ML19340D137

Testimony on Doggett Contention 1(b) (Bishop Contention 13) Re Health Effects of Coal & Nuclear Power.Pp 1-69.Prof Qualifications Encl

ML19340D137
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Site:	Allens Creek File:Houston Lighting and Power Company icon.png
Issue date:	12/18/1980
From:	Hamilton L BROOKHAVEN NATIONAL LABORATORY
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7 December 18, 1980 1

UNITED STATES OF AMERICA 2 NUCLEAR REGULATORY COMMISSION 3 BEFORE THE ATOMIC SAFETY AND LICENSING BOARD 4

I the Matter of )

5 )

HOUSTON LIGHTING & POWER COMPANY ) Docket No. 50-466 6 )

(Allens Creek Nuclear Generating )

7 Station, Unit No. 1) )

)

8 TESTIMONY OF DR. LEONARD RAMILTON ON O DOGGETT CONTENTION 1(b) (BISHOP CONTENTION

13) RELATING TO HEALTH EFFECTS OF COAL 10 AND NUCLEAR 12 Q. Please state your name and place of employment.

13 A. My name is Leonard D. Hamilton and I am employed 14 as Head of tne Biomedical and Environmental Assess-15 ment Division in the National Center for Analysis of -

16 Energy Systems at Brookhaven National Laboratory, 17 Associated Universities, Inc., Upton, New York 11973.

18 0 Would you describe your professional qualifications?

19 A. A copy of my professional qualifications _are set 20 forth in Attachment A to this testimony.

21 Q. Dr. Hamilton, have you reviewed Intervenor Doggett's 22 contention no. 1(b) (Bishop 13) ?

23 A. Yes. I have reviewed this contention.

24 Q. What is the purpose of your testimony?

25 A. The purpose of'my testimony is to respond to that 26 part of the contention relating tu the comparative 27 health effects of a coal and nuclear power plant 28 at the Allens Creek site. In addition, I will F 012 2 9 0 /604 . --

l' address ASLB Question 1 relating to the health effects of 2 a lignite plant at the Allens Creek site. I would like 3 to point out that my testimony reflects only my own 4 views and opinions, and not those of the Brookhaven National 5 Laboratory.

6 My testimony summarizes and compares the health 7 impacts of two fuel cycles, first the nuclear fuel cycle 1

8 i and then the coal fuel cycle. Reasonable comparisons 9 between the health impacts of electric power. options can 10 only be made by comparing entire fuel cycles. For this 11  ; purpose, our calculations of the health effects (merbidity 12 and premature mortality) of electrical power plants come 13 from estimates of risk due to one gigawatt-year (Gwy) of 14 electric energy production and its supporting fuel cycle 15 operating over a year [1-3]*; these and the effects there-16 upon engendered on workers and the general public provide 17 a standard base for comparisons.

18 Q. First Dr. Hamilton, please turn your attention to the 19 health impacts of the nuclear fuel cycle. Are data available 20 with respect to the induction of cancer from high doses 21 of radiation?

22 A. Yes [4]. Although it was clear since shortly after 23 the discovery of X-rays that high levels of radiation ,

24 induce cancer in humans, it is only in the last decade or 25 so that data have become available that permit ,

4 26 27 *Nu=bers in brackets [ ] indicate references listed 28 beginning on page 58.

2-t -

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4 1 quantitative risk estimations [5]. Data are available 2 on the induction of leukemia and other malignancies in 3 man frc= the Japanese atom bomb survivors and from 4 English patients treated for ankylosing spondylitis (a 5 rheumatic disease of the spine) with therapeutic doses 6! of radiation (6). These were largely high doses of 7l i radiation given at high dose rates.

8! Mortality records in the Atomic Semb Casualty i

9' Cc= mission Life Span Study Sample have been collected 10 until the end of 1972, 27 years after the bombings; b

Ild the spondylitics have been followed fully for 24 years 1

12) and, in part, for an additional 3 years. The results on 13l: the atc= bomb survivors apply to a general population 14 (41% male: 20% less than 10 years old at time of bombing) 15 irradiated with a pulse of mixed radiation (a much 16 larger neutron component at Hiroshima); results on the i

37 spondylitics apply to a largely (84%) male adult population 1

18 affected by a specific disease irradiated with fractionated 19 x-rays over long time periods. Although several revisions 20 of the estimates have improved the accuracy of dose-l 21 effect relationships, there must still be large uncer-22 tainties in the estimates of the doses of radiation received 1

l 23 by survivors.

l l 24 Amonc.the survivors, the incidence of leukemia 25 (based on mortality or morbidity data) appears to rise 26 linearly with dose up to a few hundred rads. A significant l

l 27 excess of leukemia was seen at Hiroshima in the population i

28 exposed to doses greater than 10 rad. The risk l ,

9 9

1 estimate from mortality is between one to two cases of 2 leukemia cer million per year per rad over 20 years.

3 .

This agrees with findings derived from the spondylitic 4 patients. Since the risk after 20 years in both the 5 survivors and the spondylitics has returned to that in 6 the general population, the overall risk estimate is 7 between 20 to 40 cases per million per rad for single l

g and fractionated irradiation, either whole body or part.

Other cancers among the atom bomb survivors for 9!.

I 10i which dose-effect relationships can be made, and hence, i

11 tentative risk estimates given, include lung cancer 12.

(bronchi and trachea) , 1.5 to 3 cases cer million per 13 year per rad; breast cancer among women, 0.2 to 0.4 14 cases per million per year per rad; and thyroid cancer, 15 1 to 2 cases per million per year per rad in males and 16 2 to 4 cases in females [5]. Unlike the risk of 17 leukemia, there is no way to determine whether the 18 increased risk of these tumors will continue or decrease 19 in the future. In the spondylitics, the excess risk 20 of tumors in heavily irradiated sites rose during the 21 addit; 4 3 years of observation and has continued to l

22 rise. T. 1s , estimates of cancer induction, currently 23 derived from the survivors and the spondylitics, will 24 have to be periodically revised. In the mear. time 25 approxinate allowances need to be made for the future 26 cancers in risk estimates. These risk estimates for 27 cancers other than leukemia are based on recent data 28 and a number of assumptions [5].

i 1

These human data are compatible with a simple pro-2 portional dose-response: the higher the radiation dose, 3 the higher the incidence of leukemia and, in some instances, 4 other malignant neoplasms, e.g., lung, breast, and thyroid cancer. It is clear that the latent period 5

6 for the induction of leukemia and the duration of the 7 risk differs from that of other cancers, the latter 3 appearing to take longer to appear and persisting later

~

9 than the risk of leukemia.

10 o. can the data on induction of cancer from high doses 11 of radiation be extrapolated to low doses and low dose rates?

12 A. Yes. The very low doses and dose rates given by 13 natural background radiation in the environment, and the 14 considerably lower doses that would be given at low dose 15 rates by nuclear power stations, are obviously very 16 much lower than those for which there are data on tumor 17 induction. However, to get a crude idea of risk, one l 18 ass umes that the linear propor.ional dose and tumor 19 induction observed at nut.2 nigher doses and dose rates 20 can be extrapolated down to the lowest doses and at 21 all dose rates and that a threshold is absent. These 7

l l 22 assumptions imply two important coroi. aries:

23 1. A dose delivered over a long time is as biologi-l 24 cally damaging as the same dose given over a short time.

25 This is known to be incorrect since there is some repair 26 of radiation damage. The presence of a repair mechanism t

27 means that doses spread over a long period are less 28 danaging than doses spread over a short period. Thus, I

l ,, ._ . . , . ,__ . . _ _ , .

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1 an estinate that ignores the repair mechanism - for which 2' a quantitative relationship cannot now be stated - is i

3 likely to be higher than the actual, but unknown, risk.

4 Therefore, the assumption of linear proportionality 5 down to the lowest doses and dose rates undoubtedly 6 overestimates actual risk.

7 2. Doses to individuals can be totaled (collective 8 dose) and then divided by the number of individuals 9l exposed, thereby giving the mean individual dose which, 10 l- multiplied by the rate of cancer induction, gives an 11 estimated statistical risk per individual. We use risk 12 estimators derived from the BEIR III 1980 re, ort. Since 13 the BEIR report was based essentially on the data and 14 ass ump tions reviewed above, one can appreciate that these 15 represent upperlimit estimates and that the actual 16 number of cancers induced by these very low doses, given 17 at very low dose rates, will be lower and may be zero.

18 The size of the collective dose from the nuclear fuel 19 cycle to the U.S. and foreign populations largely 20 reflects a situation in which large numbers of people 21 receive an infinitesimally small dose. A review of the 22 literature on radiation dose response done as part of E the Reactor Safety Study, led to the use of a dose and N dose-rate effectiveness factor reducing the BEIR I (1972)

E estimates by a factor of 5 for doses of low linear energy E transfer radiation under 10 rem received at a rate under 1 rem per day [8]. BEIR III does not make any statements 28 for doses below 10 rad or rates of below 1 rad / year.

W 1 BEIR III suggests that the dose-response function may be 2 quadratic at low dose rates for low LET radiation, but rec-3 ommends the use of linear dose response functions as a uonser-4 vative method in estimating risks. The BEIR III (1980) results 5 are slightly lower but essentially the same as BEIR I (1971).

6 Q. With the above-described assumptions, can you calculate 7 the risk to a population from radiation exposure?

8 A. Yes. With these assumptions, one can calculate an 9 estimate of the expected number of cancers in a population 10 following radiation exposure. These assumptions underlie 11 the estimates of cancers after radiation from the nuclear 12 fuel cycle. For the effects of nuclear power, our 13 principal reference for exposure data are Table S-3 14 (10 CFR 51) and GESMO [9].

15 o. please describe your calculation in greater detail.

16 A. The cancer risk estimators used in the remainder of this 17 testimony are derived from the BEIR III study [20]. The rescits 18 of the absolute risk model were used. Since, except in the case 19 of a possible accident, the exposure is continuous in nature, 20 the BEIR III numbers' reflecting a continuous exposure to one 21 rad per year were chosen rather than a single exposure of 10 22 rad. The model for which the low-level low-LET radiation dose-23 response is linear with no threshold (as opposed to the quadratic 24 and linear quadratic models with or without threshold) 25 was chosen for two reasons: (1) it is considered to be 26 conservative on the high side, by the BEIR III committee 27 and (2) it is the only one which can be applied when only 28 collective population doses are available (as opposed to

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

I population dose distributions). Two distinct populations 2 l. at risk are considered: (1) the general public consisting 3 of all ages and both sexes, and (2) an occupational popula-4 tion consisting of essentially all males between the ages 5 of 20 and 65.

6 The risk estimators for whole body low-LET exposure 7 for leukemia and bone cancer incidence (and mortality) 8 are taken from BEIR III page 256. The other cancer risk 9 estimators for mortality are from p. 259 and incidence 10 from p. 271 (the Nagasaki Tumor Registry results).

11 12 CANCER RISK PER 10 RAD 13 (Whole body low-LET exposure)

Population Incidence Mortality 14 15 occupational 225 102 16 Public 293 158 17 The lung cancer risk to the occupational population 18 is derived from figures presented in BEIR III p. 390. The 19 male population age distribution and life expentancy are 20 combined with the risk at time of diagnosis and a latent 21 period of ten years resulting in a risk estimator of 93 s

22 cases per lo rem lung dose.

23 Q. What is your estimate of the genetic effects which 24 would result from radiation from the nuclear fuel cycle?

! 25 A. No genetic effects have been demonstrated in the l

l 26 offspring of irradiated human populations; there are i 27 thus no direct quantitative data available for man.

I 28 3

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. i 1 But since the genetic material DNA and erotein is 2 similar in man and mouse, it is not unreasonable to 3 assume that one can extrapolate mouse data and base 4 estimates of risk primarily on experimental wor % with 5 mice [10). The major genetic hazard frem small 6 experimental radiation doses and low dose rates probably 7 results from the induction of gene mutations and small 8 deficiencies in the male. In male nice a dose-rate 9 effect is apparent in mutation induction; mutation 10 frequency falls off as a given total dose is delivered 11 over a longer time. However, below about 1 rad per 12 minute (rad / min) there is no further reduction in mutation 13 frequency for a given total dose as dose rate is lowered.

