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|From:||Healy J, Mcclellan R, Preston J, Thompson R|
JOINT APPLICANTS - CLINCH RIVER BREEDER REACTOR, OAK RIDGE NATIONAL LABORATORY
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,; BEIATED CORRESPONDE!?C3
hd'Cstil0 USNRC UNITED STATES OF AMERICA
,82 t,ni,'. _1 p 4 UJ NUCLEAR REGULATORY COMMISSION
In the Matter of )
UNITED STATES DEPARTMENT OF ENERGY )
PROJECT MANAGEMENT CORPORATION ) Docket No. 50-537
TE!!NESSEE VALLEY AUTHORITY )
(Clinch River Breeder Reactor Plant) )
APPLICANTS' DIRECT TESTIMONY CONCERNING NRDC CONTENTIONS lib) and lic)
A f l
. ~. - -- -- .-- - .
0 Q.l. Please state your names and af filiations.
A. l'. My name is R. Julian Preston. I am a Senior Research Staff Member, Biology Division, Oak Ridge National Laboratory.
My name is Roger O. McClellan. I am President and Director, Inhalation Toxicology Research Institute, Lovelace Biomedical and Environmental Research Institute.
My name is John W. Healy. I am a Staf f Member, Los Alamos National Laboratory.
My name is Roy C. Thompson. I am a Senior Staff Scientist, Pacific Northwest Laboratory.
Q.2. Have you prepared statements of your professional qualifications?
A.2. Yes. Copies are attached to this testimony.
Q.3. What subject matter does this testimony address?
- 11. The health and safety consequences to the public and l
plant employees which may occur if the CRBR merely complies with current NRC standards for radiation protection of the public health and safety have not been adequately analyzed by Applicants or Staff.
b) Neither Applicants nor Staff have adequately assessed the genetic ef fects f rom radiation exposure including genetic ef fects to the general population from plant employee exposure.
c) Neither Applicants nor Staff have adequately assessed
o the induction of cancer from the exposure of plant employees and the public.
Q.4. How does this testimony address those contentions?
A.4. In the general portion of Contention 11, NRDC claims that neither Applicants nor staf f have adequately assessed the
" residual risks" of CRBRP operations in accordance with existing NRC radiation protection standards, i.e., they have not assessed the health effects that would result from operation of CRBRP in compliance with existing NRC ;
Contention 11(b) asserts that the genetic effects from radiation exposure to the general public and plant employees resulting from operation of CRBRP in compliance with existing NRC regulations have not been adequately assessed. This testimony presents analyses of the calculated genetic effects of radiation doses to the public and to plant employees from CRBRP operation. These analyses show that such calculated genetic effects are small relative to the normal incidence of such ef fects.
Contention 11(c) asserts that the somatic effects (induction of cancer) from operation of CRBRP in compliance with existing NRC regulations have not been adequately assessed. This testimony presents analyses of the
4-calculated somatic effects of radiation exposures to the public and to plant employees from CRBRP operation. These analyses show that such calculated somatic ef fects are small relative to the normal incidence of such ef fects.
Q.5. What input data for radiation exposure resulting from CRBRP operation have you used for perf orming your analyses of genetic and somatic ef fects and from what sources were those data derived?
A.5.. The input data and their respective sources are shown in tabular form as follows:
Valuefs) Source Occupational Exposure 400 man-rem PSAR Section 12.1.5 General Population 2 man-rem FES Supple-ment, Section 5.7.3 (Table A5.5) 921,200 ER Page 5.2-19 persons within a 50 mile radius of CRBRP in the year 2020 .
Q.6. What types of genetic effects ,an be induced by radiation?
A.6. There are four different cate gories of genetic ef fects that can be induced by radiation: these are (i) autosomal dominant.and X-linked disorders, (ii) recessive disorders, l
(iii) structural and numerical chromosome alterations, and (iv) irregularly inherited diseases. Each of these categories must be considered separately, because different l
calculations apply to each. An overall effect, however, can be provided that is simply the sum of the effects estimated for each individual category. This overall effect can then be compared to the reported background frequency for the population.
Q.7. What background frequencies were used by the Applicants?
A.7. The background frequencies for the different categories of genetic effects are those utilized by the National Research Council's Report of the Biological Effects of Ionizing Radiation (BEIR III) Committee (National Academy Press, Washington, D.C., 1980, pp.71-134). The BEIR III report 1
is also the basis for the estimate of the increase in the
f requencies of the different genetic end-points as a result of radiation exposures. The rationale for using the BEIR III values kather than those suggested, for example, by Gofman, J.W., in " Radiation and Human Health," Sierra Club Books,1981, pp. 760-853, is given in the following answers.
