ML20071F742

Offers Comments on NRC Regs for Self Protecting SNM in Res Reactor Fuel Element.Asserts That Weakness in Spec Is That Dose Rate Is Not Connected W/Specific Quantity of Snm. Supporting Documentation from Med Treatises Encl

ML20071F742
Person / Time
Site:	University of Virginia
Issue date:	10/30/1978
From:	Williamson T VIRGINIA, UNIV. OF, CHARLOTTESVILLE, VA
To:	Stello V Office of Nuclear Reactor Regulation
References
NUDOCS 7811080179
Download: ML20071F742 (21)

Text

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• g e s7 univaasiry or vinaisix SCHOOL OF ENGINEERING AND APPLIED SCIENCE f

V V C H A R LOTT ESVILLE, 22901 DEPARTM ENT OF NUCLEAR ENGINEERING AND ENGINEERING Physics TELEPHONE: 804 924 7136 ftEACTOR FACILITY 4 October 30, 1978 i

Dr. Victor Stello ,

Deputy Director Nuclear Reactor Regulation U.S. Nuclear Regulatory Commission - '

Washington, D.C. 20555 4

/ 0

Dear Dr. Stello:

O , This is to comment on NRC regulations for self protecting SNM in research V reactor fuel element, i.e. the requirement of a total external radiation dose

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rate in excess of 100 rem per hour at a distance of 3 feet from any accessible surface. One m'ajor weakness in this specification is that the dose rate is j not connected with a specific quantity of SNM. If the intent of the regulation {

is to assure that a person handling the SNM would receive an incapacitating i dose before he could complete the construction of a weapon, then it seems that the specified dose should be tied to quantity of material to be handled.

I suggest that the NRC consider the following specificationsj _

2 L. i SNM quantity 5 kg [f i n  !

Incapacitating dose 1000 rem c M N Total exposure time 0.5 hr ?j [ r)

Dose rate limit 5 kg kib

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.250 kg a u iu O ,

, 0.4 rem /hr 4 gm l This specification will allow research reactor fuel elements which have less than .25 kg to be self protecting if the dose rate at one foot is less than 100 rem; specificaally the dose rate limit would be calculated as 0.4 rem /hr for each gram of SNM material.

Relating the self-protection criteria to the weight of SNM will reduce radiological concerns since the total radiation level of irradiated fuel could be lowered. The increased radioactivity of the present requirements results in at least two concerns. First is the additional exposure to the reactor staff both during normal operation and special activities, such as shipment of O

V 781108 Ol77 f

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Letter to Dr. Stello October 30, 1978 Page 2 expendeT fuel. Second, the possible consequences of industrial sabotage, as defined in 10 CFR Part 73, would be substantially increased by' the increased-activity level. Clearly the probability and consequences of sabotage and theft must be evaluated when defining the radioactivity level necessary to for SNM to be self protecting.

The basis for these recommended numbers is as follows:

SNM quantity, 5 kg: Formula quantity as defined by the NRC Incapacitating dose, 1000 rem: ,

References:

n U Saenger, E. L., Medical Aspects of Radiation Accidents, U. S. Atomic Energy Commission (undated, but preface dated 1963) .

Travis, E. L., Primer of Medical Radiobiology, Year Book Medical Pub lishers , 1975.

Saenger describes five clinical radiation injury groups with Group IV being in the dose range 600-1400 rad. This group is described in an accelerated version of the Acute Radiation Syndrome. Complications of gastrointestinal injury dominate the picture with early incidence of vomiting. Early onset of diarrhea, ataxia, disorientation, coma and cardiovascular collapse are all of importance.

Travis describes the gastrointestinal (GI) syndrome and states that doses between 1000 R and 10,000 R will result in the GI syndrome in all animals n studied. In humans some symptom of the GI syndrome appear at a dose of 600R (J (the threshold dose). The full syndrome is apparent at 1000R. The LD100 ' #

humans (between 600 and 1000R) is in the dose range of the GI syndrome Survival time does not vary with dose in the syndrome; death occurs at the same time regardless of dose. In humans death occurs within 3 to 10 days if medical support is not administered and within approximately.2 weeks even with medical support. The prodomal stage of the GI syndrome occurs within a few

! hours post exposure and is characterized by severe nausea and vomiting, which may be accompanied by severe cramps and diarrhea.

This early sickness is justification for a total dose in the neighborhood of 1000R.