14 This argues against any threshold level of dose or dose 15 rate, and one assumes that for dose rates below 1 rad / min 16 the mutational response in the male will be linearly related 17 to total dose. In female mice, the effects of radiation 18 at dose rates below abouc 0.01 rad / min are small compared 19 to those seen in the male. This applies to all the germ 20 cell (oocyte) stages tested: mature, maturing, and 21 immature arrested stages. In the arrested oocyte stage, 22 no statistically significant increase over spontaneous 23 mutation frequency has been detected, even after large 24 accumulated doses. To recapitulate, most of the genetic 25 hazard from Iow radiation dose rates is seen in male, 26 rather than female, mice; the mutation frequencies at II low radiation levels in the male are believed to be 28 linearly related to dose. The spontaneous mutation rate 9-

' e

-3

1 in the mouse is widely accepted as 0.75 x 10 per locus, o per generation, anc the increase in this rate in the

-8 3- =ouse (male) is now estimated as 17 x 10 per locus, 4 per generation, per rad. The spontaneous mutation in

-5 on,r, tic,,

5 =an is esti=ated as 1 x 10 p,r 1,cu,, p,r 6 If one assures that the induction of mutations by 7I radiation is the same as in the mouse, one rem could b

8- procuce a 1 Ti increase in the mutation rate, making 9- no allowance for repair of genetic damage or low dose i

104 rates. Thus the approximate 3 re=s corresponding to 11 an average accumulation frc: natural background radiation over the 30 year reproductive life of the human male i

12 13 could be responsible for 5.1% of the spontaneous 14 mutation rate in =an. This assumes repair has negligible 15 effect. Estimates on the contribution of natural back-16 ground radiation to the spontaneous mutation rate in 17 =an range from 4 to 101. If one accepts that 3 re 1 18 over 30 years may be responsible for 5.1% of the I 19 spontaneous mutation rate, response of the general 20 population within 50 miles of a nuclear reactor to an 21 ave. age annual whole body dose of 0.01 =re=/yr. i.e.

22 0.3 mre in 30 years, would increase the rate negligibly 23 (0.0005%), again making no allowances for repair [10].

24 There have in the past been several quantitative 25 estimates made of the genetic effects of irradiation.

26 These include BEIR [11], EPA [12], Cohen and Dance [13],

27 Cohen [14] and the estimate used by Binder, et al. [15].

28 The most comprehensive, critical and up to date review

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1 of the genetic effects of irradiation is given in the o

2: United Nations Scientific Committee on the Effects of I

t 3[ Atomic Radiation latest report [161, sources and 4lg Effects of Ionizing Radiation. This report U

5!

l' estimates that in a million liveborn children in the 6 first generation of offspring of a population exposed h

7 ". to 1 rad at low dose rate during the generation, there would be 20 cases suffering from dominant or x-linked Sli  !

diseases, 38 with chromosomally determined diseases, and 9j i

10' 5 with diseases of ccmplex etiology induced by the 11 radiation, i .e., a total of 63 genetic effects in the 12 first generation. This is equivalent to 0.06% of the 13 current incidence of these genetic effects in the first 14 eneration. Less certain are the estimates one can make 15 of total genetic damage expressed over all generations 16 (or the value in each generation reached after prolonged 17 continuous exposure). By the doubling-dose method 18 these are estimated to total 185 genetic effects in the 19 offspring of a population continuously exposed to 1 rad i 20 per generation at low dose rate for several generations l

21 until equilibrium is reached. One hundred eighty-five 22 genetic effects would be equivalent to 0.17% of the 23 l current incidence of genetic effects. since a reasonable 24 I

upper limit estimate of the irradiation the U.S. population t

i 25 will receive for the entire nuclear fuel cycle from 26 ; all nuclear power by the year 2000 (4000 GWy) is 27 l' approximately 1 = rem per generation, the genetic effects 28 would be one thousand times less than those calculated

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1 above for 1 rad. They would also be 3,000 times less 21 than the genetic effects induced by natural background 3 . over this period.

4 Q. In your review of the health effects of the nuclear 5 fuel cycle, have you estimated the impacts to persens 6-which result from the nining and processing of uranium, 7 radioactive emissions from nuclear power reactors, 8 management of nuclear wastes material, and the transporrion 1

91 of nuclear fuel and wastes?

10- A. Yes.

11 Q. First, what is the impact on the general population 12 from uranium mining activities?

13 A. Table S-3 includes no radiological effluents from 14 uranium mining to the general public. GES".0 estimates 15 the total integrated population dose commitment from 16 airborne radon emissions from the entire U.S. uranium 17 mining industry [17]. Dividing these estimates by the 18 4732 GWy, the electric production equivalent of mining 19 with no recycle for the 1975-2000 period [18), and applying 20 appropriate dose response functions [19, 20] gives:

21 Integrated Ex:ess cancer population dose per 10 6

c:-1:=ent per person-re= Esti=ated cancers per city 22 Organ Deaths

! (person-re:) cases death Incidence E bnclebcdy 82.l. 293 158 2.4 x 10-2 1.3 x 10-2 N 24.5 9;. 47 2.3 x 10-3 1.2 x 10-2 G: tract E 2 'A S . 4 4 8.2 x 10-3 S.2 x 10-3 Scne 24 12 1.2 x 10-2 6.0 x 10-3

.ive r 507.

E 23e5 55 25 1.3 x 10-1 6.7 x 10-2 Eidne:

3 1.5 140 7 2.1 x 10-4 1.1 x 10 "

Thyroid

-2 192. 133 133 2.6 x 10- 2.6 x 10 Lung Total 0.20 0.13

I i

l' O. What is the impact on uranium miners from radiation u

2 as a result of mining activities?

I 3, A. Uranium miners are exposed to many of the occupational l

disease-producing agents which exist in other metal 4l, 5? mines. These include exposure to siliceous dust, toxic 6l metals, diesel exhaust products, oxygen deficient h,

7! atmospheres, blasting powder gases, external radiation

,I 8 exposure and internal radiation produced by inhaled l'd 9? airborne radioisotopes, particularly raden-222 and I

10'l its daughter products. The latter is the most important 11 occupational hazard in uranium mining. Radon is an 12 inert gas and is substantially expelled from the lung 13 before it undergoes radioactive decay. The inhaled radon 14 daughter products are deposited in the respiratory tract 15 where decay occurs by emission of alpha particles. This 16 internal exposure is measured in " working level months" 17 CWLM). A WLM is defined as the exposure to radon in 18 equilibrium with its daughters at 100 pCi/ liter for 19 170 hours0.00197 days <br />0.0472 hours <br />2.810847e-4 weeks <br />6.4685e-5 months <br /> per month. A working level (WL) is the 20 exposure level which would produce a WLM in a miner 21 working for 1 month. Estimates of the dose to the 22 bronchial epithelium, considered to be the target cells 23 , where lung cancers originate, vary over 2 orders of 24 l' magnitude ranging between 0.1 and 20 rads per WLM [21].

25 BEIR used a value of 0.5 red /WLM. The strongest evidence 26 i of increased lung cancer in uranium miners has been among 27 those exposed to more then 400 WLM [221, although data j 28 supporting a causal relation between cumulative airborne j l

~ l.

1, radiation exposure in the 120-359 WLM range and increased l

2, risk of lung cancer has been reported [23]. EPA has l

3 estimated that exposure to 110 WLM will doubic the risk

! of lung cancer [24]. Present standards allow 4 WLM 4

exposure per miner per year [25-27]. GESMO assumed 5l. that the combined external gamma radiation and the internal 6

0 7 radon daughter exposure in underground mines was 1.1 g: rem / miner / year [28). Measurements in surface mines g! indicate exposure levels are generally less than 0.3 WL with an average concentration of 0.06 WL. Average 10' 11- external exposure rate was found to be in the order of 12 0.5 mR/hr 1 0.5 mR/hr [29]. GESMO assumed that the average 13 whole-body dose in surface miners was 0.5 R/ miner / year [28].

14 Assuming that, on the average, uranium mine production 15 over the years 1975-2000 will be 40% surface mining 16 and 60% underground mining [30], GESMO estimated occupational 17 external radiation exposure in mining associated with 18 the I"" ';__ . .le during these years to be equivalent 6

19 to 1.14 x 10 6 cerson-rem whole-body; 6.4 x 10 person-rem 20 to the lungs of the miners [31]. Both estimates are 21 based on no recycle of uranium or plutonium. To obtain 22 an estimate for 1 GWy (e) supply of fuel, we divide by 23 the GESMO equivalent production for mining of 4732 GWy(18) :

24 241 persen-rem whole-body per GWy from external exposure 25 1353 person-rem per GWy lung dose.

6 Applying 225 excess cancers and 102 deaths per 10 p,r,,,_

26 27 rem whole body, yields:

2B 0.054 cancers /GWy 14 -

I

I l

l 1 j 0.025 deaths /GWy I s 6

21 Applying 93 lung cancer cases per 10 person-rem dose 3 to lung yields:

l 4 0.126 cases /GWy -

l 5 The total impact on uranium miners for 1 GWy(e) of LWR operation without recycle is (0.025 + 0.126) = 0.15 6li i

7 cancer deaths. This estimate is subject to uncertainties I

f 8; in estimation of the exposure level and the dose-response 9- function and also to assumptions concerning the amount 10 of ore required per GWy, miner productivity, and 11 cercentages allocated to underground and surface mining.

12 Applying somewhat different but perhaps equally credible i 13 estimetes and assumptions sinder, et al., estimate 0.01 14 cancer deaths - org miners per plant-year [33]. WASH-1224 15 estimated 0.01 total cancers per plant-year among miners [341 l

16 Q. What is the impact on uranium miners from accidents?

i 17 A. Based on an analysis of the 1964-69 data, WASH-1224 l 18 estimates the accident rate in uranium mines to be 1.92 6

19 fatal and 73.9 nonfatal injuries per 10 tons ore from l 20 underground mining, and 0.29 fatal and 10.8 nonfatal l

21 injuries from open pit mining.

t 22 3 This rate is even higher than that in coal mir.es l

1 23 but the amount of uranium ore that must be mined is over f

24 l

an order of magnitude less than the amount of coal to I

25 support one GWy of electricity. If we take the ore 26 requirement of 374 short tons U0 3g per GWy in the no-l 27 recycle option [36] and assume that 60% comes from under-l 28 ground mines with an ore grade of 0.2% U 038 and 40%

i i

15 -

1 comes from open pit mines of 0.1% grade, the fatalities 2 would be:

3 Underground:

374 6 tons = 0.22 deaths /GWy tons x 0.6 x 1.92 deaths /10 5- 0.002 374 6 6 tons + 0.6 x 73.9/10 tons = 8.3 injuries /GWy 0.002 7

St Open Pit:

9~ 374 6 tons x 0.4 x 0.29 deaths /10 tons = 0.043 deaths /Gff 10l- 0.001 4 6 tons x 0.4 x 10.8 injuries /10 tons = 1.6 iniulies/My 12 0.001 13 Adding the underground and open pit mining deaths and 14 injuries give 0.26 deaths and 9.9 injuries per GWy.

15 WASH-1224, using slightly different assumptions for ore 16 requirements estimates 0.09 deaths and 3.6 injuries per 0.75 17 GWy (37].

18 Q. What is the impact on uranium miners from non-radiation 19 induced diseases?

20 A. sinder, et al. [381 analyze the results of an unpublished 21 report by Archer [39) to estimate occupationally related 22 lung disease other than cancer in uranium miners. The 23 number of deaths due to respiratory insufficiency was 5 24 times higher among the 3366 underground miners studied 25 than would be-expected in the general population and 1.7 20 times higher than among the control group, i.e., surface E workers. Subtracting the background risk in the general E population, they calculate 1.0 and 0.5 excess deaths per i

I i

I  !

i 1000 man-years among underground miners and surface i

2! workers respectively. From this they calculate 0.031 3- deaths among underground miners and 0.009 deaths among 4 surface miners per power plant year assuming 50% of the fuel coming from each source.

5]

6' converting this to the GESMo split of 60% under-7 ground and 401 surface yields 0.037 deaths underground 8 and 0.007 deaths surface for a total of 0.044 deaths from occupational non-radiation induced respiratory 9l:

10' disease per plant-year in uranium miners. Dividing by 11 0.75 GWy/ plant-year gives 0.06 deaths /GWy.

12 Q. What is the dose commitment to individuals working in 13 uranium crocessing facilities?

14 A. Table S-3 does not consider occupational dose 15 commitment in uranium processing (including milling, 16 uranium hexafluoride production, uranium enrichment and 17 fuel fabrication) . Gotchy reports, however, that dose 18 commitments given in GESMO are comparable to those which i-19 would result from the radiological releases in NUREG-0216, 20 which provides background support for S-3 [40]. His 21 estimate of the ef fect on workers of this exposure yields 22 0. 05 f atal cancers per GWy (e) . Also based on dose 23 commitments given in GESMO, Gotchy's estimate yields 24 ,

0.003 f atal cancers among the general public per GWy (e) .

25 It should be noted that GESMO considers only radon-26 222 emissions from active mill tailings piles. If 27 further action is not taken, these piles will continue 28 to emit radon-222 into the indefinite future, imposing

4

. i 1 ,

a dose commitment on future generations. It is clear, l

2J however, that the addition to natural background radon-3 222 levels due to the operation of the nuclear industry 4 through 2000 (as projected in GESMO) is only a fraction 5 of a percent.

6 Gotchy estimates accidental deaths among processing 7

l workers equivalent to 0.006 deaths per GWy (e) [40].

I 8': These estimates are essentially equivalent to the more 9 detailed estimates by Binder, et al. [411 derived 10 essentially from WASH-1224. Injuries are 1.6 per plant-11 year (sinder).