Q.8. What assumptions were used by Applicants in calculating genetic effects?
A.8. Several assumptions and conditions are utilized in this testimony, and these are discussed below:
(i) The dose to the reproductive organs is not specifically included, and so it is most appropriate to use the total body dose, realizing that this is probably an over-estimate as a consequence of the
routes of exposure and the predicted dose distribution throughout the body.
(ii) The population size in Year 2020 is assumed to be about 921.200 within a 50 mile radius of CRBRP (See Q/A 5, above).
- 1 Annual total body dose to the population (See Q/A 5, above) 2 man-rem Mean annual dose to each individual in population 2 man-rem 921,200 individuals
= 2 x 10-3 mrem (Background 170 mrem / year)
Dose received during 30 year =(2 x 10-3) x 30 mrem reproductive period = 0.06 mrem Background received during = 170 mr em x 30 1 30 year period
= 5100 mrem The BEIR III estimates of genetic effects are based on or normalized to a dose of 1 rem (1000 mrem) during a 30 year period, whereas the CRBRP doses for the same period are 0.06 mrem. Therefore, the BEIR III estimates must be
multiplied by (6 x 10-5) to make them applicable to. CRBRP doses. This will then give the increase in frequency of genetic disorders per million liveborn as a consequence of radiation exposure to both parents.
(iii) O'e cupational doses. The annual dose received by the occupational group is calculated to be 400 man-rem (PSAR Section 12-1.5). This occupational group comprises plant staf f and utility and contractor i
personnel. It is assumed that the mean period from the start of the particular occupation to the birth of a worker's children will be 15 years. This is a maximal estimate since it assumes that even a person who starts work at age 20 will have a first or
i middle child at age 35, and at a later age for persons who start work when they are older than 20.
A 15 year mean exposure period will give a total dose to the occupational group during this period of:
(400 x 15) man-rem The BEIR III estimates are expressed in terms of the increase in genetic disorders per million offspring produced by an average dose of 1 rem per person per generation. In order to present frequencies for a relatively small occupational group, they will be i expressed as per thousand offspring, and thus, BEIR III values (per million offspring) have to be
,,, f divided by 1000.
It is also assumed that each individual in a population has three children. Thus, the number of persons in a population producing 1000 of fspring will be 1000/3, when only one of the two parents is included in this population. The total dose received by this population on the BEIR III assumption of 1 rem per person is 1000/3 man-rem.
The ratio of the dose received by the occupational group at CRBRP (400 x 15 man-rem) to the dose received by the population utilized in BEIR III estimates is:
(400 x 151 man-rem (1000/3) man-rem = 18.0 One additional correction factor needs to be applied. Since only one parent in the occupational group is likely to be exposed, a correction has to be made for the probability that an offspring will inherit the disorder, when the other parent is une xpo se d. For dominant and X-linked disorders, this is 1/2, and for all other disorders, this would
. be considerably less. A factor of 1/2 is nonetheless assumed for all disorders, in order that the estimates are conservative, and also to make the calculation feasible.
Therefore, it is possible to calculate the frequency of the different genetic disorders per 1000 .
offspring from CRBRP doses to the occupational group by multiplying the BEIR III values (corrected for 1000 offspring) by the dose ratio (18.0) calculated above, and the correction f actor resulting f rom the exposure of only one of the two parents:
BEIR III estimate of increase in aenetic disorders x 18.0 x 1/2 =
BEIR III estimates of increase in oenetic disorder r (9.0 x 10-3)
Estimates obtained using this correction factor will
be conservative. This is because the population exposed is small, and induced frequencies and current incidences obtained simply by division by the appropriate correction factors of frequencies based on one million persons will provide maximcl values. This calculation also assumes that the entire exposure will be received by the reproductive organs, and that is not likely to be the case.
Since no appropriate correction factor can be assumed for this, none is applied. Consequently, the increases in genetic disorders estimated using the above information will represent conservative values.
(iv) The operating lifetime of the plant is proposed to be 30 years. For calculating increases in genetic disorders, it is assumed by BEIR III that doses of 1 rem are received over a 30 year reproductive period
- f or each generation. Thus, doses from CRBRP operation will be to a single generation, and any increases in genetic disorders have to be based on first generation values and not equilibrium values.
This will apply to both population and occupational exposures.
