ML19029A879

04/09/1980 Legal Correspondence Written Testimony and Qualifications of Dr. David B. Fankhauser, in Response to ASLB Order of February 22, 1980

ML19029A879
Person / Time
Site:	Salem
Issue date:	04/09/1980
From:	Valore C Lower Alloways Creek Township, NJ
To:	Atomic Safety and Licensing Board Panel
References
Download: ML19029A879 (31)

Text

• UNITED STATES OF AMER!'

NUCLEAR REGULATORY COMMISSION Before the Atomic Safety & Licensing Board IN THE MATTER OF Docket No. 50-272 (Proposed Issuance of Amendment PUBLIC SERVICE ELECTIUC .. to Facility Operating License

& GAS COMPANY No. DPR-70)

{Salem Nuclear Generating Station, Unit No. 1)

RESPONSE TO THE ATOMIC SAFETY AND LICENSING BOARD ORDER DATED FEBRUARY 22, 1980 The Intervenor, Township of Lower Alloways Creek

.* I hereby submits the testimony .of Dr. David B. Fankhauser-

. in response to the Atomic Safety & Licensing Board Order dated February 22, 1980 which provides for submission of evidence to the following question:

"In the event of a gross loss of.water from the spent fue.1 storage pool at Salem 1, what would be the difference in consequences between those occasioned by the pool with the expanded storage proposed by the Licensee and those occasioned by the present pool.

Dr. David B. Fankhauser's qualifications are attached to his written testimony.

CREE!<

April 9, 1980

e UNITED STATES OF AME.A NUCLEAR REGULATORY COMMISSION Before the Atomic Safety and Licensing Boa;r:d In the matter of PUBLIC SERVICE ELECTRIC

& GAS COMPANY Docket No~ SQ-272 (Salem Generating Station  :

Unit #1)

CERTIFICATE or SERVICE I hereby certify that copies of Dr. David B. Fankhauser's testimony response to the Board Order dated February 22, 1980 in the above captioned matter have been served upon the attached list by deposit in the United States mail, at the Post Office in Northfield New Jersey with proper postage thereon, this 9th day of April I 1980.

Da t: ed : _ _A_p...._r_i_l_9...;..,_1_9_B_O_ _

________,__..:.......:............____ ~------------------'----~** ........ ____,, -****

Gary L. Milhollin, Esq. Richard Fryling, Jr~ , Esquire Chairman, Atomic Safety Assistant General Solicitor

& Licensing Board Public Service Electric &

1815 Jefferson Street Gas Company Madison, Wisconsin 53711 80 Park Place Newark, N. J. 07101 Glen O. Bright Member, Atomic Safety Keith Ansdorff, Esquire

& Licensing Board Assistant Deputy Public Advocate U. S. Nuclear Regulatory Corrrnission Department of the Public Advocate Washington, D. C. 20555 Division of Public Interest Advocacy P. O. Box 141 Dr. Janes C. Lamb, III Trenton, New Jersey 08601 Member, Atanic Safety &

Licensing Board Panel Sarrlra T. Ayres, Esquire 313 Wocdhaven Road Department of the Public Advocate Chapel Hill, N. C. 27514 520 East State Street Trenton, N. J. 08625 Chairman, Atomic Safety arrl Licensing Appeal Board Panel Mr. Alfred C. Coleman, Jr.

U. s. Nuclear Regulatory Calmission Mrs . Eleanor G. Coleman Washington, D. C. 20555 35 K Drive Permsville, N. J. 08070 Chairman, Atomic Safety &

Licensing Board Panel Office *of the Secretary .

U. S. Nuclear Regulatory Conrnission Docketing and Service Section Washington; D. C*. 20555 U. S. Nuclear Regulatory Cornnission Washington, D. C. 20555 Barry Smith, Esquire Office of *the Executive Legal Direc~or June D. MacArtor, Esquire u~ S. Nuclear Regulatory Corrrnission Deputy Attorney General Washington, D. C. 20555 Tatnall Building, P. O. Box 1401 Dover, Delaware 19901 Mark L. First, Esquire Deputy Attorney General Mr. Frederick J. Shon Department of Law & Public Safety Atomic Safety arrl Licensing Board Environmental Protection Section U. S. Nuclear Regulatory Carrnission 36 West State Street Washington, D. C. 20555 Trenton, N. J. 08625 Mary O. Herderson, Clerk Mark J. Wetterhahn, Esquire Township of Lower Alloways Creek for Troy B. Conner, Jr., Esq. Municipal Building 1747 Permsylvania Avenue, N. W. Hancock's Bridge, N. J. 08038 Suite 1050 Washington, D. C. 20006

HEALTH EFFECTS OF A POSTULATED SPENT FUEL POOL FIRE Al: THE SALEM NUCLEAR POWER STATION.

by David B. Fankhauser, PhD.