Exposure time, 0.5 hour: For elements loaded with .25 kg a person would have to handle 20 elements to obtain a formula quantity of SNM. The handling time would have to be less than 1.5 minutes per einment to keep the total -

7 _

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Letter to Dr. Stello October 30, 1978 Page 3 -

exposurMbelow1000 rems. It is likely that the handling time per element in -

an unshielded configuration would be greater than 1.5 minutes and the absorbed dose correspondingly larger.

Impact on Research Reactors: The attached table lists research reactors with approximate fuel loading per element and operating power. Those in category I and III have less than .250 kg so the requirement for self protection would be less than 100 rems by an amount which is the ratio of the individual element loading to .25 kg. The reactors in category, II are all more heavily ,

loaded than .25 kg so their fue1 ~would have to give a dose rate greater than 100 rem /hr. These four reactors all operate at higher powers and the loading O per element per megawatt is comparable to those facilities in category I.

It appears from this table that the requirement of dose rate for a speci-fied quantity of SNM as suggested here would not have an adverse effect on the operation of these reactors.

It is significant to note that an average fuel element in category I has about .16 kg so that one attempting to divert this fuel would have to transfer more than 30 elements.

In summary, I consider that relating the definition of self protecting SNM to the mass of SNM as recommended above results in an effective deterrent i

to theft while' reducing the radiological concerns. I, therefore, recommend that 10 CFR Part 73 be revised to exempt from the requirements of Part 73 SNM which is not readily separable from other radioactive material and which has a-total external radiation dose rate in excess of 0.4. rem per hour per gram at a distance of three feet.

Sincerely, b b%

T. G. Williamson, Director Reactor Facility

. TGW:ec cc: Mr. A. A. Sinisgalli U.S. Nuclear Regulatory Commission Mail Stop 228 Washington, D.C. 20555

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APPROXIMATE SNM LDADING PER ELEMENT

.-.li I 1.-Plate-Elements with,less than .25 kg: .

Fuel Loading Reactor Power Babcock & Wilcox .190 kg 1 MW Georgia Tech.. .188 5 University of Lowell .124 1 University of Michigan .140 2 Rhode Island .124 2 Union Carbide .196' 5 University of Virginia .192 and .162 2 II. Plate Elements with more than .25 kg General Electric (GETR) .511 50 M.I.T. .445 5 University of Missouri (Columbia) .775 10 NBS .300 10 1 III. TRIGA Elements greater than 20% enriched Ore. State, Texas A&M, Wisc. .123 1 Washington State, G.A.

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I Gadiobiology Total Dody Radiation Response l Wst, 113

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9-Radiation Syndrome in Humans '

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crease in fat. C, three weeks postexposure, contents now appear relatively normalindicating regeneration (absence of bony trabecurae in C is not a re-sult of irradiation but is due to the area of the tissue sectioned). (H & E stain; j-

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, e,pf , '.

4

(,.g. 1 p 'f . tract are profo w 3.;. ntt y, . .

r uvg.

o n.

<< t. g .g mater als actc

d. . y~ $ . a.

. y ,

y s.v **- a,... g- CI tract resutt

.- - 6.

n, 4 - . s inM p . .:-(,.

,3 -

v- - o p fiPj. T bacteria that o 5$$fl Sf6 *-Mh N. Y k k .c.. .

& stream throug t - - M Poun ed b w

g. a4 b+y3w; .c ., .c /4 3r/v, e - y\. *- effects ofdar vT-q.k

,[^-

.4j '. E. pg,9[,

,s., $@- ,

, , the GI tract !!

5&

~$;f;. h.'.'*

'NEg' +k'p.'fi

h>p

~

.,.s J. %'%

. p-severe decrea:

sion occurs as w .4 p .t q.u rx-7.g. -M ~ . -

t g therefore com p[1;5s ti .3 T , ,j,, - *' 4 s i , blood cells m I.

[w. # A 2A. gbbh act that death

-'7 *e A'f.6 g Eh, 6m~h g%N ; &

s. i lines.

4

%y.4t: % ,

N':%

0;\$ b

@M a (.A y.r%A +

ih bYr $*b h; L Y . $ih

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=

. m . m n . a Mi

w. w &. L. ,S..'G. M. W. .=~ Q. o,4 u.M a . hn m (x-bnM y

.' .+ h,,f

. p.ac>..',y*[n 9p>2+f~*%.

m. a e. m* r . ~. =.i~h "M%., .F,

,a. p . . _* m

%w'y.'y'Q2k?S&%*M,&';

t y *.;*Qye. +.w # .'.1.