Q.9. What are autosomal dominant and X-linked disorders? '
i A.9. Autosomal dominant disorders are determined by genes located on one of the 22 pairs of autosomes, i.e.,
excluding the X and Y chromosomes. A dominant mutation will be expressed in any individual who carries the gene (assuming complete penetrance) even in the heterozygous form. Thus the frequency of dominant disorders will be equal to the frequency of dominant mutations induced in the population. Dominant mutations are eliminated f rom the population, because of selection, with an average persistence of five generations.
X-linked disorders are determined by genes located on an X-chromosome. A mutation in an X-linked gene will be expressed in males if the gene is dominant or recessive since males have only one X-chromosome. In general, in females normal conditions of expression for dominants and recessives will obtain.
Q.10. What frequency of autosomal dominant and X-linked disorders can be calculated for doses associated with f CRBRP operation?
A.10. BEIR III estimates a first generation value of 8-40 autosomal and X-linked disorders per million liveborn off spring using the relative-mutation-risk method for 1 rem per individual per 30 year dose, or 5-65 using the absolute-mutation-risk method. The current background I
incidence of such disorders is 10,000 per million liveborn.
The relative-mutation-risk calculation uses a doubling dose range of 50-200 rads for low dose rate exposures.
The alternate calculations of Gofman differ only by a )
factor of two in the upper estimate of autosomal and i l
X-linked disorders. This higher upper estimate is the
!~ result of assuming a lower minimum doubling dose estimate of 25 rads, but sAnce this value ignores experimentally demonstrated dese rate effects, it is not legitimate. The average persistence of autosomal dominant or X-linked mutations in the population is 5 generations; theref ore,
- equilibrium values (40-200) obtained by the relative-mutation-risk method have to be divided by 5 in order to give the first generation value (8-40). The absolute-mutation-risk method gives first generation values dirpctly, and these (5-65) are essentially the same as those obtained f rom the relative-mutation-risk analysis.
The frequency of autosomal dominants and X-linked disorders as a result of CRBRP exposures to the surrounding population using BEIR III estimates will be:
Upper estimate: 40 x (6 x 10-5) per million liveborn )
= 2.4 x 10-3 per million liveborn )
Lower estimate: 8x (6 x 10-5) per million liveborn
= 4.8 x 10-4 per million liveborn Current incidence in population - 10,000 per million liveborn.
The frequency of autosomal dominants and X-linked disorders as a result of occupational exposure at CRBRP can be obtained by multiplying the BEIR III estimates by the correction factor derived above (9.0 x 10-3): l Upper estimate 40 x (9.0 x 10-3) = 0.36 per 1000 offspring Lower estimate 8 x (9.0 x 10-3) = 0.07 per 1000 of fspring The current incidence for this group can be obtained by multiplying the current incidence in the general population per million liveborn by 1000 (the number of offspring indicated for the occupationally exposed group):
1***' 10 00 x 1000 = 10 per 1000 of fspring 1f Q.11. What are recestive disorders?
A.ll. A recessive disorder is the consequence of a mutation (designated as m) that is generally expressed only when in the homozygous form (mm), i.e. , when both parents carry the mutation in the unexpressed heterozygous form (Mm) there is a probability that an offspring could obtain the mutant gene from each parent and thus will be homozygous (mu) for this mutation. The important point is that any recessive mutation that is induced by radiation will be expressed as a recessive disorder only when the other parent of an offspring also has this same recessive mutation.
Q.12. What frequency of recessive disorders can be calculated for doses associated with CRBRP operation? 1 A.12. The increase in recessive disorders is very small as estimated by the calculations used by BEIR III or by Gofman. The only difference between the two is a
consequence of the lower limit for the doubling dose used by Gofman as discussed in ( A.10. ) . The correction of the BEIR III values required to estimate the incidence as a result of CRBRP exposures makes the frequency less than 105 times lower than the already very small value.
Specific values are not given, since BEIR III merely gives an estimate of "very few" in the first generation, with "a very slow increase" at equilibrium. The current incidence of recessive disorders in the general population is estimated pt 1,100 per million liveborn.
Q.13. What are chromosome alterations?
A.13. Chromosome alterations are generally defined as any alteration in chromosome structure or number than can be y e detected microscopically or genetically. Three types, deletions, translocations, and trisomy-21, are discussed in this testimony because they can occur in viable offspring, and have been identified as causative in human or laboratory animal disorders. These types are two structural alterations, deletions and translocations, and one numerical alteration, trisomy-21: these will be defined in the appropriate answer below.
- - - _ - - . _ _ _ ~ _ _ ___ ________ __ _ _
Q.14. What is a deletion and what effects from chromosome deletions can be calculated for doses associated with CRBRP operation?