Biology Department Clermont College University of Cincinnati Ba ta via, Ohio )+5103 .

March 31, 1980

TABLE .QE CONTENTS I. Introduction p. l II. Accident Parameters p. 2 III. Biological significance or Sr, I and Cs . p. 2 IV. Radiological scope of Salem Spent Fuel Accident . p. 4

v. Doses attendant to Spent Fuel Accident p. 5 VI. Spectrum of Dose-Related Health Effects A. Acute Somatic Effects p. 6

.. B* Carcinogenesis p. 8

c. Genetic Effects p. 9 VIT. Projected Population Dose-Effects: p. 12 VIII. Conclusions p. 13 IX. Bibliography p. 15

I. INTRODUCTION Significant quantities of radioactive materials are projected to be released and.dispersed as a result of a Zirconium fire in the Salem spent fuel pool following a gross loss of cooling water (Richard E. Webb; Review of Draft Testimony). This paper* deals with the scope of somatic and genetic effects of the resulting radiation exposure. It is important to note at the outset that only three isotopes will be considered: Strontium-90 (SR-90), Iodine-131 (I-131}, and Cesium-137 (Cs-137}. These isotopes are particularly significant because tney would be gaseous under accident conditfons and are important bioligically. Actual exposure calculations will be performed only for Cs-137 *. Because the accident scenario proposed by Dr. Webb's testimony clearly carries the potential for violent explosion, additional analysis should be performed to assess the im~act of particulate contamination as well.

II. ACCIDENT PARAMETERS The capacity of the Salem spent fuel pool with assemblies re-racked amounts to approximately 1,100 fuel assemblies. *The . I I

storage time for the assemblies ranges from freshly stored to thirty years old. Therefore, except for the fresh assemblies, most of the short-lived fission products will have decayed to relatively low levels. Table I lists the characteristics of the three isotopes considered in this paper. Sr-90 and Cs-137 will be present in large quantities in all assemblies, while I-131 will be found primarily in the recently added assemblies.

• *During the course of the accident in which cooling water is lost from the spent fuel pool, decay heat will build up. Once the temperature in the dry pool reaches 900 C, the*

Zirconium cladding will undergo a self-sustaining fire. The heat from combustion will vaporize the isotopes under considera-tion, and they will be easily dissipated through any breach in containment. Note that only Sr-90 has a boiling point above 1000 C.

I II .. B-IOLOGICAL SIGNIFICANCE OF STRPNTIUM, IODINE AND CESIUM.

Strontium is chemically similiar to calcium. It is concentrated at each step. up the food chain (notably in milk) becoming incorporated into bone in man.. (Cronkit~, in Schwartz, p. 191). Once deposited there, radioactive decay exposes bone, and more importantly, bone marrow to irradiation.

Bone marrow exhibits a high degree of sensitivity to radiation, being exceeded in sensitivity only by lumphoid cells and the gonads. (See Table 4) .

Iodine is rapidly accumulated in the thyroid gland where it is stored and incorporated into thyroxine. This growth hormone usu~lly carries three or four atoms of*Iodine per molecule. 98% of the Iodine in the body is concentrated in the thyroid and the kidney retains 97% of the remaining 2%

~

within the body. {Ganong, p. 25.0). Any absorbed radioactive isotopes of Iodine will deliver a dramatically concentraqed dose to this gland. Due to bioaccumulation, seemingly small quantities of radiiodine in the environment are concentrated in milk and result in a high dose*to humans. Milk winds up being laden with both I-131 and Sr-90 and exposes nursing infants and children in particular. This group is notably more sensitive to radiation than adults.

Cesium belongs to Group I of the periodic series.

Like Potassium {of the same Group) it exhibits a st~ong affinity for muscle and nervous tissue. (Silver, p. 305}.

