding with a lead sheet or with plaques

, , , . , .-- , . - - _ _ - . _ , _ . , _ _ _ _ , _ _ - _ - - . . . .-g._, , ,

t EP Ti 10 was generally used to protect the face, eyes, and ears. Subsequent simulation of the irradiation preceduce indicated that even though only 100 kV X-rays were used, substan:ial doses were received by the brain, eyes, thyroid, and ears (20,J2).

Ccepared to catched controls, excess brain, thyroid, and parecid tumors were detected. In additien, excess skin cancers were also observed a subs:antial p,roportion of which were just outside of the

, hair-c:vered regions of the scalp and on the face (JI). About one-fourth of the individuals treated were ncnwhite; no skin tumors were detected in this group. Sunlight-induced skin cancer is very rare in pigmental ucrsas acne 12:ented skin.

t Thus, it vould appear tha: an enhanced expression of skin turers resulted frc the ccabined effects of icnizing and nenioni:ing radiations in whi:e pa:ien:s treated for tinea capitis.

Cancer theraov a'nd tunerigenesis. It is, no' doubt, biologically significan: that many of :he agents effectively used for the sterilization of tumor cells are also capable of inducing cancer (if). Fur:her, as

rea::en: pr:cedures be:: e Ore effective, with the consequent result t tha: ::re pa:ien:s may be cured er more patients will at least have an increased life expectancy, :he likeliheed of de:e :ing treatment-induced new primary cancers intresses. This situatien is illus: rated in c nnet-ti:n with the trea::ent of Hedskin',s disease since relatively high frequen: des cf n n-H:dgkin's disease ly:phc a and acute myeloid leukemia are being de: acted (!!.J4).

The impreved treatmen: of cancer with radia:icn and/cr drugs alces:

always inv:1ves large d:ses of be:h kinds of agents. It is no: unexpected, therefore, :ha: new primary cancers would be induced (JE) To date the resui:s de not supper: the inference :ha: :he e.:bination of radia:1cn ,

and :hert:herspy is :: t effe::ive in inducing new cancers than either

, :dali:y alene alth: ugh such a :: 1usi:n say be:::e justified in tire as

re data are eclietted (JJ).

J.adiation-induced cancer and occupational hazards. Studies of the j at :10 bc=b survivers in Japan have made clear :he cancer-inducing i N pctential of high deses of both high and Icw LET radiatiens. Efforts have been made :: explore the possibilities that, in some instances, the occupational histories of the survivors ray have contributed to the leuke:ia induced. The data available do not clearly support such associations although a tenden:v for a higher risk was noted anang survivors expcsed to ben ane or its deriva:ives, and tc redi:21 I-rays (JJ).

Recaritulation i Trin the esterial reviewed, the questi:ns raised in this Issue Paper ray be answered as follows.

It is clear free cell studies, and c nfirred in a general way by anical s:udies, :ha: radiation produces effects that are interactive with l

. Qi 11 those due to other physical agents, chemicals of various types, and viruses.

Our understanding is limited, however, in respect to the techanis s of action in cells and, accordingly, even less penetrating in respect to our cc prehension of effects in animals. In the first instance, the foregoing lack of knowledge reflects our incomplete understanding of the co=plexities of the effects of radiation acting by itself in living syste=s. Since the other agents considered involve techanists of action which also =ay be subtle and involved, combinea actions perforce =ust be even more co plex.

Thus, the conclusion follows at this time, th:: >e are unsbie to predic:

resp:nsce in r.umans due to a:=hined : tion because o,', cur incomplete

. f . .. . , ,

un:ctst natng os snatuscua an: c:n tnea responses o,r raatatt n anc otner cgent: in c= peri = ental s.ustems.