A deletion is defined as the loss from a chromosome of a A.14.
terminal or interstitial piece as a consequence of i
" breakage." The deleted piece of chromosome will be lost from the cell at division since it will not contain a centromere, that is necessary for accurate segregation of chromosomal material. Cells containing deleted chromosomes will, theref ore, contain less than the normal amount of DNA.
BEIR III does not consider this as a separate category of effect. The majority of deletions, ranging in size from those involving several genes up to microscopically i observable ones, cause cell lethality, because of the loss of genetic material. Thus, they will not contribute significantly to the categories of genetic disorders. For microscopically observable ones, this has been demonstrated by correlating the inability of cells in' vitro to divide and form micro-colonies with the presence of deletions (Joshi, G. P. et al., 1982). It has also i
- been shown that the frequency of deletions is very much ;
j higher in spontaneous abortions than in liveborns, i suggesting that the presence of a deletion in a developing i
embryo usually produces lethality. The frequency of very small deletions is measured genetically in the specific f
e-~ve--,,, y ewr-,----- - -- -me,we--s--w--m-m -~
--wwn---- ,wew - , -
- - - - - - - - ~ ~ - - - - - - - - - -
- locus assay as recessive mutations (Russell, L. B., 1971),
and is considered by BEIR III in this category. Such recessive mutations are recovered in the F1 (first generation) at a low frequency following low dose rate exposure, and have a doubling dose of about 100 rads. An analysis of these mutants shows that they do not include larger deletions, involving the selected loci and several adjacent ones. These are cell lethal.
Gofman's estimates assume that radiation-induced deletions could be induced at and transmitted with high frequency, and thus contribute to a high-frequency of genetic l
disorders. The preceding discussions show that this will not be the case. , Larger deletions will not normally be transmitted because they are either lethal to the cell in which they occur, or would cause lethality of the embryo if they were present in the female or male germ cell involved in fertilization (dominant lethality) . Very small deletions are considered in the category of specific
- clocus mutations, and, for the mouse, are shown to be recovered at low frequencies in the viable offspring of irradiated mal:s or females (approximately 5 x 10-8 4 mutations / locus / rem). No separate estimates of the increase in genetic disorders as a consequence of radiation-induced deletions are warranted.
l Q.15. What is a translocation and what frequency of disorders I
from translocation induction can be calculated for doses 1
1.-.______._._ _ _ _ _ _ _ , , _ _ . , _ _ _ _ _ . _ _ _ __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
associated with CRBRP operation?
A.15. A translocation is an exchange between pieces of two enromosomes, must of ten including the ends of the Since there is no loss of chromosomal chromosomes.
material, but rather a rearrangement, a translocation does not result in cell or organism lethality. In fact, persons having reciprocal translocations show little or no phenotypic effect. However, when translocations are present in germ cells they can result in genetic abnormalities in the of fspring of these translocation carriers, as a consequence of the formation of genetically unbalanced products of meiotic segregation [see (c) below).
Data on the induction of translocations in human spermatogonial stem cells by X-rays are available (Brewen, J.G., Preston, R.J., and Gengozian, N., 1975), and both BEIR III and Gofman use these in making estimates of the increase in disorders as a consequence of translocations
The effect estimated by-
,- following parental exposure.
Gofman is considerably higher than that of BEIR III.
There are three major factors that were considered by BEIR III but not by Gofman that show that the BEIR III estimate is much more accurate.
(a) Since translocations are produced as the result of an exchange between two chromosomes, the probability of this occurring will be much higher following acute rather than
chronic exposures. The data of Brewen, et al.(1975), used l 1
by BEIR III and Gofman, were for acute exposure, and so a dose reduction factor has to be made in order to estimate the effects of low dose rate exposures. BEIR III uses a f actor of 2 that is conservative, but reasonable based on ,
data from the mouse.
(b) The observed translocation frequency is for males only. The recovery of translocations in the of fspring of irradiated female parents is very low. In estimating a population effect, i.e., when an equal number of males and f emales are exposed, it is reasonable to divide the translocation frequency in males by two.
(c) The genetic disorders that are the consequence of
< translocation induction are the result of the unbalanced product of the meiotic segregation of the translocation.
The probability of recovering this unbalanced product in the first generation is 0.06 of the induced frequency, and this correction f actor has to be applied to the induced frequency. For each subsequent generation, a further reduction factor of 0.25 has to be applied to account for the fact that only one-fourth of the segregants of a translocation will result in a balanced translocation 4 being recovered in the offspring of a translocation carrier.
