ML19305E736
| ML19305E736 | |
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| Site: | Salem  |
| Issue date: | 03/31/1980 |
| From: | Fankhauser D CINCINNATI, UNIV. OF, CINCINNATI, OH |
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Text
i 8005200374 e
HEALTH EFFECTS OF A POSTULATED SPENT FUEL POOL FIRE F
AT THE SALEM 1mCLEAP POWER STATION.
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9 z
DOC g ED g
USgac 8-APR 11980
- 2 g
David B. Fankhauser, PhD.
cn b'
Biology Department Clermont College University of Cincinnati Batavia, Ohio 45103 March 31, 1980 l
l
t Gary L. M11ho111n, Esq.
Richard Fryling, Jr., Esquire Chairman, Atomic Safety Assistant General Solicitor
& Licensing Board Public Service Electric &
1815 Jefferson Street Gas Company Madison, kisconsin 53711 80 Park Place Newark, N. J.
07101 Glen 0. Bright Member, Atomic Safety Keith Ansdorff, Esquire
& Licenning Board Assistant Deputy Public Advocate U. S. Nuclear Regulatory Conmission Department of the Public Advocate Washingtm, D. C.
20555 Division of Public Interest Advocacy P. O. Box 141 Dr. James C. Lamb, III Trenton, New Jersey 08601 Member, Atcmic Safety &
Licensing Board Panel Sandra T. Ayres, Esquire 313 Woodhaven Road Department of the Public Advocate Chapel Hill, N. C.
27514 520 East State Street Trenton, N. J.
08625 Chairman, Atomic Safety and Licensing Appeal Board Panel Mr. Alfred C. Coleman, Jr.
U. S. Nuclear Regulatory Crnmission Mrs. Eleanor G. Coleman Washington, D. C.
20555 35 "K" Drive Pennsville, N. J.
08070 Chairman, Atomic Safety &
Licensing Boarti Panel Office of the Secretary U. S. Nuclear Regulatory Conmission Docketing and Service Section Washiq:.un, D. C.
20555 U. S. Nuclear Regulatory Conmission Washington, D. C.
20555 Barry Smith, Esquire Office of the Executive Irgal Director June D. MacArtor, Esquire U. S. Nuclear Regulatory Conmission Deputy Attorney General Washington, D. C.
20555 Tacna11 Building, P. O. Box 1401 Dover, Delaware 19901 Mark L. First, Esquire Deputy Attorney General Mr. Frederick J. Shon Department of law & Public Safety Atcmic Safety and Licensing Board Environmental Protection Section U. S. Nuclear Regulatory Conmission 36 West State Street Washington, D. C.
20555 Trenton, N. J.
08625 Mary O. Henderson, Clerk Mark J. Wetterhahn, Esquire Township of Lower A110 ways Creek for Troy B. Conner, Jr., Esq.
Municipal Building 1747 Pennsylvania Avenue, N. W.
Hancock's Bridge, N. J.
08038 Suite 1050 Washington, D. C.
200 %
I.
INTRODUCTION Significant quantities of radioactive materials are projected to be released and dispersed as a result of a Zirecnium fire in the Salem spent fuel pool following a gross loss af cooling water (Richard E. Webb; Review of ' Draft Testimony).
This paper deals with the scope of somdtic 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-9 0 ), Iodine-131 (I-131), and Cesium-137 (Cs-137).
These isotopes are particularly significant because they would be gaseous under accident conditions 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 impact of particulate contamination as well.
i l
TABLE OJE CONTENTS I.
Introduction
- p. 1 II.
Accident ?arameters
- p. 2 III.
Biological significance
- of Fr, I and Cs.
- p. 2 IV.
Radiological scope of Salem Spent Fuel Accident.
- p. 4 V.
Doses attendant to Spent Fuel Accident
- p. 5 l
VT Spectrum of Dose-Related 2
Health Effects A.
Acute Somatic Effects p. 6 B.
Carcinogenesis
- p. 8 C.
Genetic Effects
- p. 9 VII.
Projected Population Dose-Effects-
- p. 12 VIII.
Conclusions
- p. 13 IX.
Bibliography
- p. 15 l
I
II.
AC'IDENT FARAMETERS The capacity of the Salem spent fuel pool with assemblies re-racked amounts to approximately 1,100 fuel assemblies.
The 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 producta 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 quancities in all assemblies, j
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.
III. BIOLOGICAL SIGNIFICANCE OF STRONTIUM, 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.
(Cronkite, 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).
4 Iodine is rapidly accumulated in the thyroid gland where it is stored and incorporated into thyroxine.
This growth hormone usually carries three or four atoms of Iodine per molecule.
98% of the Iodine in the body is concentrated l
in the thyroid and tha kidney retains 97% of the remaining 2%
within the body. (Ganong, p. 250).