12 Q. What doses and impacts to the population will result 13 from normal releases of radioactivity from nuclear power 14 reactors?

15 A. Table s-3 does not specifically address emissions

! 16 from light water reactors. GEsMo 144] estimates total 6

17 body exposure as occupational,2.3 x 10 person-rem; j 18 offsite U.S. population, 3.1 x 10 person-rem; and 5

19 foreign population, 2.1 x 10 for 1975 to 2000.

20 To obtain the estimate for one GWy one divides by 21 the 4000 GWy electricity produced in the GESMO scenario [36]:

22 Occupational: 568 person-rem /GWy 23 public: 130 person-rem /GWY 6

24 Applying 225 cancers (102 fatal) per 10 person-rem 25 yields 0.13 occupational cancers (0.06 fatal) per GWy.

6 26 Applying 293 cancers (158 fatal) per 10 person-rem l

l 27 gives 0.04 cancers among the public (0.02 fatal) l i 28 cer GWy. The Council on Environmental Quality (CEQ) [42]

i l

t

I estimated 0.013 deaths and 1.31 injuries per plant-year 2 (0. 75 GWy) due to occupational accidents at nuclear 3 power plants. The Philadelphia Electric Company [53]

4 conducted a survey and found no deatns and an estimated 5 0.7 injuries per plant-year for nuclear plants, we calculate 6 95% Poisson confidence limits on these estimates to be 7 0 to 0.2 deaths and 0.34 to 1.3 injuries per plant-year.

8 We accept the CEQ estimates as confirmed by the Philadelphia 9 Electric Company Survey.

10 Q. What impacts to the population will result from 11 the accidental releases of radioactivity from nuclear 12 power reactors?

13 A. only light water reactors have been thoroughly 14 evaluated for risk associated with catastrophic accidents.

15 Reactors, however, probably account for most of the 16 potential impact of major nuclear accidents in the i

17 uranium fuel cycle and, were an accident to occur, the 18 health impact of an accident at a reactor is likely to be 19 much larger than of an accident at other types of 20 facilities in the uranium fubl cycle.

21 t

22 On an actuarial basis, the Reactor Safety Study 23 estimated reactor accidents contribute only 0.02 deaths 24 per GWy (e) . Since almost all of the health effects 25 calculated from even the worst hypothesized accident are 26 attributable to low doses over a large population, the 27 Reactor Safety Study applied the dose and dose-rate gg factors (see above p. 6). Converting back to the BEIR I

~ _, -

I I

l i upper bound estimate yields 0.1 deaths per GWy(e).

I 21 Q. What is the impact on workers and the general 3lI population as a result of radioactive waste management?

4 A. GESMO estimates the radiation exposure in waste 4

5. management and spent fuel storage to be 1.4 x 10 l

6'; person-rem for occupational, 31 person-rem for U.S.

I 7 I population offsite, and 130 person-rem for foreign i 4 SP coculation (44]. This sums to 1.4 x 10 person-ren b occupational and 161 person-rem to the public cumulative 9p 10" fer 1975 to 2000. Dividing by the GESMo scenario, irradi-11!- ated fuel storage equivalent of 3072 GWy [36), the I,

12 estimate for one GWy is approximately:

13- occupational: 4.56 person-rem /GWy 14 Public : 0.05 person-rem /Gwy 15 Applying the same dose-response estimators as above

-3 -4 16 yields 1.0 x 10 occupational cancers (4.6 x 10 fatal)

-5 -6 14 and 1.5 x 10 cancers among the public (8 x 10 fatal) 18 per GWy. Similar analysis of the specific organ 19 exposures in GESMo [44] lead to estimates of an additional

-4 -5 20 7.2 x 10 cancers in workers and 11 x 10 cancers 21 in the public.

22 I have found no estimates of routine, non-radiological 23 effects on workers or the public. I believe that such 34 l' effects will be nil.

25 O. What will be the radiological exposure resulting 26 from the transportation of fuel and wastes to and from 27 the reactor, including transportation accidents?

28 ' A. Estimated radiation exposure from transportation of I w

t L

!i e

i 1.' fuel elements to the reactor and of wastes.from the

't .

2 reactor to waste management facilities is estimated to 3 be 4 person-rem for workers and 3 person-rem for the 4 general public-[45]. Radiation exposure due to transport 0

5i:

among mining, processing and waste management facilities 6; is estimated to be 0.4 person-rem for workers and 0.1 h

for the public per GWy {46]. Applying the dose-response 7:

-3 cancers among workers 83 functions yields 1.0 x 10

s. ~ ~4 cancers among the public 9," (4.5 x 10 fatal) and 9.1 x 10

-4 (4.5 x 10 fatal) per GWy.

10L 11 I

Secause of the low probability of a serious accident 12 cecurring in transport and the regulations providing i

13 8 for strict packaging standards and shipment criteria, 14 the risk of radioactive contamination or radiation 15 exposure from transport accidents is extremely small 16 [48, 49]. Cohen and Dance have made a quantitative l,

17 i estimate of the radiological public health effects of

' transport accidents (501 on an actuarial basis, they 18 19 estimate the overall health effects from all transportation f '

20 accidents to be in the range of 1.7 x 10

-3 to 1.8 x 10 '

-5 cancers plus 1.2 x 10

-5 to 2.6 x 10 prompt deaths 21 22 per plant-year. Short term deaths are those fatalities i

i 23

! that would result frc= the very low-probability accident i

(less than 9 x 10 per shipment) that results in the r - -8 l 24 ,

! 25

! release of irradiated fuel from a shipping cask.

26 Assuming that half of the cancers would be fatal, yields f

-4 -5 -4 -5 27 8.6 x 10 to 9 x 10 deaths and 8.5 x 10 to 9 x 10 28 ncnfatal cancers per plant-year.

21 -

.  : I l

i l

il The maximum accident considered by cohen and Dance, I

t ,

21 a release from a collision involving irradiated fuel O

3' followed by release of fuel from the cask, had an 4

4 estimated impact of 2.7 x 10 person-rem whole body, and 5

2 x 10 person-rem to the G.I. tract exposure. In 5l 6: addition, cohen and Dance estimate 14 promet deaths.

b 7j This would yield an estimated total of 25.4 deaths were 8 such an accident to take place. The probability of h -10 9l this accident occurring was estimated to be 2 x 10 i

_a 10j to 9 x 10 per shipment. For about 50 shipments per li Plant-year (uAsH-1238, Table 1) [46], this. yields an 11ll

'i 129 average of 3 x 10'I to 1 x 10 -4 deaths per plant-year.

13 Table s-4 estimates 0.01 fatal injury and 0.1 nonfatal 14 injury from common (non-radiological) causes, per 15 reactor-year.

16 O. Will there be any radiological exposure resulting 17 from decommissioning of nuclear power reactors?

18 A. Yes, but the exposure should not be very large. No large 19 commercial power reactors have been decommissioned.

20 .

Industry experience is limited to the decommissioning i

21 l cf several small experimental reactors. Before any l+

22 reactor now being built will be decommissioned, however, 23 much more experience will be acquired. Inevitably, l'

24 there will be advancements in the state of the art.

25 Furthermore, regulatory changes in the interin may 26 also have an impact on the health effects of decommissioning.

27 Radiation exposure of the public during decommissioning 28 . would be sexy low and would last only a short time. Binder,

~

1 et al. have estimated this dose to be 8 x 10- person-2i rem [58]. Applying the dose-response function yields

-7 ~7 3 2.3 x 10 cancers (1.3 x 10 fatal). Apportioning

~9 4 1 this among 30 years of useful life gives 7.8 x 10 5 cancer deaths among the public per plant-year due to decommissioning. Exposure to workers is greater. Binder, 6,I y et al. estimate worker exposure of 630 person-rem for g  ;

dismantling, the decommissioning method with the highest t

9l worker exposure [58]. This yields 0.14 cancers

-3 10- (0.06 fatal) or 4.7 x 10 fatal cancers per plant-year.

1 Il nl sinder, et al. have investigated accidents among 9

121 demolition workers in New York State and found an 13 average accident rate of 0.12 deaths and 10 injuries 6 If one estimates that decommissioning of 14 per 10 man-heurs.

15 a nuclear plant will require 206,000 man-hours, this leads to 0.025 deaths and 2.1 injuries [59). on an annual 16

~

17 basis this is 8 x 10 deaths and 0.07 injuries.

l' 18 0 Dr. Hamilton, please turn your attention to the health impacts of the coal fuel cycle. What assumptions 19 20 did you use in your analysis of the coal fuel cycle?

! 21 A. The fuel cycle necessary to support a coal-fired l

f 22 power station includes mining, processing, transportation l

23 to the generating station, coal storage at the generating 24 l, station, power generation, and transport and disposal of fly ash and scrubber sludge.

l 25 ll i

26 It is first necessary to quantify how much material i

27 must be processed at each step. One GWV (e) ecuals n

28 8.766 x 10' kWh of electricity produced.

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

I 1 In the United states, the energy content of coal is 2 normally measured in British Thernal Units (Btus).

3 There are 3413 Btus per kWh. If the plant operates at 4 38% efficiency, then it requires:

9 S 8.766 x '0 ' kNh x 3413 Btu = 7.4 x 10 13 Btu coal /GWy 6' O.38 kWh 7 Coal varies by about a factor of 2 in energy content, but if one takes 12,000 Btu /lb (2.0 x 10 Btu / ton) as typical, 8,

I then the annual tonnage required is:

93 13 10 7.9 x 10 Btu 6

11 = 3.3 x 10 tons coal per Gwy (e) .

12 2.4 x 10 Btu / ton.

13 c. In your reeiew of the health effects of the coal 14 fuel cycle, have you estimated the impacts to persons 15 which result from the mining, transportation and proc-16 essing of coal, and the burning of coal in power plants?

17 A. Yes, i

18 O. Let us examine the impacts from each of these ac-l 19 tivities. First, what is the impact on underground coal l

l 20 mine workers from occupational diseases?

21 A. The current average productivity rate in underground 22 coal mining it estimated to be 1.35 tons of clean coal per 23 man-hour, clean coal being the coal that leaves the proc-24 essing plant. To produce the requirement of 3.3 25 million tons per Gwy would require 2.5 million man-hours, 26 or the work of 1200 miners working 40 hours4.62963e-4 days <br />0.0111 hours <br />6.613757e-5 weeks <br />1.522e-5 months <br /> per week 27 for 50 weeks per year.

28 Coal workers pneumoconiosis (CWP) is the primary l

24 -

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

I l' occupational disease of coal miners. simple CWF is caused 2 solely by retention of coal dust in the lungs. It may 3 lead to several minor respiratory ailments, but does not, 4 in itself, seem to lead to permanent disability or pre-5 mature death. About 2% of simple CWP cases progress to 6 complicated CWP annually. This does not seem to require 7 -

further exposure and may occur even after the miner has 8 stopped working. Complicated CWP causes respiratory im-9  ! pairment, permanent disability and premature death.

I 10'! other major diseases that have a high incidence rate 11 among miners -- chronic bronchitis, emphysema, and bronchial 12 asthma -- affect the general population as well. This 13 creates a problem in attributing the cause of the 14 disease or its aggravation to occupational factors, 15 such as coal dust exposure, or to nonoccupational fac-16 tors such as the environmental and socio-economic condi-17 tions in mining communities, cigarette smoking, etc.

18 Despite extensive study of coal miners disease, 19 specific etiologies are not known. It is not clear, 20 for example, why some coal fields seem to induce higher 21 disease rates than others, although relationships with 22 rank of coal and with trace element concentrations have 23 been suggested.

24 Eecause it takes several years of exposure for disease 25 to develop, it is difficult to separate and specify caus-26 ative factors. It is difficult to maintain a cohesive -

27 population of miners for study. Mining technology and 28 conditions in the mines change over time; it is difficult

4 1 to apply associations based on even current studies to 2' mining operations today since effects measured in these 3 studies may stem from exposures over the past 20 or more 4 years. Despite these difficulties, studies of morbidity and mortality in miners are the best source of information 5l. available fron which to estimate future impacts. We re-6:

7 view the literature and draw on an analysis of Morris

8. et. al . [ 61] to derive an estimate of disease impact as-l 9 sociatec with =ining for a 1000-Mwe plant year fuel cycle.

l  !

10 Enterline reported that in 1950 U.S. coal miners had twice 11 the risk of mortality of other workers (62). Liddell 12 investigated deaths among British coal miners frc= 1961 13 and found that their overall mortality rate was lower 14 than the population of working and retired males [63).