The data of Brewen, et al. (1975) , for translocation induction by acute exposures have to be divided by 2 ( to
allow for low dose rates), 2 (for males and females), and mutiplied by 0.06 to account for the proportion of induced translocations that are estimated to be recovered in the i
of fspring as genetic disorders. l 1
The genetic disorders resulting from induced l translocations following population exposures of 1 rem /30 yr. period are estimated by BEIR III as about 10 per million liveborn. The current population incidence is 6,000 per million liveborn.
The estimated frequency in the first generation as a consequence of CRBP.P population exposures (0.06 mrem) will be 10 x (6 x 10-5) = 6 x 10-4 per million liveborn, that is an immeasurably small frequency.
For the occupationally exposed individuals, the estimated f requency of disorders f rom translocation induction would ce:
Frequency of translocations/ rem /30 yr x correction factor for occupational group
,' 10 x (9.0 x 10-3) = 9 x 10-2 per 1000 of fspring The current incidence for this group would be:
Incidence per million liveborn x No. of offspring in group 6,000 x 1000 = 6 per 1000 offspring 106 Q.16. What is trisomy-21 and what calculations of possible increases in trisomy-21 frequency have you made for doses l
1 associated with CRBRP operation?
i A.16. A trisomic cell is one that contains three complete or l almost complete copies of a chromosome instead of the l
, normal two. It can result from the failure of a chromosome to segregate at the first or second meiotic division, thus giving two copies of the chromosome in the post-meiotic germ cell instead of the normal one. On fertilization with a germ cell containing the normal one copy, an embryo with three copies will result. The most common trisomy recovered in viable of fspring is f or chromosome 21 (trisomy-21) , usually ref erred to as Down syndrome or mongolism. The mis-segregation of chromosomes at meiosis is more frequent in females.
A separate estimate of the increase in frequency of trisomy-21 as a result of radiation exposure was not made by BEIR III, but was by Gofman. There is no conclusive evidence that parental (particularly maternal) irradiation causes increases in trisomy-21. The data availalle are
, , equivocal, largely because the dose estimates are very uncertain, and f actors other than radiation that could affect the results are not considered. An estimate of increases in trisomy-21 as a consequence of CRBRP exposures is not warranted.
j Q.17. What are irregularly inherited diseases?
A.17. A definition of this category of disorders is given in the BEIR III report. "The population survey in British l
l Columbia reported that at least 9% of all liveborn humans will be seriously handicapped at some time during their lifetimes by genetic disorders of complex etiology, manifested as congenital malformations, anomalies expressed later, or constitutional and degenerative diseases." These are referred to as irregularly inherited disorders.
It is difficult to provide exact estimates of spontaneous and induced frequencies of this class of disorders; howevr. a range including a maximal value can be calculated. The BEIR III Committee used the current incidence values based on the British Columbia population survey (Trimble, B. K. and Doughty, J. H. , 197 4) . This value, 90.000 per million liveborn, is a valid estimate based on the best available data.
The estimates of the increase in frequency due to population radiation exposures derived by BEIR III and Gofman differ considerably. This difference is largely due to the concept of the " mutational component" of these irregularly inherited diseases. In making their estimates, BEIR III clearly define this, and apply it accordingly. The " mutational component" is the proportion l
of these disorders that would yary directly with the mutation rate. This does not imply that some proportion of these disorders are not the consequence of mutations, but rather because of the complex genetic nature of many 4
of these disorders, mutations will not necessarily be expresse d. For example, many irregularly inherited diseases appear to involve multiple genetic loci (polygenic), and thus a mutation ".n one of these genes will not result in an observable genetic disorder. BEIR III use a range for the mutational component of 5-50%,
where 50% can be considered an excessive maximal limit.
Gofman uses a value of 100% for the mutational component, l
thus proposing that all irregularly inherited disorders would vary directly with the mutation rate. This supposition is not supported by any experimental evidence, and is clearly inappropriate where polygenic inheritance is involved. The consequences will be that Gofman's estimates of the increased frequency of irregularly inherited diseases will be 2-20 times higher than those of BEIR III.
Q.18. What calculations have you made of the frequency of irregularly inherited diseases from doses associated with s (CRBRP operation?