Although muscle is relatively resistant to radiation, the high energy ganuna radiation (660 Kev) released during decay results in whole body exposure and notable gonad exposure.

(Tubis & Wolf, p. 272)' *.

The signi.ficance of these three fi~sion products in terms of human exposure is underscored by experience gained as a result of inadvertant exposure of the Rongelapese, natives in the Marshall Islands to fallout from U.S. weapons testing.

Eight years after exposure 15/19 children who were younger than ten when exposed developed thyroid nodules. Furthermore, the exposed population carried 24 times more Sr-90 and 300 times more Cs-137 than the average U.S. citizen, {Behrens, et al, pp.

308-339, and Rahn, pp. 192-193).

IV. RADIOLOGICAL SCOPE. OF SALEM SPENT FUEL ACCIDENT In order to gain some perspective on the mag'nitude of the releases described in the previous section we can compare the sume of the three isotopes currently under consideration with the total released by the bomb dropped on Hiroshima. The three isotopes released due to the postulated accident comprise 3

a total of 10 curies. (See Table Il. In contrast, the number 6

of curies released at Hiroshima is estimated at 15 x 10 (Berger,

p. 48). Therefore, the fraction of releases from Salem in Table I amount to more than 6.5 times the radioactivity of the Hiroshima bomb. In .fact, the postulated Salem releases assume even greater proportions in view of the substnatially shorter half-lives of the Hiroshima releases. The latter decay much more rapidly than the half-lives of Sr-90 and Cs-137. The Salem releases would be much more persistant in the environment, allowing more time for bioaccumulation and incorporation into human tissue.

Furthermore, much of the Hiroshima activity was propelled by the blast into the stratosphere where it did not expose the local population (Berhens, et al, p_. 309). On the other hand, The Salem accident would result in a much more concentrated plume of activity. The heat from the Zirconium fire would not cause the contamination to rise to great heights. Enough height would be ensured to permit wind dispersal, and local weather conditions would have a major effect on who would be exposed, and to how much. Figure 1 clearly illustrates, based on the path of fallout along the East Coast, that Salem releases could easily strike the major population centers of the region, particularly Wilmington (lS mi.), Philadelphia (39 mi.) ,

and New York City (122 mi.). The clear implication.is that there is a probability for uncommonly high levels of total person-rems for the quantity of radioactivity released.

DOSES ATTENDANT TO SPENT FUEL FIRE.

Dr. Richard Webb's draft testimony indicates the following results from his dose calculations for various locations around the Salem Plant:

Next to Plant, after 30 days: 2,000 rem/hr 1 mile from Plant, rainfall precipated Cs-137-specific dose: between 44,000 and 1.9 x106;30 yr Dose to average Philadelphian: 1500 rems/30 yr.

(due to Cs-137)

• I have independently calculated the Cs-137 doses to three metropolitan areas: Wilmington, Philadelphia and New York City. The dispersal factor used for this calculation was empiric~lly derived from the dispersal relationships observed-at Three Mile Island (TMI).

There, the dose delivered.was found by curve-fitting to be roughly proportional to the inverse square of the dis-tance from the source (l/R2) (NUREG-0558, p. A-2). This dispersal or dim~nution factor was applied to.the 30 year dose from Cs-137 at 1 mile from the Salem facility as derived bY Webb. It should be noted that localized contamination may be. expected to be more severe where heavy deposition occurs. The results of these calculations are summarized in Table.5.

VI. SPECTRUM OF DOSE RELATED HEALTH EFFF,CTS VI. A. Acute Somatic Effects.

The effects of acute whole body exposure to greater than 100-200 rads are we'11 established as outlined in Table 2 (Merck Manual, pp. 1729-1733). The median sick-ness dose is that dose which produces obvious signs of acute radiation poisoning in t of the exposed pe~sons.

It is placed at 175 rads (Behrens et al., p. 65). The dose at which t of the exposed persons die is termed the Lethal Dose50 (tn 50 ) and is placed at 450 rads. Doses in excess of 600 rads are uniformly fatal. In those exposures which are sub-lethal, ~here is a characteristic interim period after initial nausea and vomiting in which the individual is apparently well. However, the hematopoeitic effects become pronounced with massive hemorrhaging 3 to 6 weeks later leading to infection and anemia.