Any absorbed radioactive isotopes of Iodine will deliver a dramatically con'centrated dose to this gland.
Due to bioaccumulation, seemingly small quantities of radilodine 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 strong affinity for muscle and nervous tissue.
(Silver, p. 305).
Although muscle is relatively resistant to radiation, the high energy gamma radiation (660 Kev) released during decay results in whole body exposure and notable gonad exposure.
(Tubis & Wolf, p. 272).
The significance of these three fission 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. m - 5 w.....m... _ mm ; :dQL __
.i;3.cggg3
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 a total of 10 curies.
(See Table I).
In contrast, the number 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 l
j.
ensured to permit wind dispersal, and local weather conditions l
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 (15 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:
i Next to Plant, after 30 days:
2,000 rem /hr 1 mile from Plant, rainfall precipated Cs-137-specific dose:
between 44,000 6
and 1.9 x10 /30 yr Dose to average Philadelphian:
1500 rems /30 yr.
(due to Cs-137) l l
I have independently calculated the Cs-137 doses to three metropolit&n araas: Wilmington, Philadelphia and How York City.
The dispersal factor used for this calculation was empirically 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-2 tance from the source (1/R )(NUREG-0558, p. A-2).
This dispersal or diminution factor was applied to the 30 year dose from Cs-137 at l 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 summari::ed in Table 5 VI.
SPECTRUM OF DOSE RELATED HEALTH EFFFCTS VI. A.
Acute Somatic Effects.
The effects of acute whole body exposure to greater than 100-200 rads are well 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 i of the exposed persons.
l It is placed at 175 rods (Bohrens M al., p. 65).
Tho 1
j dose at which i of the exposed persons die is termed the 1
Lethal Dosego (LD50) and is placed at +50 rads.
Doses in excess of 600 rads are uniformly fatal.
In those exposures which are sub-lethal, there is a characteristic interim period after initial nausea and vomiting in which the individual is ap'arently well.
However, the hematopoeitic p
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 et 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 radiciodine during childhood has been shown in the Rongelapeso to ilead to atrophy of the thyroid,
~
with attendant features' of hypothyroidisn.
The 9 million curi os of I-131 would pose an extraorainerily increased risk to cchildren and the unborn.
An excesgivesnqmber of hypothyroid infant -
I have recently been born in the three counties surrounding TMI.
The probability of this occurring is, according to a recent article in Nature, 1/107 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.)
Humerous 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 maximum sensitivity of women to radiation as measured by the in-duction of breast cancer is 6.5x higher in adolescent women than the average for all ages (BEIR, p. D-1). (2) The maximum sensitivity 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. L77-500).
An additional fcetor which tends to lead to an under-estimation of dose-effect for carcinogenesis is the latent period between exposure and the appearance of the malig-nancy.
Five to 20 years is a common length, with greater i
1 !
latent periods occasionally being observed (Bodmer &
CavaZi-Sforza, pp. 176-177).
John W. Gorman has pointed to the above factors and also mentioned shorg pomings of the absolute risk estimations as presently derived and the low estimates of thyroid cancer mortality due to the ordtracted course of thyroid cancer.
He suggests a figure of 7,200 6
cancers /10 person-rems.
On the other hand, the United Na tions Scient.ific 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 10 person-rems (UNSCEAR, section H. pp. 411-412).
This latter figure was used recently by the NRC in assessing the health 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 Gorman figure as probably being more realistic.
VI.C.
GENETIC EFFECTS There are also considerable difficulties in estbuating i
i genetic effects (Salthe, p. 233-, Newcombe,1978, and Neel, 1978).
Noel 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 es timates to have been cons erva tive.
He postulates that roughly 14.7% of con-ceptions will have serious disease potentialitics maintained by background mutation pressure.
_9-
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 es'inatos are that only 2 7% of the recently induced mutations appear per generation (Casarett, p. 343).
For this reason, a major impact on the gene pool would be required before it would be detected.
The actual damage 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 population has led. to a doubling in observed chromosomal abnormalities in their children.
(Bodmer &
Cavalli-Sforza, pp. 176-177).
The amount of radiation to which our 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 now mutations (Casarett, p. 343).
At some time, all 8000 mutations will result in genetic death, the process taking many generations to completely " cleanse" the gone pool.
According to currently accepted models, the initiating j
stop for both mutagenesis and carcinogenesis is the alter-O
r ation of DNA.
Indeed, 90% of all known mutagens are car-cinogens (Ames Sd; 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 con-trolling cell division obviously constitute a small frac-tion of the total genes in a cell.
With thase 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 (Mausner and Bahn, p.135), times 30 years.
(We _ssume for simplicity'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.