15 standard mortality ratios (sMa's) were: face workers 16 60: other underground workers 76; surface workers 108 17 (SMR = 100 x observed deaths h expected deaths) . This 18 might be explained on the basis that only those with 19 exceptionally strong constitutions were able to work in 2f the mines. Compared to the general population, they 21 were healthier even after the effect of the mine environ-

22 ment. The mortality rate for occupational pneumoconiosis,

(

23 however, was several times that of the standard population.

l 24 The mortality rate for occupational pneumoconiosis in the 5

25 standard population was 2.2 deaths /10 . In the groups of 26 miners examined it was 1.9 to 5.6 times higher, indicating 27 an occupationally induced increase in the miner's mortality

. 5 28 rate of 4.2 to 12.2 deaths /10 . It is difficult to es-

- 2A -

n 1 timate the coal production associated with these excess l

2. deaths. The U.S. production rate for 1959 was about 2,200 l 6 3 tons / man-year or 450 man-years /10 tons, and for 1952 6

l 4 about 1,320 tons / man-year or 750 man-years /10 tons [64].

I 5 Assuming a simple linear relation, (4.2 to 12.2 excess I 5 6 6 man-years) x 450 man-years /10 tons yields deaths /10 I 6 0.019 to 0.055 excess deaths /10 tons. Using the 75 7)

I 6 8 man-years /10 ton figure, the estimate is 0.032 to 0.092 l1

! 6 E' attributable deaths /10 tons, and, assuming 3.3 million 10l tons per GWy, the estimate is 0.1 to 0.3.

11 Hollingsworth reported significant excess mortality 12: rate in a cohort of 553 miners followed from 1938 to 13 1971 [65, 66]. Hollingsworth reported the number of 14 active miners in the cohort for each year. Morris coupled 15 this with the national average production per man-year for 16 each year to estimate the total coal production of the 17 cohort [67]. The estimated effect of mortality (excluding 6

l 18 occupation accidents) was 1.7 excess deaths /10 tons (95%

i i 19 confidence interval 0.8 to 2.8) or 2.6 to 9.2 per Gwv.

l 20 Rockette analyzed mortality in a cohort of 23,000 coal 21 miners covered by UMFA Health and Retirement Funds between 22 1959 and 1971 [68]. No significant excess was found in I

23  ; overall total mortality (SMR for all causes was 101.6);

24 SMR = 100X observed dealths/ expected deaths; expected i

! 25 death based on 1965 white male mortality rates. All 26 SMR's tested for significance at the 5% level. Signif-l 27 icantly increased mortality rates were reported for lung 28 l

n l

Il and stomach cancer, non-malignant respiratory diseases, li 24 asthma, tuberculosis, accidents and ill-defined causes.

Il Si The total excess death rate for the diseases for which coal mining apparently produces increased mortality is 4{

5, 49 x 10

-5 Using the estimates of 450 and 750 man-years /

6 h 6 6 10 tons yield 0.22 to 0.37 attributable deaths /10 tons, l

Ti, or 0.73 to 1.22 per Guy.

S 0

E Summarizing the results of analysis of these studies, n

l' 9: the best estimate would seem to range from 0.1 to 2.0 10 excess deaths in coal miners per million tons or from 0.3 11 to 6 excess deaths per GWy. To take into acemmt 12 the current higher productivity of miners, these num-13 bers should be reduced by a factor of two.

14 Based mainly on British data, EASE 1224 (69] es-15 timated attributable morbidity as 0.2 cases of coal 16 workers pneumoconiosis and 0.002 cases of progressive 17 massive fibrosis per million tons. In an analysis of 18 data collected by the Appalachian Laboratory of Oc-19 cupational Respiratory Disease during 1970-71, Bohm, 20 Moore, and Schmidt-Bleek estimated 900 to 1800 miners 21 were newly disabled (both partially and totally) by 6

22 pulmonary disease [70]. With about 350 x 10 tons 23 of coal mined underground annually in preceeding years, 24 this leads to an estimate of 2.6 to 5.1 cases of at-25 tributable disability per million tons, or 8.6 to 17 26 cases attributable to the 3.3 million tons recuired per 27 uwy. This estimate seems more consistent 28 with the mortality effect estimate than those of WASH-

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

1 r 1224. One expects the incidence of disease to be re-2 duced by the implementation of the 1969 Federal Coal f A major purpose of that 3' Mine Health and Safety Act.

4 legislation was to reduce dust concentrations in the 5 mines from a national average of 7 milligrams per cubic 6, meter to less than the new limit of.2 milligrams per 7 cubic meter. The effectiveness of this Act will not 8 be known for some time because it will be necessary to '

9/ study a new generation of miners who were not exposed i

10' to the higher, earlier concentrations. Again to take 11 into account current higher productivity of miners the 12 numbers should be reduced by a factor of two and in 13 addition to get a rough approximation of the effect 14 of the new dust standards -- assuming a linear relation-1 15 ship between dust concentrations and effects which wou~d 16 give an upper estimate -- the resulting numbers multiplied 17 by 2/7. This adjustment and a doubling of productivity 18 would reduce deaths to 0.04 - 0.9 and pulmonary disease 1

19 to 1.2 - 2.4 cases per GWy.

(

l

! 20 O. What are the impacts on coal miners from mining j 21 accidents?

22 A. The average accident fatality rate for underground i

6 23 coal mining (1972-75) was 0.36 deaths per 10 tons (95%

24 confidence interval 0.33-0.40). This is 1.2 deaths 6

25 per GWy for the 3.3 x 10 tons of coal required l 26 (95% confidence interval 1.1 - 1.3 [61].. There has 27 been a steady downward trend in this fatality rate.

28 This trend provides a statistically significant fit to I

i

I the model 6

2 log (deaths /10 ton) = a + bt 3' where t is time in years.

4 Using this model with data from 1965 to 1976 yields an 5 estimate of the 1977 fatality rate of 0.33 deaths per 6

10 tons (95% confidence limits 0.27-0.41). This is 6l 1.1 deaths per GNy (95% confidence interval 7l 8 0.9 to 1.4).

h 9 Surface mining is a safer occupation. The mean ac-10 cident death rate (1965-76) in surface mines was 0.10 6

11 deaths per 10 ton (95% confidence interval 0.09-0.12).

12 This is 0. 33 deaths per plant year (95% confidence 13 interval 0. 3 - c. 4) . A clear downward trend has not 14 appeared in these data [1].

15 c. would you discuss your' estimate of accidents which 16 result from the transportation of coal by rail?

17 A. Statistics are not maintained for accidental deaths (8 . and injury in railroad transportation by type of freight 19 carried; thus, it is not possible to determine directly 20 the mortality effects of transporting coal by rail.

21 There are several ways to estimate this value. All in-22 volve assigning a proportionate share of all railroad 23 deaths'to coal transport. One way is to apportion 24 deaths on the basis of total weight or bulk of material i

25 transported. A second is to make the apportionment on l

26 the basis of miles traveled. Third, the most commonly

[

t 27 used basis of comparing transport statistics is to l

l 28 apportion on the basis of ton-miles traveled. The basis i

l

1: of comparison should be selected on criteria most likely fl This requires

to result in a realistic apportionment.

i l an understanding of how railroad associated deaths occur.

4 Over 60 percent of these deaths result from rail-highway 5 grade crossing accidents, primarily due to collisions be-tween trains and motor vehicles (7). The crucial parame-6l' then, are the number of intersections crossed and ters, 7l Sj the relative risk of an accident at each.

There is some reason to believe that unit coal trains 9l! may create different exposure situations than the average 10' 11 freight train. Coal has a greater density than average 12, freight, coal cars are generally bigger and coal trains 13 l longer than average. Train velocity may be different.

14 Unit trains generally operate on well used and raintained 15 lines and it has been suggested that they are less likely 16 than average freight trains to pass signal-less crossings.

17 Concerning the 40 percent of accidents not at grade cross-18 ings, unit trains generally can avoid hazardous switching 19 and yard operations. While one might suspect that unit 20 trains are less likely to be involved in fatal accidents 21 than are average freight trains, there is no quantitative 22 basis on which to base an adjustment.

23 24 There were 5,251 billion ton-miles of frcight move-25 ment on U.S. railroads from 1966 to 1972 [71], and 10,704 26 deaths and 46,460 injuries were associated with freight 27 traffic [72]. This yields 2.0 deaths and 8.9 injuries E per billion ton-miles. The average haul length for the 31 -

l

l t

b l

l! railroad industry as a whole is about 600 miles, but coal .

li

! 2! shipments are reported to have an average haul length of If 3 300 miles (73]. Thus, coal transported by rail results in l

- l 9

- 2.0 deaths per 10 ton-miles x 300 ton-miles per ton or 5 0.6 deaths per nillion tons transported, and 8.9 injuries I 9 per 10 ten-miles x 300 ton-miles per ton or 2.7 injuries 6'

7 per million tons transported based on the current average 8' haul distance of 300 miles. This results in an estimate '

l!

I of 2. 0 deaths and 8.3 injuries attributable to the 3.3 9"1 1

10' nillion tons required per owy.

f More recent estimates suggest calculations on a 11!

l 12! train-mile rather than a ton-mile is more realistic.

I l.

13' This leads to reduction in the above estimates by about 14 a factor of 5 [61).

I 15

16 17 18 t

19 20 21 22 23 24 25 26 Tl 28

' 4 l 1 i Q. What is your estimate of accidents resulting from l

. 2- the transportation of coal by water? ,

3 A. Estimates of mortality due to water transport were 4 made in the same manner as rail haul. The average trip 1

5 length for all domestic water-borne commerce is 325 miles.

6 No published estimates of trip length specific for barge l

l 7 transport of coal was available, but the National Coal l l

8' Association has estimated the average would be roughly 9' 100 miles. Since accidental death rates and the amount of 10 coal transported vary considerably among coastal waters, l'

! 11 the Great Lakes, and river systems, the estimates for each 12, of these locations has been calculated to be 1.4, 0.1 and l

13' 2.1 respectively. The resulting total of 3.6 deaths I

14 annually results in an estimate of 0.04 deaths per million 15 tons transported, or 0.13 deaths per Guy.

16 o. Have you looked at the impacts from a coal slurry pipe-17 line?

18 A. Yes. Slurry pipeline accident rates have been estimated f

i 19 by EPA to occur at a rate of 0.0019 fatalities and 0.0032 non-

! 12 Btu transported. Health damage is 20 fatal injuries per 10 21 entirely occupational.

1 22 one Gwy converts to a coal requirement of 7.9 x 10 23 Btu, assuming a plant efficiency of 38%. This allows con-24 version of the above rates to 0.15 deaths and 0.25 injuries l 25 per GWy. The average length of proposed slurry pipelines is I

26 700 miles; thus, assuming typical subbituminous heat content 27 of 10,000 stu/lb, one Gwy is equivalent to 700 miles x 4.0 6 9 Using this factor for 28 x 10 tons = 28 x 10 ton-miles.

O s

-11 -11 1 renormalization yields 5.4 x 10 deaths and 9.0 x 10 2 injuries per ton-mile.

3 Although the numbers of accidental deaths per unit 4 energy in coal transport can approach that in mining, the 5 level of individual risk is much lower due to greater 6 numbers of exposed individuals.

b No air emissions are directly attributed to the transfer 7l-g of coal by slurry pipeline under normal operating conditions.

9 The pump stations, located 100 to 160 km !%) to 100 miles) 10l. apart, are electrically powered. Noise from pump stations 11 is not considered an offsite problem since these stations 12, are usually located in remote areas and the buildings in 13 which the pumps are housed provide a shield to reduce the 14 noise.

15 Because availability of water in the western states is 1 16 relatively low, the matter of water usage raises the most 17 controversy concerning possible the operational impacts 18 of slurry pipelines. The exact impacts of water withdrawals 19 for a slurry pipeline have not been determined.

I 20 ' Another concern is the possibility of an accidental 21 release of slurry by a pipeline break or pump station 22 malfunction. The slurry could cause damage to agricultural 23 crops or local vegetation, and the runoff could adversely 24 affect nearby water bodies.

25 A pipeline break could cause fine particles of coal to 26 be spread over the surface of the soil and to be mixed 27 with it. The surface particles may prevent absorption of l water into the soil. Additionally, the fine particles 28

s y may become a source of fugitive dust, l Use of saline water in the slurry involves an additional gl 3

i '""if ^**"t*1 h***#d if

• P i P*li"* hr**h CC"#8 fl di"9 4

of alkaline soils in arid areas even in a one-time release e uld c nsiderably worsen their suitability for vegetation.

5 6

In good soils, however, absorption of salts would have less 7

effect, and impacts would diminish with progressive rainfall.

i g The potential. rupture of a coal slurry pipeline is an g unsolved environmental problem, although the technology gg for monitoring breaks is sophisticated enough to prevent gi their occurrence under normal circumstances. Protection g from internal and external corrosion is provided by use of high-grade welded seamless pipe of adequate wall thickness, 13 34 by protective wrapping of the pipe, by use of corrosion 15 inhibitors and cathodic protection during operation, and i 16 by placement deep in the ground.

17 At the power plant the slurry must be dewatered, a 18 particularly difficult aspect of slurry pipeline operation.

19 com nly encountered problems include: (a) loss of coal l

l 20g fines through the system from inadequate flocculation; and 21 (b) removal and plastering in feed ducts and boiler when l 22 the coal remained too moist. The higher the moisture content l 23 of the coal, the greater the heat loss through the boiler.