Delayed effects resulting from exposures of less than 450 rads are summarized in Table 3. Doses below 100 rads produce blood effects, but are not generally fatal {Bond .

~al,, p. 156). Carcinogenesis, number 9 in Table 3, will be dealt with separately below in section VI.B.

The various tissues of the body exhibit a marked var-inbility of sensitivity to radiation. Table 4 lists the tissues in order of decreasing sensitivity. It is a gen-eral rule that the most rapidly dividing cells show the greatest sensitivity. It is also.important to note that the gonads are the second most sensitive tissue, a fact.

which bears directly on the estimation of genetic effects.

The fetus exhibits increased sensitivity as compared to the adult, presumably due at least in part to the high rate of proliferation of his cells. Microcephaly has been observed in about 25% of fetuses irradiated with several hundred rads (BEIR Report, pp. 74 & 75).

Exposure to rndioiodine during childhood has been show:i in the Rongelapese to !:lead to a trophy of the thyroid, with attendant features* of hypothyroidisr'l. The 9 million curi cs of I-131 would pose an extraor&in~~ily increased risk to (children and the unborn. An exce9~~y~*1].~*~er of hypothyroid infant

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have recently been born in the three counties surrounding TMI. The probability of this occurring is, according to a recent art~cle in Nature, 1/105' years.

. It therefore seems likely that it is in some way associated with the TMI accident (Nature; 283:807, 28 Feb. 1980).)

VI *. B. CARCINOGENESIS Carcinogenesis is a delayed effect of radiation exposure which has received a great deal of attention (see Shapiro, pp. 260-264 for a tabulated summary.)

Numerous uncertainties plague the precise determination of the dose-effect. Individual variability in sensitiv-ity is pronounced, particularly with regard to age. Two notable examples of this phenomenon are (1) the max:1,.mum sensitivity of women to radiatio~ as measured by the in-duc-!:ion of breast cancer is 6.5'x higher in adolescent women than the average for all ages (BEIR, p. D-1). (2) The ma:dmum sensi ti vi ty of the very young as measured by leu-kemogenesis

• is 17x greater if the exposure occurs pre-natally rather than postnatally (Upton, in Hiatt et al.,

pp. 477-500).

An additional fnctor which tends to lead to an under-esti::.ation of dose-effect for carcinogene~d*s is the latent period between exposure and tho appearance of the malig-nancy. Five to 20 years is a common length, ~Ti th greater la tent periods occ.:::sionally being observed (Bodmer &

CavaJ1i-Sforza, pp. 176-177). John W. Gofman has pointed to the above factors and also mentioned shori(_comings of the absolute risk estimations as presently derived and the low estimates of thyroid cancer mortality due to the protracted course of thyroid cancer. He suggests a figure of 7,200 cancers/106 person-rems. On the other hand, the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) does not take into consideration many of the above factors and suggests a figure of 450 cancers/

6 20 person-rems. (UNSCEAR, section H. pp. 411-412). This latter figure was used recently by the NRC in assessing the heal th effects of the TMI accident (NUREG.-0558, p. D-1).

I have used the latter figure to estimate the lower bounds of the induced cancers, but have also* included the projections based on the Gofman figure as probably being more realistic.

VI.C. GENETIC EFFECTS There are also considerable difficulties in estimating genetic effect~ (Sal the, P* \23~i~ N~wcombe, 1978, and Neel, 1978). Neel specifically emphasizes that his esti-mates of the absolute minimum contribution ..of mutation *to disease will "increase *** rather dramatically in the next decade *** " showing many previous estimates to have been conservative. He postulates that roughly 14.7% of con-ce_Ptions wi~l have serious disease potentialities maintained by background nutat:i,on pressure.

Man is diploid, receiving a set of genes from each *parent.

It is to be expected therefore that the majority .of:~ induced muta-tions will be masked. Only when the induced mutation is homozygous will it appear as a mutant *. Current estirnatos are tha~ only 2.5% of the recently induced mutations appear per generation (Casarett, p. 343). For this reason, a major impact on the gene pool would b,e required before it would be detected. The actual da~age would be roughly forty times as great as the observed effects. It comes as no surprise therefore that pronounced genetic effects have not been observed in the single generation since the Hiroshima bombing. None-the-less, 100 rads delivered to the exposed porula tion has led.: to a doubling in observed chromosomal abnormalities .in their children. (Bodmer &

Cavalli-Sforza, pp. 176-177). The amount of radiation to which oul' sex-cells are exposed has tripled in modern times, with as yet no clearly demonstrable effects (Singer,-

pp. 96-97).