-l Other effects which cannot at present be quantified include the induction of mutant strains of pathogenic bac teria 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 officiency.
New strains of agricultural dis-eases will also be anticipated as a result of increased environmental mutagens such as radiation.
VII.
PP0JECTED POPULATION DOSE-EFFECTS We have not had the opportunity to examine compre-hensive. demographic and meteonlogic 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 perform emergency procedures would do so at severe risk even in such a short exposure as y 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 /> af ter the accident would be expteted to de-velop the full spectrum of acute radiation sickness out-lined in Table 2.
Effects on the major urban centers would vary accord-ing to dispersal parameters, and. populations should most certainly be evacuated before doses shown in t.' ables 5 and 6 were received.
However, in the event th' t such relocations a
were not undertaken, the health of the exposed populations would be severely 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 makes a persuasive argument, the effects would be cata-strophic, with a total of 370 million cancer-dose-equivalents marking the upper bounds of these 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 24,000 and 10 million in the three urban areas.
It must be retembered also that only.about 2.7% 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.
Major relocations of millions of persons would be advis-able due to the projected health offects accruing to unrelocated populations.
Evacuations of such scope would present difficulties bordering on the insurmounL-I able.
Finally, it must again be emphasized that these 1
calculations could well represent a pininum effect of the postulated accident.
Only Cs-137 related exposure has been calculated.
As can be seen from Table 1 nearly 3
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-ably. be in transit, and exposure would be difficult to monitor and control.
Ho 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 bicaccumulation.
An additional means of exposure which should be quantified is the aquatic pathway.
It is anticipated tha t inventories of radioactivity such as those involved in this postulated accident would soon find their way
'l into carine foodstuffs, possibly being transported along the coast in this canner.
FIGURE 1 PATH OF CHINESE WEAPONS TEST FALLOUT, OCTOBER, 1976 vr.
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AfAINg
,5f -
"n
' NN A1 Ass.
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CHIO A-N. !'
/.
h\\
\\\\
1'-
Q i u,, Cogy-E ort.,
Note that radioactive materials released from tho Salem facility, if dispersed in a similar fashion, would expose the most heavily populated regions, of the North Atlantic Coast. (From Hon-ecker, 27.)
i l
TAnTR I ClildiAC'IIIiISTICS OF Sr-90, I-131 end Os-137 rele ased due to postuited accident.
~Sr-90 I-131 Cs-137 half-lifa :
28.1 yecrs' 8.05 days 30 ye ars boiling point 1,366 183 (sublimes 690
'C:
below 114)
Tissues affected; bone thyroid
- muscle, nerve.
iuantities rele ased t
according to hebb 40 x 106 ci 9 x 196 Ci 50 x 106 Ci scenario; e
v w
e v
TABLE 2 SYMPTOMS AND SIGNS OF ACUTE WHOLE-BODY RADIATION EXPOSURE.*
A.
Cerebral syndrome, follows exposures greater than 3000 rads, is invarihbly 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).
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 24 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.
p'.
Reduced resistance to diffusion.
4.
Hemorrhage in skin and bowel yeild to bacteria.
E.
Exposures greater than 600 rads are fatal due 'o B. and c
C, with the probability of surviving lower exposures being inversely related to dose.
l
- From the Merck Manual, pp. 1730-1731.
i l
TABLE 3 DELAYED EFFECTS _ O_F DOSES LESS THAN 450 RADS
- F l.
Amenorrhea 2.
Decreased fertility 3
Decreased female libido 4.
Anemia Si.
Iaukopenia 6.
Thrombocytopenia 7.
Cataracts 8.
Loss of hair 9.
Carcinogenesis 10.
E ceteva From Merck Manual, p. 1731.
l I
TABLE 4 HEIRARCHY 0F_ TISSUES ACCORDING TO F
RADIATION SEUSITIVITY*
Most Sensitive:
1.
Lymphoid cells 2.
Gonads (testes and ovaries) 3 Proliferating cells of bone marrow 4.
Epithelial cells of bowel 5
Epidermis 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.
e l
r
- m__,
1 TABLE 5 DOSE AND CARCINOGENIC EFFECTS OF Cs-137 RELEASED FEDM SALEM SPENT FUEL ACCIDENT IN SELECTED METROPOLITAN AREAS.