?*e'3 .~:.% .C.2. :

~ . .

r. -w '--

p w s s .' e1 ?s- -" jai C"." y.,y

. . -o ar /'3*/l a.. .w ,*'"~.u.es}'.!

/ ,e *=* '

7 * -- A -p w.-

Q.C4. . M % 5.?g'.3** . C'e m .e . .' e g .yy M +p-wd m.

~ h 4'.:WM*'%T 2- '~ LW - 1"..-~-

j bNdhik$((ibh _ _ __= M' 24A PINDI meYdA. N [_ds$$N.2;W.Y"&'i'r

_~

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=

E,.MMMMMh%GiswhEEM%WF!d

'; $ hYk  ? ?-$ h ? & S N & h W $ & 5 % W$ M W A mu@ss i

V r.&. '.'rW:W

~C-A h

Total Body Radiation Response 117 0 d

'.',M, ,3.yy.g,$N

-w 4 ., 3.gg.Aw in the dose range of the GI syndrome. Survival time does not vary 4 g

" m d

'.5,.% Q3;@.7..

with dose in this syndrome; death occurs at the same time regardless ofdose. In humans death occurs within 3 to 10 days if medical support y -N-ff6 tg MCW

,, per is not administered and within approximately 2 weeks even with med- ,

m

,. be- ical support.

@p%w y.g' '

,.cals The prodromal stage of the GI syndrome occurs within a few i i!

[-i.N hours postexposur and is chc.racterized by severe nausea and vomit-

,.heet seh ing, which may be accompanied by severe cramps and diarrhea. From c NMk:.

j;%'y

, gt: Ms the second through the fifth day, the individual enters the latent stage MWg C

and feels well. At the end of this time, there is a recurrence of severe ,

. ., s e'd diarrhea, nausea and vomiting accompanied by fever, signaling the . . N:8.f v WW onset of the manifest illness stage, which may persist from the fifth gj$2 h through the tenth day. Death occurs from the GI syndrome during the MQ[Qj;[

'Q' ,.

second week postexposure iflife. sustaining support has been admin- h' gG9,f$

N istered (fluids given, transfusions, etc.).

The GI syndrome is due to damage in two organ systems: the gas-

' dM?!jk (l y hp

, .'f, '*g*4

'* trointestinal tract and the hone marrow. The full GI syndrome does :j . gQ.yg

h not occur if only the GI tract has been irradiated because the bone ,4 - -

wr.d

'.I

.':t marrow plays an integral role in this syndrome.

The lining of the GI tract, particularly the small intestine, is se-j?C:.n n.h:Wfgh

..',+O- verely damaged by doses in this range.The mitotic activity of the cells W (.((j')bb .Q M id in the Crypts of Leiberkuhn, the radiosensitive precursor cells to the M

. #4,

.'z-' population of cells on the villi, will be decreased drastically following . n. :s

$.p$Gi:f-  %

exposure. As a residt the villi, which slough dead cells into the intes-ag4?g;g!';

7 WM

.E tinallumen every 24 hours2.777778e-4 days <br />0.00667 hours <br />3.968254e-5 weeks <br />9.132e-6 months <br /> and are dependent on the Crypts of Lei- . .m

.<.  !@p%;5 py' ..

4 I '

4 berkuhn for replacements, lose cells and become shortened, flattened L ,

"; and partially or completely denuded (Figs. 6-4 and 6-5). f, W 2'.?!! M M. .- 7. fS. .-M.,. ..

tl [f. The consequences to the individual of these changes in the GI l1

.i tract are profound.The flattened villi result in decreased absorption of ll . WW963' j,?,ig; .

materials across the intestinal wall. Fluids leak into the lumen of the -

}- H

$;hig/p d'$ C y' GI tract resulting in dehydration. Overwhelming infection occurs as bacteria that normally live within the GI tract gain access to the blood-MMW3

& stream through the intestinal wall causing systemic infection.

-[.

• The effects of thc3e drastic changes in the GI tract are com- J 1.u M4sM!~d ~

MM- - [

j (M -

poimded by equally drastic changes in the bone marrow. In fact, the efTects of damage in the bone marrow occur at a time when damage in 4

y g.jh the GI tract is reaching its maximum. Of primary importance is the o i e Asu7 severe decrease in the number ofcirculating white cells.This depres- 3%T i

. h,'s - sion occurs as bacteria are invading the bloodstream from the GI tract, q.;;', :49 '

~5  %

i thenfore compounding an already severe problem. The remaining

(* e, blood cells may not exhibit a severe decrease in numbers due to the Y. dQ My'k i fact that death occurs before radiation damage is reflected in these cell g&e[##f.