Our present inability $odealadequatelywithcc=binedeffectsdoes not reflect deficiencies in laboratory-derived knowledge alone. The -

connection between uranium :ining and seoking =akes clear that hu=an epidericlegical data are needed to help identify specific problems and specific interactants that warrant laboratory study. While it is bighly unlikely that mechanisms can be discerned fro: epidemiclegical data alone, the foregoing example illustrates that without epidemiological data the experimentalist ay =1ss important leads. .After all, it is not likely that an anical radiobiologist, who may have been studying the late effects of :-particle irradiation of the lung, will have been prescient enough to have used in his studies a colony of tice that s:cke.

Thus, the study of possible public health hacards due to ambined effects of radiation plus other agents is one that should be converged up;n si ultaneously by the laboratory investigator and the epideniologist-public health specialist. What is clear is the likelihood that agents biologically active in their own right will interact. Indeed, an irportant and significant zuiding principle ray already be extracted from current kncwledge. Relative to induced cellular changes--e.g., cell killing, altared differentiation, =utation, and neoplastic transfornaticn--agents th-t register lesiens in the genetic substance of a cell are Iiks!y to prciuce interactive effects. Such ef fects may becc e expressed in individual cells, in tissues, or in whole organisms.

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.e I 12 References i

2. D. Grahn. Biological effects of protracted low dose radiati,on exposure ,

In Late Effects of Radiation (R. J. M. Try, '

of man and anicals.

D. Grahn, M. L. Gries, and J. H. Rust, Eds.), pp. 101-136. Taylor end Francis, London, 1970.

2. E. J. Ainsworth, R. J. M. Fry, P. C. Brennan, S. P. Stearner, J. H. Rust, and F. S. Williamson. Life shortening, neoplasia and systematic injuries in mice after single or fractionated doses of neutron and gamma radiation.

In Biological and Environmental Effects of Low-Level Radiation, pp. 72-

92. International Atomic Energy Agency, Vienna, 1976.

J. Quantitative Ccncepts and Dositetry in Radiobiolocy_, Repo:t 30, pp. 14-15, International Commission en Radiation Units and Measurements, Washington, DC, 1979.

1

4. M. M. Elkind. DNi repair and cell repair: Are they related? Int. -J.

(

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.S_u_r e e rv ,. and Irrunotheraov. . (F . F. Becker. Ed.) pp. 51-99. Plenum, New York, 1977. -

6. W. C. Ceway, L. E. Hopwood, S. A. Sapareto, and L. E. G e rweck. Cellular ,

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3. F. Q. H. Ngo, A. Han, and M. M. Elkind. On the repair of sublethal da age -

in V79 Chinese harster cells resulting from irradiation with fast neutrons or fast neutrons conbined with X-rays. Int. J. Radiat. Biol. Ja, 507-511, (1977).

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(T. Fhillirs, Ed). Int. _J . Radiat. Cn c o l o r_ v_ , Biol. Phys. 5 (1979).

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Acad. Sci. 68 172'-1737 (1971). 9

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24. A. R. Ecnnedy, S. Mandel, C. Heidelberger, and J. B. Little. Enhancement of X-ray transformatice by 12-0-tetradecan:vl-phorbal-13-acetate in a cloned line of C3R =cuse embryo cells. Cance r Res. 33, 439-413 (1973),

25. R. W. Tennant, J. A. Otten, J. M. Quarles, W. K. Yang, and A, Ergwn, Cellular fa :ars that regulate radiation activa:1cn and rest'rictien of

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Yuhas, R. W. Tennant, and J. D. Regan, Eds.), pp. 227-236, Raven Press, 9

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interacti:ns with chemicals and viruses." Paper H, These Proceedings I 7. 5. E:rnsey, V. Andre ::1, and P. R. Warren. Sublethal damage in cells of the ::use gu: after mixed treatrent with X-rays and fast neutr:ns.

., .e . : =~s < , ,

._ . ... 50, 5.' .' ,517 ( .' 9 7s ') .

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s

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..nst. _3_e , . /;-ee ,3,ve

t. s ).

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22. L. J. C:le cad W. A. Foley. Modification of ure:han-lung turer inciJepce by 1:e X-radia:icn deses, :Ortisane, and transfusion of isegenic lympho-cytes. ?adia:. Ees. 39, 391-399 (1960).