A.18. The estimates of the increases in frequency in the first generation due to CRBRP population exposures are based on the current population incidence provided by BEIR III and a calculated equilibrium fraquency for the increase in disorders. The average persistence of these mutations in the population is 10 generations, and thus, the first generation value for the increase in irregularly inherited
diseases is obtained by dividing the equilibrium frequency by 10. It was given above that 9% of all liveborns will be affected by an irregularly inherited disorder. Thus the frequency per million liveborn will be:
Current incidence: 1,000,000 x 0.09 = 90.000 per million liveborn Increases due to CRBRP exposures:
- 1. Upper limit - Equilibrium frequency using a doubling dose of 50 rem, Upper estimate of current incidence x mutational comoonent x CRBRP dose-rem 106 liveborn doubling dose ~ (rem) 1.e., 90,000/106 liveborn x 0.5 x (6 x 10-5) rem 50 rem
. = 5.4 x 10-2 disorders /million liveborn The first generation frequency, assuming a mutation persistence of 10 generations, will be:
= 5.4 x 10-2 disorders /106 liveborn 10 ,
= 5.4 x 10-3 disorders /106 liveborn
- 11. Lower limit - Equilibrium frequency using a doubling dose of 200 rem, Lower limit of current incidence x mutational comoonent x CRBRP dose-rem 106 liveborn doubling dose ~ (rem) 90,000/106 liveborn x 0.05 x (6 x 10-5) rem 200 (rem)
= 1.4 x 10-3 disorders /106 liveborn First generation frequency = 1.4 x 10-3 disorders /106 liveborn l
= 1.4 x 10-4 disorders /106 liveborn The estimates for the occupationally exposed group are approxima tely:
First generation frequency /10 6 liveborn x population size-dose correction factor Upper limit 90 x (9.0 x 10-3) = 0.8 Lower limit 2x (9.0 x 10-3) = 0.02 per 1000 offspring Current incidence 90.000 x 1000 = 90 106 From the preceding discussion, it is considered that these estimates include a maximal value and are not an underestimate.
Q.19. Can you summarize your calculations of total frequencies of genetic effects from doses associated with CRBRP operation?
A.19. Yes. An estimate of total genetic disorders induced by population exposure from the CRBRP is obtained by adding the estimates for individual disorders:
Values are civen as per million liveborn Upper Limit Lower Limit Current incidence Autosomal dominants + 1 X-linked 2.4 x 10-3 0.8 x 10-4 10,000 l Recessive disorders very low very low 1,100 ;
Chromosome alterations 6.0 x 10-4 6.0 x 10-4 6,000 Irregularly inherited _4 diseases 5.4 x 10-2 1.4 x 10 90,000 Total (per million liveborn) 5.7 x 10-2 1.2 x 10-3 107,000 The estimate of the total increase in genetic disorders f rom occupational exposures can also be calculated:
Values are aiven as per 1000 liveborn Calculated Upper Lower Current Limit Limit Incidence i Autosomal dominants 0.4 0.07 10.0 1
. Chromosome alterations 0.1 0.1 6.0 Irregularly inheritec 0.8 0.02 90.0 Total (per 1000 liveborn) 1.3 0.19 106.0 l- The estimates derived in the preceding sections indicate that any discernible increase in genetic disorders would only be for the group that is occupationally exposed, and even then any increases will be small in comparison to the I
Q 20. Do you believe that these values overestimate the expected genetic effccts from doses associated with CRBRP operation?
A.20. Yes. The upper estimate frequencies provided are clearly a maximal estimate, particularly for the occupational
exposures. There are several factors that account for this (as discussed in each section above): an exposure period of 15 years, three children per occupationally exposed person, entire exposure to reproductive organs, simple division of frequencies of disorders for a large population to obtain those for a small population, a minimal estimate for the doubling dose used in calculations of mutation frequency, and, for irregularly inherited diseases, a maximal value for the mutational component .., The upper estimate is calculated on the basis that all these maximal assumptions pertain.
Q.21. Have you calculated the somatic effects for exposure associated with CRBRP operation?
, A.21. fYes. Applicants addressed the NRDC contention that "neither applicants nor staf f have adequately assessed the induction cf cancer from the exposure of plant employees and the public." Estimates were made of cancer deaths among the general public and among plant workers that may 1 result from CRBRP operation. These were shown to be l
extremely small relative to the normal Ryerage incidence of cancer in the U.S. population.
Q.22. What somatic health effect is of concern in connection with exposure to radiation?
A.22. Data for the estimation of the number of cancers that may result from a given dose of radiation arise from studies l of groups of people who have received high doses of radiation. These include the survivors of the Hiroshima and Nagasaki bombs, people treated with radiation for medical disorders, and some radiation-exposed industrial workers, such as the radium dial painters.