3$ . T' .f lines.

i t '

d w

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-p.

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W. !.$$,pl

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m. :w. m: n a.p 7=.gm

--cpf us

>.. %c.wnum +& m?.=.

W.y4a.: w y x w.= ,y: ..n.L,n e. M w;.~4!.,. w. aw.7y;.w?y. gmwy p +w.w.u.r . w p-

? wwsm -

.: q ,.:  % m.w.=:

/ km ms" m e. 4. .m.;

h5 5 .& h YEffY k i- k 15 kk

• wuu w w dum a n?am a mK A k m: us a.w

~ . . i

.. m .. , m ,,, ,,,,,,, ..-. ,,,,,,,, - - . r - 7 . . .. . .' . .._ dar

3 s Wg. u. ,,. s Nhm -~..-' N;k. ..N[h~,s. b.

~ .g- o./ 3 w. y,.k M w .$ . g.e,.,_

. 5,f k.hs.h.. mw Nbb hrh.,

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• , % s,x.

7 .o.= g .n , y,. ,a,. ,,,,, y..

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,sfW&m Q't Q:

"l% h 118 Primer of Medical Radiobiology Total Bod

, Q; h;, 9 ' -

villi y pf .'

i,[A r , d _. A I l .

'{ E'M;< #~ ~ i, '- 3 J , c,[

$g* ' '

A. <C.w7 .n .

1 "

3 I i' <

g<

ffpQpt 4 '

i p I* j ' '

t e '

j M-' :'.'" .^.i,7E L i 4 1: [ h 51 h surface l

k Q 1:  : c c i epithelial '

l p h" 4 % %.". I q E .' j ': ~ S T cell l '

3 JT B $ c q', A!

[}g [cryptJ M

m M'(('.

c h ~

(

U crypt

, y 8 I u

k f y

gtd,W @ '

\ e r ' */; (

\

• , 4 ,b

• 7 .

,eq,> n . .. p tc. ,, p g===.===_--_,M3-

-=

% ,,- y- . = = - ( s q;.% _# .. . ,,.

N y T ";".

,  ; .W ws e

. . %j 2 ; .

3 villi 'My ,

NAU .S ., l l .O JJA([

l

---

hthelial

."pis:

..m-M .L N.,

p . - f".s::~~ cell die.7 Id Fig. G-4.-Diagrammatic representation of changes in the small intestine . f, n _ n' gf A ." % H ! (D following total body exposure in the dose range of the GI syndrome. A, pre- ---@

$.:.-fQ

., irradiation; B, postirradiation. { '

<m . . . ,,

.A &.

a g N tl. * .

n . .{.- - a ,

g hl[,Eg g Although attempts at regeneration occur in the GI tract after irra-

h7A:

WM

_ _l diation, particularly at the lower dose levels of the GI syndrome, the damage incurred by the bone marrow will probably still result in

]Q, death (Fig. 6-6). Death from the GI syndrome is due primarily to n47%{

W.yc.N ti, ,

sj $ infection, dehydration and electrolyte imbalance resulting from the destructive and irreparable changes in the GI tract and bone marrow.

~ .

,t ...

w , g S,' n.

'f f.y9 y(,-Q' CENTRAL NERVOUS SYSTEM (CNS) SYNDROME.-The full CNS syndrome occurs at a dose of greater than 5000 R in humans. Although Q, Q;,J, ,f' .

CNS damage is evident at lower doses (2000 R), death from the full g

CNS syndrome occurs within 2 to 3 days following an exposure of  ! [,b,,2 W;*-s :T. N 5000 R to all individuals.

Fig. 6 5.-S

'rcye;f The prodromal stage varies from a few minutes to a few hours diation. ali sa<

i.% ri d dependent on dose. The signs and symptoms of this phase are extreme (C). B,500 ra NJ & - nervousness, confusion, severe nausea and vomiting, a loss of con. dent.C,1000 sciousness and complaints of burning sensations of the skin. A latent contain mitot

! ". M.5.M period next appears and may last for several hours, although often it is and edema o u'r ,;W; -: rows).(H & E a of shorter duration. The manifest illness stage begins 5 to 6 hours6.944444e-5 days <br />0.00167 hours <br />9.920635e-6 weeks <br />2.283e-6 months <br /> post-l exposure, at which time there is a return of watery diarrhea, convul-4[3Q n..%

'M L sions, coma and finally death.