24 Coal fines discharged to a waste pond can <ause ft tea l

l 25 dust emissions if the water is allowed to evarorate.

26 The dewatering of slurry and treatmert of coal fines 27 pose continuing problems likely to be encountered with 28 future pipelines.

i I

1h The literature indicates that a variety of chemicals l 2j!' may be added to coal slurry to prevent corrosion of the h i 3,! pipeline, to improve the velocity of the slurry and o

to maintain pH. Chemicals for this purpose include 4l1  !

5 chromates, phosphates and various organic compounds.

6; Dese rates may be as high as 1000 ppm.

O 7:l Dissolved solids in slurry water include natural

, SjI impurities, soluble components of coal, corrosion products I'I from the pipeline and additives. Mineral species in the coal 9l can include a range of soluble metals such as iron, aluminum, l 10' 11 calcium, sodium and manganese, as well as anions such as 12 chlorides, sulfates and carbonates. Dissolved organic 13 compounds have not beer. specifically identified.

I 14 At the power plant , use of clarified slurry water as 15 part of cooling tower makeup has the potential for releasing i 16 metals into the atmosphere. Disposal of this water as 17 blowdown from cooling towers may also present a problem 18 if the water is leacned underground from the storage ponds.

l 19 The severity of these problems depends on the trace metal 20 content of the slurry water and the extent to which it 21 is concentrated. Additional study is needed to determine 22 the ef fects of metals discharge in coal slurry water.

23 Q. What estimate of accidents have you made for workers gg in coal processing plants?

25 A. Based on 1965-75 experience estimated accidental death 6

26 rates in coal processing plants are 0.021 deaths /10 tons 27 input to the plan: (95% confidence interval 0.017 to 28 '

O.027) [61]. Accidental injury rates in coal processing l

l l l 1 f

6 I plants are 1.3 disabling injuries /10 tons input to the 2 plant (95% confidence interval 1.0 to 1.6) (1965-73 mean).

3 This leads to estimates of 0.07 deaths and 4.3 injuries li 6

! 4 for the 3.3 x 10 tons coal per GWy.

I 5

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1 0. What estimates of air pollution effects have you 2 made which would result from power generation at a I

3! coal- fired power plant?

4 A. Coal combustion results in the emission to air 5 of a wide range of pollutants, including particulates, 6 So . No , CO, polycyclic aromatic hydrocarbons (PAH),

2 x 7 and trace elements such as iron, mercury and cadmium.

8 These primary pollutants contribute to atmospheric 9 chemical reactions producing secondary pollutants such as 10 ozone, sulfate, nitrate, and peroxyacetyl nitrates (PAN).

11 Federal New Source Performance Standards (NSPS) limit 12 emissions of particulates, So , and NO [74).

2 x 13 State standards may be more restrictive in some geographic 14 areas than Federal standards.

15 The full health and environmental impact of emissions 16 from coal-fired electric power plants has not been assessed, 17 but estimates have been made of the impact of some of the i

18 emissions.

19 There is considerable evidence linking sulfur-par-20 ticulate air pollution with health effects. It is cur-21 rently hypothesized that the causative agents of this l

22 linkage are sulfate compounds, both directly emitted

, 23 and produced by oxidation of SO in the atmosphere.

l 2 l 24 This hypothesis is detailed in an EPA position paper 25 [75]. Other power plant pollutants may also be harm-l 26 ful to human health. Thus, based on comparison with 27 studies of the effect of cigarette smoking, Lundy [76, 28 77] has estimated the effect of polycyclic aromatic emis-l t ,

i

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

. t I

sions for a coal-fired power plant. Since it is uncertain whether all, or whether part of these effects are the 2

3-N same effects attributed to sulfur pollutants, we have not added them to avoid possible double counting. We use 4

5 estimates of the health ir. pact of sulfate pollution from coal-electric pcwer plants developed at Brookhaven National 6;l.

7j Laboratory based on linear regressien studies of the type gi t

conducted by La.ve and Seskia [78,79]. These studies b correspond to air pollution and other environmental and 9'

and socio-economiu factors with mortality in U.S. Standard

! 10l Metropolitan Statistical Areas (SMSA). An analysis of 11' 12 these and similar studies for consistency was made by Finch 13 and Morris [30). The latter report derives an early version of the damage function used here. The Lave and Seskin 14 15 studies are subject to rethodological problems (e.g.,

16 assuming uniform -- or proportional -- pollution exposure 17 and socio-economic patterns over all SMSA's, using a 18 single air monitoring station to represent the pollution 19 exposure for an entire SMSA, not including important 20 pollution variables). Equally as great a problem is 21 the poor cuality of the pollution measurements (from ,

22 the National Air Monitoring Network) used in the studies.

23 Major problems include adsorption of So 2 onto the filter followed by oxidation of the 50 to sulfate (resulting 24 2

25 in a varying, but positive, bias in sulfate level, 26 leading to an underestimate in the dose-response func-27 tion); potential variability amont blanks (leading to pos-28 sible errors of unknown magnitude and direction); loss 1

1 i

l 1 of material from the filter during the interval between 2 samplinc and analysis (negative bias of unknown magnitude i

3 leading to possible overestimate in dese-response function):

4 and errors due to variation of collection efficiency with wind speed and direction [811 Inclusion of different 5l socio-economic variables [82) and use of alternate regres-6.

7 sion techniques (83] can lead to changes in the estimate. The j gj geographic scale of the analysis may be a factor. Lipfert re-h g: ports that when a similar analysis was done at the scale 10 of cities rather than SMSA's, the sulfate effect disap-11 peared, although the combined effect of all sulfur and 12 particulate pollutants generally remained the same [84).

13 It seems clear that there is a health effect produced 14 by the sulfur-particulate mix. Standing alone, the re-15 gressions studies are inadecuate to ascribe this effect 16 to sulfates. Toxicological studies [85-87], which find 17 effects of sulfates far exceed those of SO or inert 2

18 particulates or combinations of the two, provide a stronger 19 base of support. The regression studies then provide 20 a means of calibrating the magnitude of the effect.

21 We have not attempted te disaggregate sulfate ex-22 posure-response by specific compound because I be-23 lieve the data available to be insufficient. Toxi-24 cological studies indicate that the specific chemical l

25 form and particle size of sulfates can have a major 26 effect on the exposure-response function [85-871 since 27 sulfates formed from oxidation of atmospheric SO (the 2

2B source of most sulfates due to coal combustion), are

f

. 1 1 in the respirable size range and are in more toxic 2, cremical forms [85] than larger sized wind blown dust 3 and sea salts [s7A1, included in general urban air, it 4l seems likely that sulfate compounds produced by coal I

5- combustion in power plants are at least as toxic as the b

6: total sulfate measured in urban areas.

N 7- Local effects within 50 miles due to sulfate air 3, pollution were estimated in a stochastic model developed I

g at Brookhav4:n by Morgan and co-workers [88]. This model b

10 is similar in foem to that used by North et al. [89),

11 F ;t considers uncertainty in meteorological, air chemistry 12 and health damage functions.

13 The model is linear in sulfur emission rates and in 14 exposed population. If one adjusts emissions to match 15 those from low sulfur coal coupled with Best Available 16 Control Technology (BACT), scaling linearly in our healths 17 effects estimates leads to an annual impact within 80 km 18 of 0.3 deaths per GWy per million people exposed for a 19 northeastern site. Since the average population within 20 50 miles around power plants in U.S. is 3 million, this 21 leads to a national average of 0.9 deaths per GWy.

22 It is important to repeat that these effects es-23 timates are limited to the 50 mile (80 km) radius around 1

' 24 the site. sulfates emitted from tall stacks are subject 4

25 to long-range transporr. It has been suggested that a 26 substantial fraction of the high sulf ate levels in North-27 eastern cities results from long-range transport of power 28 plant emission [90]. This is an area of intense current

I research. Preliminary results of modeling studies at 2 Brookhaven suggest that the health impact, due to 3 long-range transport of sulfates beyond the 50 mile 4 (80 km) radius of a power plant may be as much as an 5 order of magnitude higher than the impact within the 50 6 mile (80 km) radius [3,91). Thus one would estimate the 7 central value for total health effects of air pollution

! frem a GWy (e) using low sulfur coal combined with BACT, 8

9, to be 9 annual premature deaths.

10 Other estimates have been reported. EPA has proposed 11 a set of best judgement air pollution dose-response 12 functions based largely on the CHESS studies [92-94).

13 These are generally for short-term effects. Note that 14 the EPA dose-response function for mortality is based 15 on studies linking increases in daily deaths with daily 16 air pollution. This is not directly comparable to the 17 BNL estimates which are based on studies linking annual 18 average air pollution with annual mortality rates. There 19 is no definitive study available which estimates the 20 amount of life shortening associated with an air pollution 21 related death. Daily increases in death rates may rep-22 resent people who would die anyway within weeks. It 23 has been suggested that while the population susceptible 24 to death during air pollution episodes probably has 25 severe respiratory disease, death is not necessarily 26 imminent. Susceptible people might live as many as .

27 20 additional years in the absence of additional stress 28 caused by an air pollution episode.

J 1 The linkage of increased deaths on days with high i

2 air pollution levels (or days following high air pol-3 lution) with the air pollution level is based on the 4 hypothesis that the additional stress of an air pollution 5 episode is sufficient to cause death in susceptible in-dividuals. Susceptibles are presumably those with 6l.

7' severe heart and/or respiratory disease. The theoretical 8 basis for linking increases in long-term (annual) mortality 9 rates with increased annual average air pollution is dif-10 ferer. and more comprehensive. I hypothesize that air 11 pollution produces respiratory disease, creating a popula-t 12 tion with increased susceptibility to any stress. Thus 13 air pollution may result in an increase in premature 14 deaths not specifically linked with air pollution, and 15 not necessarily occurring on days with high air pollution.

16 This increase in susceptibility is likely to result from 17 years of exposure and may continue years af ter exposure ends.

18 0 What are the impacts from radionuclide emissions from 19 coal-fired power plants?

20 A. Coal contains trace amounts of uranium-238, uranium-235, 21 and thorium-232, and, of course, the daughter radionuclides 22 in the three decay series which ther head. These radio-23 nuclides are contained in the ash which escapes frc= the 24 stack. They can then be transported through the environ-25 ment and expose the general population by direct external 26 radiation or internally via inhalation and ingestion.

27 The Environmental Protection Agency has prepared 28 an assessment of the human health impacts [99]. The

I assessment is a modelling effort based primarily on the 2 AIRDOS ccde of Oak Ridge National Laboratory. One of the facilities modelled is a "new" coal-fired power station.

3 4

The model plant has a bottom / fly ash partition coefficient of 5

20%/80%, 35% thermal efficiency, 99% particulate control 6

efficiency, and burns Western U.S. bituminous with 975s Btu /lb 7

heat content, 1.9 ppm natural uranium content, and 5.0 ppm thorium content. Health effects are assessed for plant loca-g g

tion at four sites with dif fering populations within 50 miles 10 and differing food production and consumption patterns: urban 11 (17,100,000 people), suburban (2,490,000), rural (592,000) and rem te (11,900). Af ter renormalizing to one Gwy (e) , the EPA 12 results are 0.294 (urbsn), 0.024 (suburb an) , 0.007 (rural),

13 and 0.0001 (remote) car.cer fatalities per GWy. Since 14 the d se is dominated by lung and bone doses, these figures 15 can also be used to represent cancer incidence.

16 Q. What are your conclusions regarding the comparision 17 of health effects of the coal and nuclear fuel cycles?

yg gg A. In the nuclear fuel cycle, the major health effect is in the mining of uranium. In the coal cycle, when one in-20 21 cludes the long-range transport of pollution, the major health effect is on the general population from the 22 electricity generating plant.

23 Nevertheless, in concidering the human damage pro-24 25 duced by a single electric generating plant, although 26 in the coal cycle air pollution is usually the largest 27 proportional contributor to deaths, in actual numbers the ef fects are very small. Thus in a population of 28

1! three million people within 50 miles of a plant, including 2,h those working at the plant (65% capacity factor) one 1

3 would expect 30,000 deaths from all causes each year.

4 of these, one estimates that 0.7 (0.02-3) could be 5 attributed to a 1000-Mwe coal plant, and 0.21 to a 1000-6 Mwe nuclear plant (the latter figure being the effect on 7 i the entire U.S. population and including catastrophic I

81 accidents). Again, for overall perspective the annual b

9 mertality rate from all causes is approximately 0.0095.

3 10 This rate would increase in the population within 50 miles 11 i of0s coal-fired plant by 0.0000002, whereas with a nuclear 12ll plant if one assumed that its total effects were con-13l centrated in the three million people within 50 miles, 14 the rate would go up by 0.00000007 or not at all.

i 15 i

16 17 18 19 20 21 22 23 24 25 26 27 28

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

1 Q. Dr. Hamilton, did you do a similar comparison of nuclear  ;

i 2 versus coal health effects based upon site specific parameters 3 at the ACNGS site?