In order to use these data, two types of extrapolation must be made. The first extrapolation involves extending the data to lower doses. Conventionally, this has been done by assuming that effect is linearly related to dose and that no dose threshold exists below which no effect will occur. The BEIR-III report postulated that the proper curve to use was one that was linear at low doses with a term proportional to the square of the dose at higher doses. Because of current uncertainties in the data employed by the BEIR-III Committee in the derivation of their linear-quadratic estimates, we have chosen to apply the more conservative linear, no-threshold hypothesis in the estimates that follow.
Sacause' the exposed populations from which the data were obtained to estimate the potential risk from radiation I have not lived their full life-span, a second extrapolation f.s needed to estimate the total number of
l cancers that may eventually develop. Two methods have been used for this extrapolation. The first method, known as the absolute risk approach, expresses the results in increased number of cancer cases per million person-rem.
The second method, known as the relative risk approach, 1 expresses the results as a percentage increase in normal cancer incidence per million person-rem. The International Commission on Radiological Protection and the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) employ only the absolute risk approach, while the U.S. National Academy of Sciences used both methods in the BEIR reports.
Both absolute and relative risk estimates can be obtained f rom the BEIR-III report (Page 212, footnote a) and the absolute risk estimates can be obtained f rom the UNSCEAR t
l report (page 414, paragraph 318). These values are given in Table 1.
I - TABLE 1. TOTAL CANCER MORTALITY PER MILLION PERSON REMS Method Used Source Absolute Risk Relative Risk BEIR-III (Linear) 167 501 UNSCEAR 75-175 Q.23. What somatic effects have you calculated for the radiation exposures associated with CRBRP operation?
A.23. For purposes of estimating the number of cancers that may occur during the lifetime of the individuals exposed, the BEIR-III linear estimates are conservative and have been used. The total annual collective dose from CRBRP operation is about 2 person-rems to members of the public and 400 person-rems to workers at the facility (See Q/A 5.
above). The estimated effects calculated using these doses are 0.0003-0.001 cancers among the public and 0.07-0.2 cancers among the workers for each year of operation of the plant. By way of comparison, one in six of these people would be expected to die of cancer from other causes.
References Brewen, J.G., Preston, R.J., and Gengozian, N., " Analysis of X-Ray-Induced Chromosomal Translocations in Human and
,,Marmose t Stem Cells," Nature, 253, 468-470, 1975.
Gofman, J.W., Radiation and Human Health, Sierra Club Books, San Francisco, pp. 760-853, 1981.
Joshi, G.P., Nelson, W.J., Revell, S.H., and Shaw, C.A.,
"X-Ray-Induced Chromosome Damage in Live Mammalian Cells, and Improved Measurements of Its Effect on Their Colony-Forming Ability," Int. J. Radiat. Biol., 41, 161-181, 1982.
National Research Council, Advisory Committee on the Biological Effects of Ionizing Radiations, "The Effects on Populations of Exposure to Low Levels of Ionizing Radiation," National Academy of Sciences, Washington, D.C.,
Russell, L.B., " Definition of Functional Units in a Small Chromosomal Segment of the Mouse and Its Use in Interpreting the Nature of Radiation-Induced Mutations," Mutation Res.
11, 107-123, 1971.
Trimble, B.K. and Doughty, J.H., "The Amount of Hereditary Disease in Human Populations," Ann. Human Genet. 30, 199-223, 197'4.
STATEMENT OF QUALIFICATIONS R. Julian Preston Senior Research Staff Member Biology Division Oak Ridge National Laboratory Oak Ridge, TN 37830 Dr. R. Julian Preston is a Senior Research Staff Member in the Biology Division, Oak Ridge National Laboratory, that is oper.ated by the Union Carbide Corporation f or the Department of Energy. His current positon is Group Leader of the Mammalian Cytogenetics Group. He is particularly involved in studies of the estimation of the genetic effects of radiation and chemical
, - agents for man from human and laboratory animal studies.
Dr. Preston has worked at the Oak Ridge National Laboratory since 1970. Prior to this, he was a Staff Scientist at the Medical Research Council Radiobiology Unit, Harwell, England. He was a member of the Biophysics Group with emphasis
. . on the genetic effects of radiations of different qualities.
Dr. Preston received a Bachelor of Arts (Genetics) and Master of Arts degrees from Cambridge University, England, and a Doctor of Philosophy degree in Radiation Biology from Reading University, England. He was born in London, England, on J une 5, 1942, and presently resides in Oak Ridge, Tennessee.