-W4 6.ikl...*.V'?, p;

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w"* ( w,g-  !,'

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Da maym$W L$g$?M.:ym. Q2 y w M. - u.5M9,%S/ , g?

GW'WI3%P M ._ Jg.QMW; .MT g--go. p.* 7 c yg;# n.... g. e.::;y,.q;;. y. ,. y MM M. &. .p%;).WWWQQ";a995.

w . . . p. . .

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. b

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g

. t; m 1. n . , a n3p pMQQ pp

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n./4:,ne,L;M-:&k'Q~G.%;? & Q&d.t -scQd; . w;.3 ]. [..J :-yNf

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a

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7 9i

.- Primer of Medical Radiobiology Total Body Ra H /s 4), . ', - 120 long enough. &

.r-

w , y . g,, * . .jrv n p- tation ofdrams y% j g g -

. 'S y

G^

L

' 'f-(

jugg ?J f

• 1

-The three

" n.nCV 4 p.* E[ f % /k d

~

$ldW r' 1[& 9, :,QQ..vj.6

.r

? -;1 T. T  ? %. 4

,MaA ' N P . .. .

lV Hadiation !

4}.fy  !

g ' *g fects on the d

%M p 'o'#~g p p { %q ,7 '

studies of thec

-* - p' 1 .

.g ..y. " .d ,.. - condu'eted in 1 h .' 9' studies have r, 1 E'. i ' b \

$q, ,' '

4 k.s<-

j ciuding the def There are 3 Q- UN,1- .% @e/kyg, '

/. 7< f.p~ , fetus:

l

,e - ,.

1. Lethality.

e'.vf

p. R! . -4 5y

& - ./-

2. Congenital; N *~.Ye/

1

c . ;.

y . ! .; s. a p

%.1% dj

3. Long-term e

f c ," /

W-N ' '.,

. f.

g 7 g,, o,1

.s j n , er .

hese eh

! . -h' '

c . _

tion in the ovo Fig. 6-6.-GI tract and bone marrow of rat exposed to 1000 rads total body they can be dir N'

irradiation. A, high-power view of edematous villi exhibiting atypical epi.

-r *;.* thelial cells (arrows) and crypt with numerous mitotic figures. Insert indicates genital).

t'y{..j. ,1 regenerative attempts (arrows). B, bone marrow from same animal. Note the This sectic g

$e i .- _1 absence of all stem cells. only red blood cells are present. Although regener-ative efforts occur in the crypts. the damage in the bone marrow is sufficient utero (congem.t ovum or spern h [7 to cause death of the animal. (H & E stain; A and B. magnification x 175;in. limited to the I Qi ' . . IIj sert, x 350.) radiation that ,

e'N l'  %:

P j' 1 will be discuse The cause of death in the CNS syndrome is not fully known or 4 understood. Examination of the CNS after an individual has been have been the l efTects discuss <

.~.f. ,

exposed to a dose within this range reveals few changes in the paren-

! n.i *

• chymal cells of the brain. This is not sumrising keeping in mind the erwise stated.

E'4- t fact that these cells are nondividing and do not manifest damage as do humans and ol I chapter.

I the cells in the bone marrow or Cl tract in which division of stem cells is necessary to provide the end cell to carry on the function of those G. , ' Lethality a systems. Damage in the CNS may be a result of damage to the blood and fetus by ra M' vessels that supply the system resulting in edema in the cranial vault, gyy vasculitis (inflammatory changes in the vessels) and meningitis (in-the part ofday a basic knowle

-{'t} . ., flammation of the meninges). Death is suggested to be due to in-T*g e understandins

1. " W creased pressure in the confining cranial vault as a result ofincreased Russell an fluid content caused by these changes.

DW 5& The bone marrow and the Cl tract do not exhibit dramatic general stages (growth) stage changes in the CNS syndrome because the individual does not live A. IL .v

!4 ]p

.c ..:

[ .y h

.+

%%w%

A;W

%.,M .