4 A. Yes.

5 Q. What assu.mptions did you use for your comparison in terms 6 of types of plant?

j 7' A. Tables S.D. 4 and S.D. 5, pages S.D-4 and S.D-5, of the 8 Final Supplement to the Final Environmental Statement (FSFES)

{.

9' give the parameters of the alternative nuclear and coal power 10 i plants to use in making environ = ental assessments. The

, 11 nuclear station wor.1d be a single 1146 MWe (net) capacity 12 unit with a thermal efficiency of 0.32 and a capacity factor 13 of 0.60. Thus 0.6876 GWy electricity would be produced per 14 year. The coal alternative parameters are identical except 15 that two 573 fM units are used operating with 0.38 thermal 16 efficiency.

17 Q. In evaluating the health effects of the 1146 MWe nuclear 18 plant at the ACNGS site, what calculation technique did you

19 use for radiological effects?

! 20 A. The effects from the part of the nuclear fuel cycle other 21 than the power station itself are obtained by multiplying the 1

22 values set forth at pp. 12-23 by 0.6876 to reflect the output 23 of ACNGS. The radiological health effects from oceration l

[ 34 of the nuclear station are obtained by multiplying the esti-25 mated population dose as given on page S.5-28 of the FSFES by l 26 appropriate dose response functions discussed at pp. 7-e.

! 27 Q. What were the results of your evaluation?

l 28 A. The results are set forth in Table 1 attached to this 46 -

L

__ _ _ =

I testimony. Table 1 generally summarizes for a nuclear 2 plant, at the ACNGS site, the results of the nuclear fuel 3 cycle evaluation which I discussed earlier including 4 assumptions regarding non-radiological injuries and deaths.

i 5 As you will note, the radiological and non-radiological 6 effects of the nuclear plant and its associated fuel cycle I 7 account for 10.8 excess morbidity / injuries and 3.68 deaths 8 per year of plant operation.

9 Q. Describe your approach to evaluating the health effects 10 of the two 573 MWe coal plants.

11 A. We ran a Gaussian plume dispersion model using 1972-12 1975 meteorological data from the Allens Creek FSFES and 13 the Rice center-Dames and Moore population estimates (the 14 first 10 mile ring was assumed to have zero population; 15 this simplification will have little effect on the output).

16 The plant was assumed to have a 200m stack, 6m in diameter, 17 emission velocity 20m/sec, stack gas exit temperature 18 400K, and ambient outside temperature 290K. The fuel was 19 assumed to be Texas lignite with a 0.95% sulfur content 20 and 7469 stu/lb coal energy density [98], for an overall 21 emission rate of 177 gGO /sec.

2 The model bases the health 22 effect on population exposure to sulfate particles with a 3

23 damage function of 3 attributable deaths per 10$ person-ug/m 24 sulfate. Sulfate exposure is calculated in the model by l

25 assuming 1.5% of the sulfur is initially emitted as sulfate l is transformed in the atmosphere to 26 and the emitted SO 2 l 27 sulfate at a rate of 1.7%/hr. So 2

and sulfate loss rates 28 were assumed respectively to be 2%/hr and 0.5%/hr.

l j .

i

. 1 I

1! The result was a population weighted average exposure 2 of 0.025 ug/m 3

sulfate. Applying the health damage function 3 (see p. ) yields an eatimate of 0.3 deaths per year 4 attributable to plant air pollution within the 50 mile 5 radius. Based on an expected total mortality using average U.S. mortality rates, this would mean an increase of 0.0014%

6-l' in the total mortality rate of the population. Increase in 7

l

! g incidence of respiratory disease morbidity would be at least g; equal to the increased mortality of 0.3 cases per year and m re likely is about 5 times this value or 1.5 cases / year.

10 Frcm previous estimates of uncertainty associated with this 17 type of estimate, one would put 90% confidence limits on the 3

13 m rtality estimate of 0 to 1.6 attributable deaths per year.

The results of our evaluation are reported in Table 2.

14 Q. Have you made any other adjustments or assumptions in your 15 16 evaluation of the coal health effects?

17 A. In Table 2 for Texas lignite, and in Tables 3-5 for other 18 coal-fired alternatives which I discuss below, the coal i

I 19 tonnage requirements are adjusted by the heat content of the

(

20 specific kind of coal. The health effects due to sulfur l

21 emissions from the coal station alternatives were obtained 41, assuming 22 by running the Brookhaven model discussed at p.

l 23 90% sulfur emission control, and the appropriate sulfur and 24 heat content. Texas lignite, for example, averages 1.14 lbs.

6 Btu and 7469 Btu per lb.

25 sulfur por 10 26 0 Does the radioactive content of coal contribute to adverse 27 health effects?

28

1 A. Yes. The Texas lignite sample averages on a whole coal

2. as received basis (99] are 1.69 ppm natural uranium, 4.58 pom 3l thorium, and 11.3% ash content. The EPA airborne radionuclide 4 assessment [99] " suburban site" is very close in character to 5 the region around Allens Creek. Scaling the EPA result of 6 O.024 cancer deaths per GWy by 0.6876 GWy/ year; 38% versus 35%

7l' thermal efficiency; 11.3% versus 12.0% ash content; 7596 Btu /lb 8 versus 9755 Stu/lb; and 1.69 ppm uranium versus 1.9 p;n; yields 9 0.019 deaths per plant year.

10 Q. What population estimates did you use in arriving at the f

11 results shown in Tables 2-57 12 A. The coal effects model was run for both the new (Rice-13 DsM) population estimates for 1980 and the older estimates 14 (T3WD7 7) used in the FSFES. The result from the former is 15 reported in the Table 2 as 0.30 deaths / year attributable to 16 sulfate air pollution from the coal plant fired with Texas 17 lignite. The latter population estimate results in 0.24 10 deaths / year, 20% lower. Since the effects of the nuclear 19 plant were based on older population estimates, this 20%

20 upward bias of the coal effects should be considered in 21 making a comparison between the two, although the difference 22 in considering this effect is essentially insignificant.

23 Q. Did you evaluate the health effects of the use of any 24 other coal resources?

25 A. Yes. We looked at surface-mined coal from New Mexico and 26 Wyoming and Texas bituminous from the North 27

• Central area of the state.

28 Q. What are the chara,.:teristics of the New Mexico and Wyoming l-l Ir

• v l

a .

I coal?

2 A. The reserves and sulfur content are shown below by coal 3 rank (100):

4 RESERVES AND SULFUR CONTENT  !

5 6 new Mexico Wyoming Bituminous Subbituminous Bituminous Subbituminous 7 250 2008 0 23740 Reserves 8

(106 short ton) 1.02 Sulfur content (%) 0.67 0.88 -

g Sulfur / heat content (% per 1.02x10 -4 BTU /lb) 0.54x10 ' O.88x10-4 -

10 11 Over 90% of the available strippable coal reserves are Wyoming 12 subbituminous. For Wyoming coal, we assumed 10,000 Btu /lb 13 coal with a sulfur-to-heat content ratio of 1 x 10-4 and a 14 haul distance of 1250 miles by unit train. For New Mexico 15 coal, the weighted averages are 0.78% sulfur, 10,277 BTU /lb, 16 0.76 x 10-4 %S per Stu/lb and a haul. distance of 1,000 miles, 17 Q. Did you calculate the health effects associated with i 18 burning Wyoming subbituminous coal?

19 A. Yes. They are reported in Table 3. I used the same f

20 damage factor employed in my calculation of the health effects l

21 of burning Texas lignite and the same assumptions with regard 22 to meteorology and plant parameters.

23 C. Did you evaluate the health effects of using New Mexico 24 coal?

25 A. Yes. The results are reported in Table 4. I used the 26 same assumptions employed in connection with my evaluation 27 of Texas lignite and Wyoming strippable coal.

2B Q. Did you perform a comparable analysis of Texas bituminous l

l

I coal?

2. A. Yes. However, we have no characterization data for this 3 coal. We assumed typical low-sulfur bituminous coal (1%

4 sulfur and 12,500 Btu /lb and a haul distance of 500 miles 5 by unit train. The health effects are summarized in Table 5.

6 0 In reviewing Tables 2-5, there are differences in the 1

7 health effects associated with the different coal resources.

8 To what is this attributable?

A. Variations among the four coal alternatives are due l 9l-10 mainly to specific heat content (higher value decreases mining accidents and air pollution per unit electricity output),

11 i sulfur content, and haul distance.

12 13 Q. Can you summarize the results of your evaluation of l the health effects of the operation of a nuclear plant versus 14 15 the alternative coal fired units at the Allens Creek site?

i A. Yes. The results are summarized in Table 6 and, in each 16 instance, take into account the associated fuel cycle. In

! 17 i 18 general, although nuclear has a slight advantage, none of the 19 alternatives is a statistically significant contributor to 20 morbidity and mortality rates in the population within 50 21 miles of the plant.

22 l

23 t 24 25 26 27 28 gp C*

t TA3? E 1 AOVERSE EEALTH IPPECTS PER TEAR OF PLANT OPERATION Nuclest .

Excess Morbiditv/In juries Excess Deaths Process Mining

• Occupa:lonal 0.10 Radiological 0.12 4

Nonradiological 0.15 Accidents 6.81 0.14 0.038 Disease 0.13 Public 0.20 Processing

• Occupational 0.034 Radiologi:a1 -0.064 1.6 0.004 Nonradi:1cgical 0.003

~0.006 Publi:

Transper:a:icn Radi:* gi:a1 (included under pcwer plan:)

0.1 0.01 Nenrafielegical P ver Plan:

Radi:1:gi:a1 0.05 Occupa:ional 0.11 0.03 0.015 Public Nonradielegi:a1 0.013 Occupa:icnal 1 31 Waste Management <0.001 Radiolegical <0.001 n.c. n.c.

Nonradiological 0.07 0.005 Dec ==issi:ning 0.20 0.10 Catas:rophic Power Plant A::idents (ae:uarial risk) 10.8 0.68 TOTAL

• Heal:h ef f ects of low level but long te ns saissions 'of raden-222 included.

f rm:

i abandoned open pit sines and stabilized mill tailings not t

(

- S2 -

• ~ '

D** '*b Y n

%g ,a D l

- n,-_ . . - - .- , . - -

Table 2 A"!!ESE HEALW EFFEC-75 PER YEAR OF PLANT OPERATIO';

Texas Lignite .

Excess Morbidity /In juries Excess Deaths Process Surface sining 18.8 0.36 Occupa:1onal accidents Processing 0.08 Occupa:1enal a::iden:s 4.7 Transper: (rail, 100 miles) 0.15 0.64 Ae:iden:s 1

Power Plant 0. 3 Publi:, air pollu: ion 1.5 0.02 0.02 Public, radienuclides 0.1 Occupa:icnal accidents 3.3 i

29.0 1.01 To:a1 f

f l

I l

l I

i

.53 -

2 t

6

._ . . . ~ . -- _ _

4 Table 3 A0 VERSE 121.C4 EFFIOTS PER YEAR OF Pl. ANT OPERATION i

k'yo ing Subbituminous Process Excess Merbidity/Infuries Excess Deaths _

Surface mining 14.0 0.27 Oc:upational 4::1 dents Prc:essing

3. 5 0.06

! Occupa:ional a::idents Transport (rail, 1250 rdles) 1.36

6. 0 Ae:idents i

Pcver Plan 0.27 Public, air pc;!utien 1.35 0.02 0.02 Public, radienuelfdes 0.1 0::upational accidents 3.3 28.2 2.08 Tc:a; i

0 m

~ ~ ' ' ' ' ' * ' ^ r n - _, __ _ , _ _ _ _

• Table 4 A *iERSI REA1.Tri EFFIOTS PER YEAR OF PLANT CPERATION New Mexico Bituminous and Subbituminous

• 1 Excess Morbidity / Injuries Excess Deaths Process Surface mining 0.26 Oc:upational accidents 13.7 Precessing 0.06 Oc:upa:ional acciden:s 3.4 Transpor: (rail. 1000 miles) 3.87 1.06 Acciden:s Power Plant 1. 0 0.2 Public, air pellution 0.02 0.02 Public, radi:nuclides 0.1 Occupa:icnal a::idents 3.3 25.3 1.7 To:a1 i

1 e

i i

d e

55 -

Table 5 i

ADVERSE HF.C.T:! EFFECTS PER YEAR OF Pl. ANT 0? IRA!!ON Texas Bituminous Excess Morbidity / Injuries Excess Deaths Process Surface mining 0.21 occupational accidents 11.3 Processing 0.05 occupa:ional accidents 2.8 Transpor: (rail, 500 :ciles) 0. /.4 Accidents

.l.9 Power Plan: 1.05 0.21 Public, air po!!u:fon 0.02 Public, radionuclides 0.02

3. 3 0.1 Occupational accidents 20.4 1.03 Tc:a1 t

{

l l

t N

i i

- 56 -

i

(

Table 6 i

e CO.WJARATIVE HEA1.Td ASSESSMENT Excess Morbidity / Injuries Ex:ess Deaths Alternative 10.8 0.68 A. Nuclear 29.0 1.01 ,

3. Texas Lignite 28.2 2.08 C. Wyo:ing subbitu inous 25.3 1.70 D. New Mexice coal 20.4 1.03 E. Texas bi:u=inous l

d i

[

l l

I I

57 -

1 2 REFERENCES 3

4 1. Hamilton, L.D., ed., The health and environmental 5 effects of electricity generation - A preliminary report, i

6' BEAG-HE/EE 12, BNL Report No. 20582, Biomedical and 7 Environmental Assessment Group, Brookhaven National 8 Laboratory, Upton, NY, 1974.