STATEMENT OF QUALIFICATIONS R. O. McClellan President and Director Inhalation Toxicology Research Institute Lovelace Biomedical and Environmental Research Institute Albuquerque, NM 87185 I received a Doctor of Veterinary Medicine degree with highest honors from Washington State University in 1960 and a Master of Management Science degree from the University of New Mexico in 1980. In 1967, I was certified (by examination) as a Diplomate of the American Board of Veterinary Toxicology and, in 1980, certified in General Toxicology by the American Board of Toxicology.
Following graduation f rom Washington State University, I was employed in the Biology Laboratory, Hanford Atomic Product Operations, General Electric Company, Richland, Washington, progressing from a position as Biological Scientist to Senior
,, Scient/st. My responsibilities included the design, conduct and interpretation of studies on the metabolism, dosimetry, and toxicity of internally desposited radionuclides. This included studies with 90S r,137 Cs, 131I and transuranic radionuclides. A major portion of my effort was directed to conducting a multigeneration study of the effects of daily ingestion of 90 r S in minature pigs.
From 1965 to 1966 I served as scientific staff member 1
i-in the Medical Research Branch, Division of Biology and Medicine, U. S. Atomic Energy Commission. In this position, I had responsibility for monitoring a major portion of the Commission's research on internally deposited radionuclides and providing advice and counsel to senior management on such matters.
In September 1966 I joined the staf f of the Lovelace Foundation for Medical Education and Research in Albuquerque, New Mexico, with responsibility for directing the Foundation's extensive program on the toxicity of inhaled radionuclides. This program was initially concerned with fission product radionuclides and in the late 1960's was broadened to include research on plutonium and other transuranic radionuclides. More recently the program has been expanded to include research on airborne materials associated with utilization of coal and use of diesel-powered vehicles.
Since 1976 I have served as Pres'ident of the Lovelace Biomedical and Environmental Research Institute (a subsidiary of the Lovelace Medical Foundation) and as Director of the Inhalation Toxicology Research Institute, which is operated by the Lovelace organization for the U.S. Department of Energy. My responsibilities include management of the Institute and participation in the design and interpretation of studies on the toxicity of radioactive and non-radioactive airborne materials.
I am especially interested in the late-occuring ef fects of exposure to pollutants and the use of data from laboratory animals to estimate health consequences for people.
I have served on numerous advisory groups concerned with assessing the health ef fects of occupational and environmental exposure to a wide range of materials.
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STATEMENT OF QUALIFICATIONS ,
John W. HEALY l Staff Member Los Alamos National Laboratory Los Alamos, NM 87545 Mr. John W. Healy is a staff member in the Health Division of the Los Alamos National Laboratory which is operated for the Department of Energy by the University of California. In his current position, he is advisor to the Division Leader, Health Division. He is extensively involved in DOE activities related to plutonium in the environment.
Mr. Healy received training at Oak Ridge in radiation protection in 1944. Following nine months of training, he moved to Hanford where he spent the next 16 years. During this period of time, he established the environmental monitoring, low-level analytical radiochemistry, and bioassay programs for the laboratory. During this period he also was involved in the '
internal dosimetry, dose assessment, reactor saf ety and meteorology programs. In 1960 he transferred to New York where he was concerned with reactor safety and product safety for the General Electric Company. In 1968 he moved to the Los Alamos National Laboratory where his activities have included the bases f or and development of radiation standards and regulations, radiation dose assements, and the application of risk estimates
to such dose assessments.
Mr. Healy received a Bachelor of Science degree from Pennsylvania State College in 1942. He was born in Corry, Penns}1vania, on May 9, 1920, and presently resides in Los Alamos.
i STATEMENT OF QUALIFICATIONS Roy C. Thompson Senior Staf f Scientist Pacific Northwest Laboratory Richland, WA 99352 Dr. Roy C. Thompson is a Senior Staf f Scientist in the Biology Department of Pacific Northwest Laboratory, which is operated for the Department of Energy by Battelle Memorial Institute. His current position title in the Biology Department is Coordinator of Nuclear Programs. He is extensively involved I in DOE activities related to the toxicity of plutonium and other actinides.
,' Dr. Thompson has worked at the DOE /ERDA/AEC laboratories in Richland, Washington since 1950. Prior to that time he held positions as Assistant Professor of Chemistry at the University of Texas, and as Research Assistant at the University of California in Berkeley and at the University of Chicago Metallurgical Labortory (Manhattan Project).
Dr. Thompson received Bachelor of Arts, Master of Arts, and Doctor of Philosophy (Bio-Organic Chemistry) degrees f rom the
University of Texas. He was born in Kansas City, Missouri on June 19, 1920 and presently resides in Pasco, Washington.
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