." .a I

Y

$  ? ,,s

~I

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~wnw G szas.:n+o Q

wy.w wn

.y:QLJg'?"f;ip a

M. b ww . m

~ fm;.;w&w..y" a -

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. op.Q..-

q .. f. M gvQ.wG :b pe%M.

m$ 3 33.m g c,wR n w w n. m 3Q r,.;

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1. 1. iiiESMMNfdid@n!s!EY...: @n y E % M I y i M A E M @ @ H M

ge MMT5 i meygy

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W.t.% g} b,,,

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. P~ - s ~ ~ "' ? ; :: :-% :- , .- ---:nNUN di ~.--h:mw.!@gny"d5$h9,g;fpyyv..,:.

9$N(?

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.s.

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i

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.N M TABLE 6-3.--

SUMMARY

OF ACUTE RADIATION SYNDROMES IN HUMANS AFTER [!gi'

$Q.h.+f.Y.[di$.

i >

'GQ'@ '

.i i *

"" 5 DY IRRADIAEN*

ORGAN AND pt.

7 $h,, 3 kvi. SYNDROME DOSE RANCE TIME OF DEATH SYSTEM DAMACED SICNS AND SYMPTOM 5 FINDINCS RECOVERY'nME  %[ i,.

f ) . Hemeipoietic 100-1000 Rf 3 weeks to 2 months Bone marmw Decreased number ofstem cells in Dose dependent--3 weeks ,3, v' kh. pp'j , bone marrow, increased amount of to 6 months; some Q4 -

jh,$@'(*;.

- y f4y.P,*M^/Tj' cft ~

$l,. Clgk' fat in bone marrow, pancytopenia, anemia, hemorrhage, infection individuals do not survive 5.M -

. : 1000-5000 3! S to 10 days Smallintestine Denudation of villiin small intestine, None r D.M'l J5-i 4' ;,7 $'glItp neutropenia, infection, bone marrow 7 Y-[f, gl h.hf.Ae I $b depression, electrolyte imbalance, g

.g.

1 $^;?@M,].l.'p,k'Ci:

h*:2 8

W. CNS

> 5000 R < 3 days Brain watery diarrhea Vasculitis, edema, meningitis None

, o . . t .qb-M*,

3 h',h.'[.(d h

• Frem Rubin, P., and Casare tt, C. W.: Clinical Radia tion Pathology, Vol. II (Philadelphia: W. B. Saunders,1968).

4jNy[.p' th -d

g ( LD., for humans in this dose range (450 R .

!!.D, or humans in this dose range (1000 R .

{

o o.

h),;y 1./.

'='

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c yn CM

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7 A4 DO

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gs -

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m o g o -@ g" a[a 3'o~5 a- o 3.a= ~.'r.a'e g-a ~ :r = s m o s e -

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> A IIANDilOOK FOR M:.x;.c @. 4 r...e iM, . -&

l'IlYSICIANS, IIEALTII PIIYSICISTS .

1,. AND' .

.d.v.a r ' ... .%

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INDUSTIIIAL IIYGIENISTS .

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l l Eugene L. Saenger, 31.D., Editor .

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J@.. .. h, College.of 3fedicine -

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SECTION 31 41 ;3n , 1,. ,' .

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The Group III and IV Patients will rejuire skilled care in order to E'.-M.SI, M... .

. achieve survival.

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TAsLE 3.1-CI,1NICAL RADIATION INJURY GROUPS ' g tg. 4 ;#,  ; g.. , '

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Dese classif! cation by-oroup citnical roantfutatie.s )%g,,e).

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noms and wald* oerstner**

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I Mostly asymptomatic. Occasional 10- 100 rad. . . . .51-100 r ye . -

minimal prodromal symptoms. 101-150 r II Mild form of Acute Radiation Syn. 200-400 rad. .. 150-400 r @M@ @M .}~ .

AW drome. Transient prodromal nau-sea and vomiting. Mild labora-IIematopoietic. M'.f*.(Q=I

• '  ? $ C ' $ 'd.f) tory and clinical evidence of h'c . P.r: . 7B. .-

hematopoietic derangement.

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.y F'e n III A serious course. IIematopoietic 400-G00 rad 401-000 r A -

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complications servere, and some esidence of gastroenteric damage (297+). IIematopoietic. h$I;X.'

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. present in upper port. ion of group.

':%. ,(;{r.p%ax:!$ v IV An accelerated version of Acute G00-1400 rad... Castroin- W.

Radiation Syndrome. Gastrb- testinal. g' q 'h.:ht.;hM m

.-e e nter.ic complicat. ions dom. mate D..