9 2. Hamilton, L.D. and S.C. Morris, Health effects of 10 fossil fuel power plants, Proc. Symp. Population 11 Exposures, CONF 741018, Knoxville, TN, 1974, p. 317.

12 3. Hamilton, L.D., Alternative sources and health in 13 Ed., R. J. Budnitz, CRC Forum on Energy Session II, U.S. Electricity through the Year 2000: Coal or Nu-14 15 clear?, crc Forum, CRC Press, Inc., cleveland, Ohio 16 44128, 1977, pp. 1-49.

17 4. Hamilton, L.D., Assessment of risk of damage to the 18 environment in Environmencal Damage Costs, Record 19 of a Seminar held at the OECD in August, 1972, l 20 organization for Economic cooperation and Develop-21 ment, Paris 1974, pp. 264-281.

22 5. Ionizing Radiation: Levels and Effects, Vol. 1 and l 23 2, Report of the United Nations Scientific Committee 24 on the Effects of Atomic Radiation to the General 25 Assembly, United ~ Nations, N.Y., 1972.

26 6. Brown, W.M. Court and R. Doll, Mortality from cancer 27 and other causes after radiography for ankylosing l

28 spondylitis, Br. Med. J. 2,.1327,.1965.

! l-l

1 2 7. Environmental Analysis of the Uranium Fuel Cycle, 3 Part III, Nuclear Fuel Reprocessing, EPA 520/9-73-003D, 4 USEPA, Washington, D.C., 1973.

5 8. Reactor Safety Study, Appendix VI, WASH 1400 (NUREG 6 75/014), U.S. Nuclear Regulatory Commission, October 7 1975, pp. 67, 8.

8 9. Final generic enivornmental impact statement on the 9 use of recycle plutonium in mixed oxide fuel in light 10 water reactors. (GESMO) U.S. Nuclear Regulatory 11 Commission (NUREG 0002) , August 1976.

12 10. Hamilton, L.D., OECD, 1974 op cit.

13 11. BEIR, The Effects on Populations of Exposure to Low 14 Levels of Ionizing Radiation, Advisory Committee on 15 the Biological Effects of Ionizing Radiation (BEIR).

16 Division of Medical Sciences, National Academy of 17 Sciences. National Research Council, Washington, D.C.,

18 November 1972.

i 19 12. " Environmental Analysis of the Uranium Fuel Cycle, l

20 Part I -- Fuel Supply," Office of Radiation Programs, 21 U.S. Environmental Protection Agency, EPA-520/9 22 003-B, October 1973.

l l 23 13. Cohen, S.C. and K.D. Dance, Scoping Assessment of f

24 the Environmental Health Risk Associated with

( 25 Accidents in the LWR Supporting Fuel Cycle, Teknekron, l

l 26 Inc., Washington, D.C., November 1975.

i 27 l

l 28  !

l l

l 1

l - er

1 .

I 2h 14. Cohen, B.L., " Conclusion of the BEIR and UNSCEAR 3 Reports on Radiation Ef f ects per Man-Rem," Health 4 Physics, Vol. 30, pp. 351-52, 1975.

5l, . 15. Binder, D.J., et al., Testimony before N.Y. State 6l. , soard on Electric Generation Siting and the Environ-7 ment on Jamesport Units 1 and 2, LILCO, March 1977, 3 p. A-6.

I gi 16. Sources and Ef fects of Ionizing Radiation, United 10 Nations Scientific Committee on the Effects of 11 Atomic Radiation 1977 Report to the General Assembly, with Annexes, United Nations, New York, 1977.

12 13 17. GESMO, pp. IV J(E)-1 to IV J(E)-8; NRC, "Modifica-tion to Table IV J(E)-1 and corollary changes result-14 15 ing from 210Pb MFC correction," 3 April 1977.

16 18. GESMO, p. IV J(E)-17.

17 19. Environmental Analysis of the Uranium Fuel Cycle, 18 Part III, Nuclear Fuel Reprocessing, EPA 520/9-763-19 003D, 1973, p. C-16.

20 20. BEIR III, Committee on the Biological Effects of Ionizing 21 Radiations, the Effects on Populations of Exposure to Low 22 Levels of Ionizing Radiation, National Academy of 23 Sciences, Washington, D.C. 1980 24 21. American Physical Society, Nuclear fuel cycles and waste 25 management, July 1977, Appendix IV, p. 23.

26 22. Ibid., Chapter V, p. 19.

27 23. Holaday, D.A., Evaluation and control of radon daughter hazards in uranium mines. U.S. Department 28

I 1:

2 Health, Education and Welfare publ. (NIOSH-75-ll7),

3 November 1974.

4 24. Potential radiological impact of airborne releases 5 and direct radiation to individuals living near in-active uranium mill tailing piles, EPA 520/1-76-001, 6,l l

7! 1976, p. 38.

i 81 25. Federal Radiation Council, Guidance for the control b

9' of radiation hazards in uranium mining. Rep. No. 8, 10,; FRC, Washington, D.C.

11 26. 41 FR 22430, June 3, 1976.

12: 27. APS, oc cit., Chapter V, p. 19.

1 13 28. GESMO, p. iv, F-18.

14 29. Miller, H.T., Radiation associated with surface min-15 ing for uranium. Health Physics 32: 523-527, 1977.

16 30. GESMO, p. iv. F-16.

17 31. GESMO, p. iv. F-19.

l 18 32. BEIR I, p. 171.

19 33. Binder, D.J., et al., Testimony before the New York 20 State Board on electricitf generation siting and 21 the environment. iiarch 24, 1977, LILCO, p. A-19-20.

22 34. Comparative Risk-Cost-Benefit Study of Alternative 23 Sources of Electrical Energy, WASH-1224, _1974, pp. 5-33.

24 35. WASH-1224, pp. 3-70.

25 36. GESMO, IV J(E)-17.

26 37. WASH-1224, Table 3-6, pp. 3-67.

27 38. Binder, D.J., et al., p. A-20-A-27.

28

i

• 1 l

1 2 39. Archer, V.E., et al., Radiation and Smoking Relation-3 ships to lung cancer in uranium miners. Unpublished.

4 Cited in Binder et al., on cit.

5 , 40. Gotchy, R.L., Testimony before the Atomic Safety I

1 and Licensing Board, September 20, 1977. Shearon 6

I 7 Harris Plant, Carolina Power & Light.

.l

41. Binder, D.J., et al., Testimony before New York State 8[

l 9d Board On Electricity Generation Siting and Environ-h LILCo, March 24, 1977.

10.' ment.

11 42. Council on Environmental Quality, Energy and the Environment: Electric Power. Washington, D.C.,

12 13 August 1973, p. 57.

14 43. Bertolett, A.D..'and R.J. Fox, Accident Rate Sample Favors Nuclear. Electrical World 182:40-41, July 15, 15 16 1974.

17 44. Final Generic Environmental Statement on Use of 18 Recycle Plutonium in liixed Oxide Fuel in Light Water i Cooled Reactors. NUR2G-0002 Vol. 1, U.S. Nuclear j

19 I

20 Regulatory Commission, August, 1976, Table S(A)-1.

21 45. 10 CFR 51, Table S-4.

22 46. WASH 1238: Environmental survey of transportation 23 of radioactive materials to and from nuclear power 24 plants. U.S. AEC Directorate of Regulatory Standards, i

I 25 December 1972. This report was the basis of the 26 Commission's transportation rule codified in 10 CFR 27 Part 51,- Section 51. 20 (g) and Table S4.

l l 28 l

l -

l

~ ,

a e -n , - , , - - . , , .

a -- , -- g ----,--- ,s , , , y -

1 l

2J 47. Enviro mantal analysis of the ure.nium fuel cycle c 3l' Part III Nuclear Fuel Reprocessi.1g. EPA 520/9 4 003D. USEPA, Washington, D.C.

5 48. WASH-1238, oc cit., p. 9.

49. 10 CFR 51, Table S-4, Note 4.

6l 7 50. Cohen, S.C. and K.D. Dance, Scoping assessment of 8 3 the Environmental health risk associated with acci-dents in the LWR supporting fuel cycle. Teknekron, 9E b

10 Inc., Washington, D.C. 1975, Table S-8, p. 5-21.

11 50A. Nuclear and Systems Sciences Group of Holmes and 12 Narvey, Inc. Transportation Accident Risks in the 13 Nuclear Power Industry 1975-2020. Prepared for 14 U.S. EPA Office of Radiation Programs, November 1974, 15 p. 119.

16 51. EPA-520/9-73-003D, p. C16.

17 52. The effects on populations of exposure to low levels 18 of ionizing radiation, National Academy of Sciences, 19 Washington, D.C., 1972, p. 171. A 30-year risk 20 plateau was used.

21 53. 10 CFR 50. 34 (c) .

22 54. ANSI N18.17 (in Binder, D.J. , et al., 1977, p. A131f).

23 55. Safety and security of nuclear power reactors to 24 acts of sabotage. Sandia Laboratories (SAND 75-0504),

25 March 1976.

26 56. Reactor Safety Study, WASH-1400, U.S. Nuclear Regu-27 latory Commission, 1975.

28 .

i s

I' .

11 i

2'l: 57. Safety and security of nuclear power reactors to 3 acts of sabotage. Sandia Laboratories (SAND 7 5-05 04 ) ,

4 March 1976, og cit.

I 5' 58. Binder, D.J., et al., p. A123.

6 59. Binder, D.J., et al., p. 126.

t 7! 60. Project Independence Evaluation System (PIES) Docu-8, ,

mentation, Vol. 1, The integrating Model of the Pro-l' 9 ject Independence Evaluation System, 1976. FEA/N-10 76/411.

11 61. Morris, S.C. and K.M. Novak and L.D.' Hamilton, Databook 12 for the quantification of health effects from coal 4

13 energy systems , Brookhaven :iptional Laboratory, Upton 14 NY, May 1979 draft.

15 62. Enterline, P.E., Mortality Rates Among coal Miners, 16 American Journal of Public Health 54:758-768, 1964.

17 63. Liddell, R.K.K. Mortality of British Coal Miners 18 in 1961, Oritish Journal of Industrial Medicine 19 30:15-24, 1973.

20 64. Estimated from U.S. Bureau of Mines data.

21 65. Hollingsworth, C.G., M.S. Thesis, Univerisity of 22 Pittsburgh.

23 66. Enterline, P.E., Annals of the N.Y. Academy of 24 Sciences 200:260-273, 1972.

25 67. Morris, S.C., Sc.D. dissertation, University of 26 Pittsburgh, 1973.

27 28

I i l 2l 68. Rockette, H.E., Mortality Among Coal Miners Covered 3l by the UMWA Health and Retirement Funds, DHEW (NIOSH) 4 Publ. No. 77-1. Morgantown, West Virginia, 1977.

5 69. WASH-1224, USAEC, pp. 4-27.

6- 70. Bohm, R.A. et al., Benefits and Costs of Surface 7 l Coal Mine Reclamation in Appalachia in M.G. Morgan, t

8 ed., Energy and Man, IEEE Press, New York, 1975.

91 71. Association of American Railroads, Yearbook of Rail-i 10; road Facts, Washington, D.C., 1977, p. 29.

11 72. U.S. Department of Transportation, Federal Railroad 12 Administration, Office of Safety, Accident Bulletin 13 Nos. 135 through 141, 1966-72, Table 108.

14 73. Association of American Railroad, Yearbook of Rail-15 road Facts, 1973.

16 74. 40 CFR 60.42.

17 75. USEPA, Position Paper on Regulations of Atmospheric 18 Sulfates, EPA 450/2-75-007, Research Triangle Park, 19 North Carolina, September 1975.

20 76. ANL Special Task Group, Preliminary Assessment of 21 Health and Environmental Impacts of fluidized Bed 22 Combustion of Coal as Applied to Electrial Utility l

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23 Systems, Argonne National Laboratory, 1977.

24 77. Lundy, R.T. and D. Grahn, Predictions of the Effects 25 of Energy Production in H'iman Health, presented at 26 the 137th Annual Meeting of the American Statistical 27 Association, Chicago, August 1977.

28 [

i 11 Il 20 78. Lave, L.B. and E.P. Seskin, An analysis of the Asso-3 ciation Between U.S. Mortality and Air Pollution, 4 Journal of the American Statistical Association 5 68:284-290, 1970.