Extrapolation from high dose experiments suggests that 1 rad to the parents/106 live births induces 8000 new mutations (Casarett, p. 343). At some time, al18000 mutations will result in genetic death, the process taking many generations to completely "cleanse" the -gene pool.

According to currently accepted models, the initiating step for both mutagenesis and carcinogenesis is the alter-ation of DNA. Indeed, 90% of all known mutagens are car-cinogens (Ames et al., and Mole in Duplan, p. 31-32). For this reason, in the absence of direct measurement of human*

mutagenesis, it is prudent to assume that doses to the gonads will be at least as efficient in mutagenesis as they are in carcinogenesis, -and probably an order of mag-nitude more so since regulatory genes involved in aon-trolling cell di vision Obviously cons.ti tute a small frac-tion of the total genes in a cell.

With these reservations in mind," we will make an esti-mation of the minimum genetic effect from the postulated exposures. The number of live births per population center over the thirty year period can be estimated by multiplying the population times the crude birth rate for the U.S.,

17. 5/1,000/year (i-1ausner and Bahn, p. 135), *times 30 years.

(We assUID.e for simpl:J.c:tty' s sake, that the population will not change in size over the 30 year period.) The cal-culated number of live births is shown in table 6".

Other effects which cannot at present be quantified include the induction of mutant strains of pathogenic bacteria and viruses. The havoc created by new virulent strains of influenza virus is an example of this problem.

Such variants are particularly troublesome since there exists no herd immunity, and therefore transmission occurs with great efficiency. New strains of agricultural dis-eases will also be anticip~ted as a result of increased envirorunental mutagens such as radiation.

-* .e VII. PROJECTED POPULATION DOSE-EFFECTS We have not had the opportunity to examine compre-hensive. _demographic and meteonil..ogic data which would allow more specificity* in making dose calculations. It is hoped that the board will permit additional submission of testimony on this subject. However, the scope of the impact can be appreciated by the use of the data assembled in this---**-****

paper. *.

A person standing next to the facility would receive an invariably fatal dose within 20 minutes. Persons at-tempting to perf()rm emergency procedures would do so at severe risk even in such a short exposure as 5 to 10 min-utes. Likewise, persons within 1 mile of the facility for 24 hours2.777778e-4 days <br />0.00667 hours <br />3.968254e-5 weeks <br />9.132e-6 months <br /> after the accident would be expected to de-velop the full spectrum of acute radiation sickness out-*

lined in Table 2.

Effects on the majo~ urban centers would vary accord-ing to dispersal parameters, and .* populations should m_ost certainly be evacuated before doses shown in ~,?ables 5 and 6 were recoived. However, in the event that such relocations were not undertal{en, the heal th of *the exposed populations would be severGly impacted. The lower bounds, as marked by low exposure, and using the UNSCEAR risk factor, would produce a total of more than 10,000 cancers in the three

metropolitan areas considered, this from Cs-137 alone.

If Gofman's risk estimate is more accurate, for which he maltes a persuasive argument; the effects would be cata-strophic, with a total of 370 million cancer-dose-equivalents marking the upper bounds of thes~ calculations.

The genetic effects are also projected to be sub- -

stantial. As can be seen on Table 6, the number of genetic deaths is projected for the first generation to be between 24,ooo and 10 million in the three urban areas. It must be remembered also that only.about 2.5% of the total genetic deaths will occur in the first generation, and that ultimately, as many as 430 million deaths may be caused over many generations.

VIII. CONCLUSIONS From these preliminary calculations, it is obvious that the postulated spent fuel accident at Salem would have severe, wide-ranging and long-lasting effects.

Hajo::- relocations of millions of persons would be advis-able due to the projected health effects accruing to unrelocated populations. Evacuations of such scope would present difficulties bordering on the insurmount-able.

Finally, it must again be emphasized that these calculationscould well represent a minimum effect of

.the postulated accident. Only Cs-137 related exposure has been calculated. As can be seen from Table 1, nearly as many curies of Sr-90 are postulated to be released, and duration of exposure would be at least as severe since Sr-90 is incorporated into bone. The I-131 released would not be a major factor over the 30 years, but would be particularly troublesome in the initial period after the accident, when large numbers of persons would presum-ab)S.. be in transit, and exposure would be difficult to

• • 1 monitor and control.