Metropolitan Area:
'.Wilmington Philadelthia New York City Population (Rand Mc-Hally, 1966):
318,700 4,200,000 15,400,000 Distance in miles from Salem Plant:
15 39 122 Dose dinimution factor relative to the dose at 1 mile 2
(1/R ):
1/225 1/1520 1/14,900 Estimated 30 year doseperson 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 8
1 3 x 10 4.6 x 107 to to to 2 7 x 109 5.6 x 109 2.0 x 109 Total cancers induced in 30 years:
UNSCEARriskfab-2.8 x 103 5.8 x 103 2.1 x 103 tor of 450/10 t
to 6
6 t
6 person-rems:
1.2 x 10 2.5 x 10 0.9 x 10 Gorman risk fac 4.5 x 107 9.4 x 107 7
3 3 x 10 0
tor of 7,200/10 to to to 8
person-rems:
1.9 x 10 g,1 x 107 1,4 x 108
TABLE 6 GENETIC EFFECTS OF Cs-137 RELEASED FROM SALEM SPENT FUEL ACCIDENT ON SELECTED METROPOLITAN AREAS.
I Metropolitan Area:
Wilmington Philadelphia New York City 0
b.1 x 106 z
Predicted live-births 1 7 x 107 2.2 x 10 over 30 years:
3 Dose to each parent:
19 to 30 to 3 to in rems 8, 40 1,300 130 (6m Tafe 6)
Y 7
7 4
Total induced muta-2.7 x 10 5.3 x 10 1.9 x 10 tions in 30 yrs:
(rems x live birtha x 10-6x to to to 8
1.2 x 10 2 3 x 10 8.2 x 107 5
Deaths in first gen-eration due to 3
y induced mutations:
6.7 x 10 1.3 x 10 4.8 x 103
( Z,5 fo o(line4.}
to to to 6
6 6
3 0 x 10 5 8 x 10 1.2 x 10 l
l l
l l
- IX.
BIBLTOGRAPHY Ames, B.N. and McCann, J, 1976.
Carcinogens are mutacens:
A simple test system.
In Screening tests in chemical carcinogenesis, 12:493, International Agency For Re-scarch on Cancer, Lyon, France.
Behrens, C.F.
King, E.R. and Carpender, J.W.J. 1969.
Atomic Medicine, 5th Ed., Williams and Wilkins, Balticore.
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.
Bodmer, W.F. and Cavalli-Sforza. 1976.
Genetics, Evolu-tion, and Man, W.H. Freeman, San Francisco.
Casarett, Alison P. 1968.
Radiation Bioloey, Prentice-Hall, Englewood Cliffs.
1977 Duplan, J.F. Ed./ Radiation-Induced Leukemeonenesis and
_Related Viruses, North Holland Pub. Co., Amsterdam.
Ganong, W.F. 1965. Review of Medical Physioloey, Lange Medical Publications, Los Altos, CA.
Gofman, John W. 1977 Cancer Hazard from Low-nose Radiation, Testimony before USNRC, Docket no. RM
$0-3, Oc tober 3,1977 Hiatt H.H, 21 al., 1977 Orieins of Human Cancer fBookA: Incidence of Cancer in Humans), Cold Spring Harbor Laboratory, N.Y.
Honicker, Jeannine. 1978.
Honicker vs Hendrie, The Book Pub. Co., Smnarton, TN.
National Academy of Sciences.1972.
The Effects on Pon-ula tiens of Enosure to Low Levels pf_ Ionizinc Rad-iation, Washing ton, D.C.
Neel, James V.
1978.
Mutation and Disease in Man, Can.
J. Genet Cytol. 20:295-306.
Howccabe, Howard B. 1978.
Problems assessine the Genetic Innnet of Mutacons on Man, Can. J. Genet. Cytol. 29:
459 l+70.
1 Mausner, J.S. andBahn, A.K. 1974, Enidemiolony, W.B. Saun-dors, Philadelphia.
IX. BIBLICGRAPHY (continued).
Rand McNally. 1967.
World A;.la s, 1967 Edition, Rand McNally, Chicago.
Schwartz, Emanuel E. 1966.
Th: Biological Basis of Rad-istion Therany, J.B. Lippincott, Philadelphia.
Shapiro, Jacob. 1972.
Radiation Protection: A Guide for Scientists and Physicians, Harvard University Press, Cambridge, Mass.
Salthe, Stanley N.1972.
Evolutionary BioloRV, Holt, Rinehart and Winston, New York.
Singer, Sam.
1978.
Human Genetics, W.H. Freeman, San Francisco.
Tubis and Wolf, 1976., Radiopharmaev, 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 Protec tion Agency,1976, Radioloei-cal Quality pf, the Environment, Washington, D.C.
l U.S. Nuclear Regulatory Commission,1979.
Pouulation Dose and Health Imnact of the Accident at the Three Mile Island Nuclear Station, Washington, D.C.
1
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C '.i First Ciass Mail l
VALORE. MCALLISTER. ARON.
WESTMORELAND & VESPER A,, PROF ESSION AL CORPOR ATION ATTORNEYS AT LAW 535 TILTON ROAD NORTHFIELO. N. J. 08225 TO:
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Washington, D.
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