61 79. Lave, L.B. and E.P. Seskin, Air Pollution and Human 7 Health, Johns Hopkins University Press, 1977.

8. 80. Finch, S.J. and S.C. Morris, Consistency of Reported i

t 9: Hea.Lth Effects of Air Pollution, in J.R. Pfafflin I

10' and E.N. Ziegler, eds.. Advances in Environmental 11 Science and Engineering, Gordon and Brench, New 12 York (in press).

13 81. CHESS: An Investigative Report, Committee on Science 14 and Technology, U.S. House of Representatives, 94th 15 Congress, 2d Session, November 1976.

16 82. Olsen, A.R., " Air Pollution and Mortality", pre-17 sented at the 137th Annual Meeting, American Sta-18 tistical Association, Chicago, August 1977.

19 S3. Schwing, R.C. and G.C. Mcdonald, " Measures of Associa-l I 20 tion of Some Air Pollutants, Natural Ionizing Radia-l 21 tion and Cigarette Smoking with Mortality Rates,"

22 Tr. 2 Science of the Total Environment 5:139-169, 23 1976.

24 84. Lipfert, F.U., " Association Between Urban Mortality l

25 Rates and Air Pollution", presented at the 70th 26 Annual Meeting Air Pollution Control Association, t

i 27 Toronto, June 1977.

i i 2B l

I 2 85. Amdur, M.o., " Toxicological Guidelines for Research 3, on Sulfur oxides and Particulates", in Fourth 4 Symposium on Statistics and the Environment, National 5 Academy of Sciences, Washington, D.C., March 1976.

86. Amdur, M.o. and M. corn, "fhe Irritant Potency of 6l I

zine Ammonium Sulfate of Different Particle Sizes",

7'f 8! American Industrial Hygiene Association Journal D

d 9 24:326, 1963.

10' 87. Amdur, M.o. and D.W. Underhill, The Effect of Various 11 Aerosols on the Response of Guinea Pigs to Sulfur 12 Dioxide, Archives of Environmental Health 16:460, 13 1968.

37A. W. Wilson, et al. Sulfates in the Atmosphere, A 14 15 Progress Report on Project Mistt. EPA 600/7-77-021, 16 Research Triangle Park, March, 1977, p. 8.

Shenk, 17 88. Morgan, M.G., S.C. Morris, A.K. Meier and D.L.

18 A Probabilistic Methodology for Estimating Air

! 19 Pollutant Health Effects from Coal-fired Power It 20 Plants, Energy Systems and Policy, in press.

21 89. North, D.W. and M.U. Merkhojer in National Academy

! 22 of Science Air Quality and Stationary Source Emission 1

23 control, printed by U.S. Senate committee on Publ.e i

I 24 Works, March 1975.

i 25 90. Altshuller, A.P., Regional Transport and Transforma-26 tion of Sulfur Dioxide to Sulfates in the United l 27 i

! 2 1 I

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1 2 States, EPA /600/3-77/054, USEPA, Research Triangle 3 Park, North Carolina, 1977.

4 91. Meyers, R.E. and R.T. Cederwall, work in progress.

5 92. Finklea, J.F., et al., The Role of Environmental 6: Health Assessment in the Control of Air Pollution, 7 in J.N. Pitts and R.L. Metcalf, eds., Advances in i

8' Environmental Science and Technology, Vol. 7, J.

9- Wiley and Sons, New York, 1977.

10 93. Nelson, W.C., J.H. Knelson, V. Hasselblad, Air 11 Pollution Health Effects Estimation Model, in USEPA, 12 Environmental nodeling and Simulation (EPA 600/9-13 76-016), July 1976.

14 94. For a general critique of the CHESS studies, see:

15 Committee on Science and Technology, U.S. House of 16 Representatives, "The Environmental Protection 17 Agency's Research Program with Primary Emphasis on 18 the Community Health and Environmental Surveillance 19 System (CHESS): An Investigative Report". Washing-1 l 20 ton, D.C., November 1976.

l 21 95. Hamilton, L.D., " Comparative Risks from Different 22 Energy Systems Evolution of the Methods of Studies,"

l 23 International Atomic Energy Bulletin, Volume 22, i

24 Number 5/6, October 1980, Table 9, p. 59.

f l 25 96. U.S. Nuclear Regulatory Commission, Final Supplement 26 to the Final Environmental Statement -- Allens Creek 27 Nuclear Generating Station, Unit No. 1, NUREG-0470, 28 August 1978, p. S.5-28.

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1 98. U.S. Geological Survey, National Coal Data Base, 2 computer run, 21 February 1980.

3 99. U.S. Environmental Protection Agency, Radiclogical 4 Impact Caused by Emissions of Radionuclides into i 5 Air in the United States. EPA 520/7-79-006, 6 August-1979, pp. 4.4-1 to 4.4-27.

7 100. Hamilton, Patrick A., D.H. White, Jr., and 8 Thomas K. Matson. The Reserve Base of U.S. Coals 9 by Sulfur Content, Part 2: The Western States, 10 Bureau of Mines, Information Circular 8693, 11 Washington, D.C., 1975 12 13 14 15 16 17 18 l 19 l

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Attachment A DR. L. D. HAMILTON PERSONAL QUALIFICATIONS My name is Leonard D. Hamil ton . My address is: 6 Childs La ne ,

Setauket, New York, 11733. I am, among other responsibilities. Head of the Biomedical and Environciental Assessment Division in the Na tional Center for Analysis of Energy Systems at Brookhaven Natienal Laboratory, As soc ia t ed Univers itie s , Inc., Upton, New York, 11973. 'Ihe Bio =edical and Environmental Assessment Divis ion is jointly sponsored by the Depa r tment of Energy and Environment and Medical Department at Brookhaven. The Biomedical and Environmental Assessment Division (BEAD) aims at developing a realistic assessment of biomedical and environmental effects of energy production and use. All forms of energy, including electric power generation using fossil fue l s , hydro, nuclear, and new technologies, are assessed. 'Ih e Biomedical Environmental Assessment Division is the lead group in the Office of Heal th and Eny'ironmen ta l Research of the Assistant Secretary of Environment, U. S. De pa r tment of Energy, assessing the health and environmental e f fec t s of energy production and use and among other responsibilities is charged with i producing a health and environmental effects assessment of the National l Energy Plan.

I have been involved in assessing the risks of radiation for man for l

35 years, specifically the health ef fects of nuclear energy for electric power genera tion for 20 years, and the assessment of the compa ra tive heal th effects from various energy sources, for the y,at 7 years. The

! Biomedical and Environmental Assessment activity formally began in July,

! 1973; for the past and present year our level of effort is 204 man-months i

annually.

4.

I received my Ba chelor of Arts in 1943 and qualified in medicine from Oxford University in 1945. I am a registered medical practitioner in the United Kingdom and licensed physician in New York State . After several positions in University hospitals, which included a postion as Resident Med ica l Officer at the Radiothe ra peut ic Centre, Addenbrooke's Hospital, Cambridge , during which time I was concerned with the management of cancer pa tien t s undergoing treatment with rad ia tion , I proceeded to research at Cambridge University on histological studies of the mechanism of the action of the ra peutic doses of ionizing radiation for which I received my Ph.D. in experimental pathology in 1952. In the meanwhile, in 1951, I had rece ived my Doctor of Medicine degree from Oxford; this is a senior medical qualification in the United Kingdom, roughly equivalent to Diplo= ate in Internal Med ic ine in the United States. I am also a Diplomate of the American Board of Pathology (Hematology).

From 1950-1964 I spent 14 years on the research staff of the Sl oan-Ke ttering Institute for Cancer Research and on the clinical staff of Memorial Hospital in New York being Associate Member and Head, Isotope Studies Section at the Institute and Assistant Attending Phys ic ian ,

Department of Medicine at Memorial . During this time I was also a member l of the fa c ul ty of Cornell University Medical College and a Visiting Phys ic ian , Cornell Division, Bellevue Hospital. Since then I have maintained a continuing association with the Sloan-Kettering Institute as Associate Scientist.

At the Institute my laboratory research wa s on the molec ul a r I

j structure of the genetic material (DNA) and the cells in man concerned i

i with the immune mechanism. I provided the DNA on which the proof of the 1

i

double-helical structure of DNA is based, and wa s one of the first to establish the long life of the immune cells in man. My clinical work in Memorial Hospital involved research on the treatment of pa t ien t s afflicted with cancer and leukemia with new chemical agents and also with new applications of radiation therapy.

In 1964 I joined the seientific s ta f f of Brookhaven NationaI Laboratory as Senior Scientist and Head, Division of Microbiology, and Attending Physician, Hospital of the Medical Research Center. Since 1973 I have been Head of the Biomedical and Environmental Assessment Group which in 1976 became a Division of the Na tional Center of Analysis of Energy Syste=s.

At Brookhaven I continued my laboratory research begun at Sloan-Kettering. In addition since my Visiting Fel lowship at St.

Ca th e r ine 's College, Oxford 1972-73, I have been concerned with placing all risks in life in perspective; and since becoming Head of the Biomed ical and Environmental Assessment activity in 1973, particularly with the assessment of the hazards as soc ia ted with di f fe rent energy sources and their use. Our group has the lead responsiblity to DOE for

! the assessment of health and environmental effects from va rious energy systems, and of coordinating such assessments in national laboratories, universities and research institutes in the United States.

My interest in the risks of radiation for man began with my Ph.D.

i

! work in Cambridge in 1946 and , since DNA and the immune system are prime l

l targets of radiation damage has continued throughout ny laboratory research. I was associated informally with the United Nations Scientific Committee on Effects of Atomic Rad ia tion (UNSCEAR) almost since its inception in 1957, served as Consultant, Of fice of the Under-Secretaries l

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for Special Political Af fairs (UNSCEAR), 1960-62, and was responsible for the first dra f t of the somatic ef fects of radia tion in the 1962 report.

This section covers the effects of rad ia tion in inducing leukemia and cancer in man. I have reviewed most of the working pa pers of UNSCEAR since then. I wa s a me=ber of the Na tiona l Research Council-Na tional Acade=y of Sciences (NAS-NAS) Coc:= it t ee on Bilogical Effects of Atomic Ra d ia t ion , Subcoccittee on Hematologic Effects, 1960-64, the NRC-NAS Solar Energy Research Institute *='orkshop,1975, the NRC-NAS Cocnittee on Environmental De c is ion Making, Steering Cc=mit te e on Environmental Monitoring, Panel on Effects Monitoring 1975-76, the NRC-NAS Heal th Ef fec ts Resource Group, Risk Impact Panel of the Coc:mittee on Nuclear and Al t erna tive Energy Ssytems (CONAES) 1975-80, the NRC-NAS Panel on the Trace Element Geochemistry of Coal Resource Development Rela ted to Health 1976-80, and the NAS-NRC Coc:mit tee on Research ' Needs on the Health Ef fects of Fossil Fuel Co=bustion Products, 1976-80.

I was a member of the Mayor's Technical Advisory Co=mittee on Ra d ia t ion , New York City, since 1963 until its end, De c emb er , 1977 and have been a member of the Technical Advisory Com: nit tee on Rad ia tion to the Cor::missioner of Health of the City of New York since August, 1978.

Since 1972, I was a Consul ta nt to the Environment Directorate, Organiza tion for Economic Co-opera tion and Development; since 1976 served as DOE (formerly ERDA) Representative in the U. S. Delegation to the Environment Co=mittee and U. S. delega te to the Joint Environment-Energy Steering Group. I was a member of the United Na t ions Environmental Program (UNEP) International Panels of ^ Ex per ts on the Environmen ta l Impacts of Production, Transportation, and Use of Fossil Fuel 1978, on the Environmental Impacts of Nuclear Energy 1978-79, on Renewable Sources I

of Energy and the Environment 1980, and on the Compara tive Assessment of Environmenta l Impa c ts of Dif ferent Sources of Energy, 1980. I was a member of the Beijer Institute, UNEP, and USSR Commission for UNEP International Wrkshop on Environmental Impl ica t ions and Strategies for Expanded Coal Utilization,1980.

I as currently a member of the U. S. Department of Health and Human Servic e s , Public Health Serv ic e Centers for Disease Control, Na tional Institute for Occupational Sa fe ty & Health overview group, supervising the epidemilogical study of the employee s at the Portsmouth Naval Shipyard where an alleged increase in leukemia was reported by Najarian and Colton in 1978, and a Consultant to the Division of Environmental Hea l th , World Health Organization and the United Nations Environmental Program on the comparative health effects of different energy sources.

I have been Professor of Medicine, Department of Medicine, Health Sciences Ce n te r , State University of New York at Stony Brook, New York since 1968 and I am currently a member of the American Association for Cancer Research, American Society for Clinical Investiga tion (emeritus),

American Association of Pathologists, Inc., the Harvey Society, and the British Medical Associa tion.

f I have published more than 100 scientific pa pers , including many reports assessing the hazards of various energy sources .

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