No consideration has been given to the impact on agricultural activities, but it also would be of major proportions. Sr-90 and I-131 are particularly subject to bioaccumulation.

An additional means of exposure which should be quantified is the aquatic pathway. It is anticipated that inventories of radioactivity such as those involved in this postulated accident would soon find their way into ~arine foodstuffs, possibly being transported along the coast in this manner.

FIGURE 1 --

PATH OF CHINESE WEAPONS TEST FALLOUT, OCTOBER, 1976

.1 A1.4ss; R.1* .

. CONN N* .J.

• Dct..

Note that radioactive materials released from the Salem facility, if dispersed in a similar fashion, would expose the most heavily populated regions, of the North Atlantic Coast. (From Hon-ecker, 27.)

TABLE*I CHAfu-\CTli;. ISTICS OJf Sr-90, I-131 end Cs-137 released due to postuil:.ted c.ccident

• I-131 Half-life: 28.l years 8~05 days 30 years boiling point 1,366 183 (sublimes 690 IC: below 114)

Tissues affected: bone thyroid muscle, nerve.

• ~:C,uan ti ties released according to Webb 40 x 106 Li 9 x 106 Ci 50 x 106 Ci scenario;

TABLE 2 SYMPTOMS AND SIGNS QE ACUTE WHOLE-BODY RADIATION EXPOSURE.*

A. Cerebral syndrome, follows exposures greater than 3000 rads, is invariably fatal. Three phases are recognized:

1 *. Prodromal nausea and vomiting.

2. Listless and drowsy.

3. Tremors, convulsions, ataxia, death in a few hours.

B. Gastrointestinal syndrome, follows exposures of 400 or more rads:

1. Intractable.nausea, vomiting, diarrhea, vascular collapse, death.

2. Toxemia due to necrosis; atrophy of GI mucosa.

3. Hematopoeitic failure within 2 to 3 weeks.

c .. Hematopoeitic syndrome (200 to 1000 rads).

I

1. Anorexia, apathy, nausea and vomiting within 6 to 12 hours1.388889e-4 days <br />0.00333 hours <br />1.984127e-5 weeks <br />4.566e-6 months <br />. *

2. The following 2t1- to 36 hours4.166667e-4 days <br />0.01 hours <br />5.952381e-5 weeks <br />1.3698e-5 months <br /> are asymptomatic, but well-being declines and lymph nodes, spleen and bone marrow begin to atrophy.

3. Thrombocytopenia becomes prominent is *3 to 4 weeks, leading to massive hemorrhage.

D. Increased susceptibility to infection:

1. Decreased production of leukocytes.

2. Impaired antibody production.

3. Reduced resistance to diffusion.

4. Hemorrhage in skin and bowel yeild to bacteria.

E. Exposures greater than 600 rads are fatal due to B. and c, with the probability of surviving lower exposures being inversely related to dose.

• From the :Merck 'Manual, pp. 1730-1731.

,1ABLE 3 DELAYED EFFECTS OF DOSES LESS THAN 45'0 RADS*

1. Amenorrhea

2. Decreased fertility

3. Decreased female libido

4. Anemia

5. Leukoperiia

6. Thrombocytopenia

7. Cataracts

8. Loss of hair

9. Carcinogenesis

10. Et cetera

• From Herek Manual, p. 1731.

• TABLE 4 ~

HEIRARCHY OF TISSUES ACCORDING TO RADIATION SENSITIVITY*

Most Sensitive: 1. Lymphoid cells

2. GOnads (testes and ovaries)

3. Proliferating. cells of bone marrow

4. Epithelial cells of bowel

5. Epidermi.s

6. Hepatic cells

7. Lung and biliary epithelium

8. Kidney epithelial cells

9. Pleural and peritoneal endothelium

10. Nerve cells

11. Bone cells

• Least Sensitive: 12. Muscle and connective tissue

• From Merck Manual,. p. 1730.

TABLE 5 DOSE AND CARCINOGENIC EFFECTS OF Cs-137 RELEASED FROM SALEM SPENT FUEL ACCIDENT IN SELECTED METROPOLITAN AREAS.