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clinical picture. Severity of hema- W .4 Wi.t!,

topoietic complications is related %m.i..f.pP,'

. grfg to survival time after exposure. JM.te...'g~

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%. .15 V A fulminating course with marked 10,000 rad 150 Cerebral. i central nervous system impair- percent. (.gg' ~g.3',;,,,

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, " A pprontmste deses in r from tAtle ill and section on Dependency of Acute Radsstion Spdrome on Q. /

Atr nose of cerstner s pl. ncs doses are eipressed as air ocae. e cirosure dose, and are thus in terms m. 'p@% g;<2c.; . - . /7 o follon.na ,

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• s There is no substitute for careful daily history and physical exami-

. nati n f there patients. Only physicians, nurses and technicians f2. .*!Ih7tb.y k'cedlessly f yo .ed' l with pertinent dutics should be permitted access to such patients.

The Acute Radiation Syndrome is conveniently divided into four @?{O.agpg 5". ..

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. clinical stages as gonows: puyg

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' 4. Recovery stage The most important findings to be sought for during the prodromal gA@d'n h '?.

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stage are listed in table 3.2A. For each item, the time of onset, M.Mv. Mi Wif'M.e$

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- severity, change and duration should be charted. This list should be E.".%

reviewed and observat.ions recorded atleast da.ly, i or oftener as needed.

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. called cerebral, gastrointestinal rmd herbatopoietic forms (col.' 4, C4J9;j are derived .

_. ' t able 3.1). This classification o'iginally r based on extensive animal  %

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rom studies } studies, although of some value, may n'ot be of much help in the !g,4 pf,2%

fallout, [3]. j assessment of the individual patient, and it is suggested that the j  ; g f.,

and radio- concept of injury groups will be found more useful and will facilitate g[ .

' 76;%y.Q@i ,

e in which the proper levestigation and care of the patient.

adiation or fn addit, ion

[ Briefly, the injury groups are as follows [4,5]:

Croup I: Most of the patients are asymptomatic; a few of them Yf'UQ g."f

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. cases that 5 may have minimal prodromal symptoms. y,y.i f.f$.y. .

humans to '

Croup II: These patients developed the Acute Radiation Syndrome ,SQ* .

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in mild form. After transient prodromal nausea and vomitmg, . in a laboratory and mild clinical evidence of hematopoietic derangement , $. I U 5,U'N i OF VIRAL dominates the picture. &b '

E Croup III: A serious course occurs in these patients. Complica-

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Ws tions of hematopoietic malfunction are severe and some evidence of j gastrointestinal damage may also be present. [Q.f.jQ'h Group IV: An accelerated version of the Acute Radiation Syndrome occurs. Complications of gastrointestinal injury dominate the g@.Q,'%

picture. The severity of the hematopoietic disturbances is related W.%I$,pd to the length of survival following the exposure. f85k5MP-Croup V: A fulminating course with marked central nervous gy.;

system impairment occurs in this group. $g%ydgf-ue .g .,.-

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Tm.s 4.2-CLINICAL STAGES OF TIIE ACUTE RADIATION z'W T w 1

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1. Initial or ?.th+prodromd ..%

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, stage................ O to 4 8 hours9.259259e-5 days <br />0.00222 hours <br />1.322751e-5 weeks <br />3.044e-6 months <br />. ,

2. Lat ent s t a ge... . . . . . . . . . . . . . . . . . . . . .. . . 2 to 3 weeks.

3. Manifest illness stage.................... 2d or 3d to 6th week.

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j 4. Recov ery st a ge . . . . . . . . . . . . . . . . . . . . . . . . 8 to 15 weeks. f. Q M .r x v..%.

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Before discussing the clinical pictures and management in relation to the five groups, a few brief comments on the dose response relation .

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ning to this I ships will aid in the understanding of the problem. Q ETX h owever, will i Doses are expressed in rad of total body irradiation and relative NtF(.M o dose. uniformity of distribution of the r ilation throughout the body is ;4 7Y** h - -M. c h.vi.ded in a . thus implied. It <hould be realize- .at in most accidents there'may I), end thi*

• be marked nonhomogeneous absorpuon of radiation in the body due Me.

MNthy. @4 Pf ul from a to the proximity of the source of irradiation, partial shielding by Mk'iN io have had  : surrounding objects, and tbc attenuating effect of the inverse square , i$ Cfd3$

p:-%E veal, within  ! law. Furthermore, energy deposition in the body may be attenuated j f by absorption within the body. Thus even at considerable distances t y,3 gq(MiW'*-4 gN i the Acute I from the radiation source (where inverse square law effects are negli-  !