!!. C. J. Shellabarger and R, F. Straub. Effect of 3-ne:hy!:helan:hrene and

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.. ... .,,. i . . a d. .' .- *. n , .c '. v... .c '. . . 3 .1," c

. u- . '. .' . c .d , .-..

. . .a* --_.a.-v, carcinogenesis. d. Natl. Cancer Inst. "", 1E5-137 (19 7 2) .

22. C. J. Sheliabarger, J. P. S: ne, and S. Holtzman. Synergis: te: ween neu:: n adenocar:in ras radiation and dia:Fylstilbesterol in the pr: duction of cantarv, in the n Cancer Res. 31, 1019-102 (1976). .

!. J. E. Lit:le, R. 3. M: Candy, and A. R. Kennedy. Intera::icas be:veen p 1: nit -210 ;-radia:1:n, ben:cCa) pyrene, and 0.97. Nacl solu: lens in

.. s. ...2....<.. ..: .,x ,.<. - .:21 lun3, cancer.

7_ .

Cancer Res. 33, 1929-1933

( ..t.. : . n) .

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a- ,.* *' ~ ' * *s w*

• ...*e . 3e ,* ,*,o *.

, _'. Natl. .C.= m.t e r : n s t.. , M:nc. 14 207-217 (1964),

,r-w- e-- 3--, , ,,

7___ - . , - . .,_.s., w.,y-..y._-._..--..~m. y _wy,9_e.m.y_.p g...g. ,p w_ -m -= ,y---.--.-- y-,. ---

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3cne turcrs viruses. In Proceedings of the Twentvfcurth Svmoesium j of the_Cc_2_ston Research Society, pp. 353-366, But t e rworths , London, 1973.

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_. .. .r _- .. . s . 5, 1 s .1 , _171c ('.9 7 9) .

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),

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1 I

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e a o UNITED SI'ATES OF AM EltlCA NUCLEAll llEGULATORY COMMISSION BEFOR E Tile ATOMIC SAFETY & LICENSING BO ARD In the Matter of LOUIS!AN A POWER & LIGliT COM PANY Docket No. 50-382 (Waterford Steam Electric Station Unit 3) -

CERTIFICATE OF SERVICE I hereby certify that on November 2,1981, I mailed copies of Save Our Wetlands, Inc. and Oystershell Alliance, Inc.'s, JOINT INTERVENORS REVISED ANSWERS TO INTERROGATORIES ON CONTENTION 8/9, to all individuals or entities appearing on the attached Service List, postage prepaid, first class in the United SN, .dait l

YMA--.

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L.JO .ES,JI.-

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o-4 SE R VIC E LI_S_T_

Sheldon J. Wolfe, Esquire U.S. Nuclear Regulatory Commission

• Atomic Safety and Licensing Board Panel Washington, D. C. 20555 Dr. IIarry Foremas.

Box 395, Mayo University of Minnesota Minneapolis, Minnesota 55455 Dr. Walter H. Jordan 881 West Outer Drive Oak Ridge, Tennessee 37830 Chairman, Atomic Safety and Licensing Board Panel U.S. Nuclear Regulatory Commission Washington, D. C., 20555 Chairman, Atomic Safety and Licensing Appeal Board .

U.S. Nuclear Regulatory Commission Washington, D. C. 20555 Docketing and Service Section (three copies)

Office of the Secretary .

U.S. Nuclear Regulatory Commission Wa sh:ngton, D. C. 20555 Sherwin E. Turk, Esquire Office of Executive Legal Dir'ector U.S. Nuclear Regulatory Commission Washington, D. C. 20555 George F. Trowbridge, Esquire and E. Bhke, Esquire Shaw, Pittman, Potts & Trowbridge 1800 M Street, N. W.

Washington, D. C. 20036 i

W. Malcolm Stevenson, Esquire Monroe & Lemann Whitney Building

( 625 Gravier Street New Orleans, Louisiana 70112 l .

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