Metropolitan Area: *_Wilmington Philadelphia New York City Population (Rand Mc-Nally, 1966): 318 7 700 4,200,000 15,400,000 Distance in miles from Salem Plant: 15 39 122 Dose dini.!nution factor relative to. the dose a t 1 mile (l/R 2 ): 1/225 1/1520 1/14,900 Estimated 30 year dose/p~on due to Cs-137 in rems: 195 30 3 to to to 8,440 . 1,300 130 Total person-rems ex-

• posure in 30 yrs: 6.2 x 107. 1.3 x 108 4.6 x 207 to

• to to 2.7 x io9 5.6 x 209 2.0 x 109 Total cancers induced in 30 years:

UNSCE.iL'q risk fag- 2.8 x 103 5.8 x 103 2.1 x 203 tor of 450/10 to to to person-rems: 1.2 x 10 6 2. 5 x 106 0.9 x 10 6 Gofman risk fac- *.

tor of 7,200;10D

4. 5 x io5 9.4 x 105 3.3 x io 5 to to

• to person-rems: 1.9 x 10 8 4.1 x 107 1.4 x io8

TABLE 6 GENETIC EFFECTS OF Cs-137 RELEASED FROM SALEM SPENT FUEL ACCIDENT ON SELECTED METROPOLITAN AREAS.

Metropolitan Area: !filming ton Philadelphia New York Citx

2. . Predicted live-births over 30 years:

1.7 x io5 2.2 x 106 8.1 x 106 Dose to each parent: 195 to 30 to 3 to in rems 8,44o . 1,300 130

(.f..r'A T1-'4 lt. b) 4 Total induced muta- 2. 7 x 10*5- 5.3 x 105 1.9 x 105 tions in 30 yrs:

(rems x live births x-10-6x .to to to 8,ooo) 8 1.2 x 10 2.3 x 108 8.2 x 107 Deaths in first gen-eration due to .

.induced mutations: *6~7 x 103 - 4 1.3 x 10 4.8 x io3

( i..s {o of I111~ 4.) *to 6

. *to 6

.. to 3.0 x 10 5.8 x 10 i.2 x :io6

IX. BIBLIOGRAPHY

• Ames, B.N. and Mccann, J. 1976. Carcinogens .ftI.£ mutagens:

A simple test system. In Screening tests in chemical carcinogenesis, 12:493, International Agency For Re-search on Cancer, Lyon, France.

Behrens, C.F., King, E.R. and Carpender, J.W.J. 1969.

Atomic Medicine, 5th Ed., Williams and Wilkins, Baltimore.

Berger, John J. 1976. Nuclear Power-The Unviable Option,.

Ramparts Press.

Berkow, Robert. 1977. The Merck :Manual, 13th Ed., Merck and Co., Rahway, N.J.

Bond, Victor P., et al. 1965. Mammalian Radiation Leth-ality, Academic Press, New York.

Eodmer, W.F .. and Cavalli-Sforza .. 1976. Genetics, Evolu-tion, and Man, W.H. Freeman, San Francisco.

Casarett, Alison P. 1968. Radiation Biology, Prentice-Hall, Englewo.od Cliffs.

1977 Du:plan, J oF. Ed. /Radiation-Induced Leukemeogenesis .and Related Viruses, North Holland Pub. Co., Amsterdam.

Ganong,- W.F. 1965. Review of Medical Phvsiology, Lange Medical Publications, Los Altos, CA.

Gofman, John W. 1977. Cancer Hazard from Low-Dose Hadiation, Testimony before USNRC, Docket no. RM 50:** 3, October 3, 1977.

Hiattl H.H; et al., 1977. Origins of Hillnan Cancer tBook A: Incidence of Cancer 1n Humans), Cold Spring Harbor Laboratory, N.Y.

Honicker, Jeannine. 1978. Honicker Y.2 Hendrie, The Book

, rub. Co., Sunmrton,

• TN.

National Academy of Sciences. 1972. The Effects .Q!! Pop-

,,~la tions of Exoosure to Low Iievels 9f Ionizinr; .B!.gl-iation, Washington, D.C.

• Neel, James V. 1978. Mutation and Disease in Man, Can.

J. ,Genet.

Cytol. -20:295-306 Newco:cbe, HOi*rard B. 1978. Problems assessing the Genetic Irmact of Mutap;ens QD. Man, Can. J. Genet. Cytol. 20:

1+59-470. .

Muusner, J.S. an~ahn, A.K. 1974, Epidemiolor;y, W.B. Saun-ders, Philadelphia.

IX. BIBLIOGRAPHY (continued).

Rand McNally. 1967. World Atlas, 1.Q21 Edition, Rand McNally, Chicago.

Schwartz, Emanuel E. 1966. The Biolot;ical Basis of Rad-iation Therapy, J.B. Lippincott, Philadelphia.

Shapiro; Jacob. 1972. Radiation Protection: A Guide for Scientists and Physicians, Harvard University Press, Cambridge, Mas.s.

• Salthe, Stanley N. 1972. Evolutionary Biology, Holt, Rinehart and Winston, New York, Singer, Sam. 1978. Human Genetics, W.H. Freeman, San Francisco.

Tubis and Wolf, 197.6....... Radiopharmacy, John Wiley, new

• York.

UNSCEAR, 1977. Sources and Effects of Ionizing Radia-tion, United Nations Scientific Committee on the Effects of Atomic Radiation, 1977 report to the General Assembly, United Nations, New York.

U.S. Environmental Protection Agency, 1976, Radiolo_gi-cal Quality of the Environment, Washington, D.c.

u.s. Uu':::lear Regulatory Commission, 1979. Ponulation Dose and Health Impact of the Accident at the Three Mile Island Nuclear Station, Washington, D.C.

QUALIFICATIONS OF DAVID B. FANKHAUSER, Ph.D.

David B. Fankhauser was born November 22, 1941 and graduated from Olney Friends School, Barnesville, Ohio, 1959.

In 1963, he graduated from Earlham College, Richmond, Indiana with a B.A. in Chemistry.

From 1963 to 1965 he worked as a medical research technician at the University of Cincinnati Medical School under the direction of Dr. Michael Carsiotis.

In 1965 he entered graduated school at John Hopkins University, Baltimore, Md., in the Department of Biology.

During the summer of 1967, he participated in the Bacterial Viruses course at the Cold. Spring Harbor Laboratory for Quantitative Biology on Long Island, N.Y.

In the summer of 1969, he conducted research in mutagenesis in the laboratory of Dr. Bruce Ames, Dept.- of Biochemistry, University of California, Berkeley. (Dr. Ames has received global recognition for the devel6pment of a bacterial test which detects mutagens/carcinogen:

with extreme sensitivity.)

• During the school years of 1968-1970, he taught laboratory courses at John Hopkins in first year Biology and Genetcis.

In 19 71, he received his Ph.. D. from J.ohns Hopkins. His thesis, "The Promoter-Operator Region of the His Operon in Salmonella Typhimurium" was researched and written under .the advisor-ship of Dr. Philip E. Hartman. It concerns the effects and locations of mutations which alter the regulation of a set of genes responsible for the biosynthesis of the amino acide histidine.

From 1973 to the present he has taught Biology at Clermont College, University of Cincinnati, Batavia, Ohio. He has developed a laboratory program for first year Biology students entitled "Appropriate Biology" which incorporates many of the cottage craft skills gained in his lifestyle research as well as lab techniques which assay the quality of* the student's environment. Student response has been highly favorable.

From 1972 he has been involved in the Atomic Energy Commission's and now the Nuclear Regulatory Commission's hearings regarding the Zimmer Nuclear Power Plant, Moscow, Ohio. He has been granted intervenor status in those proceedings. Issues raised in 1972, such as waste disposal, epidemiology of low level exposure, evacuation and monitoring have recently become subjects of national interest. He maintains an active speaking schedule on these subjects, appearing at 10 to 20 engagements a year.

Qualifications of

• Dr. David B, Fankh"auser Page 2 . * .

Dr. Fankhauser also has been invited several times by members

.of the Ohio Legislature to testify on health related aspects of nuclear power.

In 1979, he served on review committees for the United States Environmental Protection Agency. The purpose of these consultations was to set limits on environmental concentrations of toxic susbstances to preclude adverse health effects.

In 1980 he accepted a position at Northern Kentucky University, Highland Heights, Ky., as lecturer in Epidemiology.

He has published papers in the following journals and publications:

Genetics Journal of Bacteriology Neurospora Newsletter Health Forum The Earlhamite

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