W ar3 the so* l- gible), inhomogenicty will result, from absorption of some of the f.

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.? 66 MEDICAL ASPECTS OF IdDIATION ACCIDENTS '

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M, . radiation within the body. This situation may be particularly so The prodrom e for neutron irradiation.

development of YY'  ; i.

i If the dose can be confidently estimated, individuals who have received 50 rad of total body irradiation or partial body irradiation that observation f',iT[T '

can be exduded from extensive investigation or study and will not to make a usefs First Post-Ez h.@ require treatment. Where only a few such individuals are involved, particularly in civilian accidents, careful study will be irrportant,

• either an overw; y(,4%b.1 from the point of view of both the patient and the responsible organi. Ou to F$@

occurs in this tu QF zation. A review of well documented cases of total body exposure in

cant dose of rad

f.0.5 7 the dose range of 50 rad or less has failed to yield evidence of symp.

dose is likely to toms, significant laboratory fmdings er short-term efTects requiring h.#F KQ any therapy.

In Group I co When the dose is 100 rad most individuals will show no symptoms. If no vomit,ing 1

p /~T m Group I.

[$Q

!&.' 'di-

- About 15 percent of cases may show some of the features of the syn.

drome in mild form. At doses of 200 rad most, of those exposed will. In Groups II e show clinical symptoms and signs and will have significant laboratory In Groups IV Y@.'Sj, ..E' j test abnormnlities. Fatalities may begin to occur at 200 rad and 1 onset of diarrhe probably approach 50 percent at 450-500 rad. Statements such as Inpse is of scrn j' '$ cases. The amc these involving percentages serve to emphasize the factor of individual

,,\@"? sensitivity which may be of the greatest importance. One man, for mjured patients i~

t risk and the ava

,. Y , gcd instance, may show prostratign re'sulting from a dose of total body Siz to Eight I

• '9 -

1. g% irradiation of, say,100 rad, whereas another man may show no appreci- symptoms reach

,i . lIl - able disability. The figures for 50 percent lethality in human beings M p~ (150 500 rad) are hypothetical since they are based on the supposition Groups III, I 9 .Y ' l'l Q ,

vitis, sweatmg a 1.uw 1 that there will be no therapeutic interwntion. It is likely that with '.

Twenty-Four t kh'h h',..:y< l, optimum treatment, according to present day knowledge, fatalities should rarely occur below a dose of 500 rad. A fatal outcome is In Group I ai

' In Group IIIt d b d. I .

probably inevitable at about the 800-1000 rad doselevel,in spite of all l*

toms with perha

-i d '! currently available treatment.

.! J In Groups.IV l

k , . $, 4.4 CUMCAL STAcE I (bm AL oR Paonnon AL SrAcE) e Thus it can f . ' W;: , *

features such as )

II . g There may be difficulty in assessing this phnse since it can be cal overlay such L'*w>

influenced by psychological factors of the individuals involved. The the first post-inc

- '.$ principal manifestations include anorexia,,pausea, vomiting, extreme ,.

bservat,on alon E...J. i

.y'y M.(

L sw'enting, prostration, and malaiseThe time of onset and the severity of these symptoms will depend on the dose. TYith large groups of

, patients a panic reaction may obscure the true significance of the 4.5 CuMCAL 81

,h( '

symptoms in the prodromal period. Mass vomiting, weakness,' diar- l5 rhea, etc., may be anticipated if groups of exposed people are kept In Group I ca

'i minimal prodror 7'

d together. For this reason, whenever possible, patients should be separated and put to bed immediately. Additional injuries, such as

- latent period. "

trauma or burns, may further complicate the picture and may tax the facilities are lim

- ' , [d diagnostic acumen of the observer. activity and shc

.'- Ib. l facilities are ava b

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The prodromal stage wdl be cons. der. d from the po.mt, of v.iew of i e development of symptoms in relation to time, and thus it, will be seen ym.g%.:.,

{.fy 9- c sh) have radiation that observations made in the first, few hours might enable the clinician will not, to make a useful preliminary assessment of the situation. ;pjy;fgf,$:3}c

.y;.[;

First Post-Exposure IIour: Symptoms during this period indicate

'E$ pr'G.G involved either an overwhelming dose or a severe psychological reaction. Mi@$5~y((('d mportant  %

' 8 One to Fire IIours Post-Erposure: The onset, of prodromal syniptoms ..QNb -c.2Jy ...W.de

.c orCani-posure in occurs in th t.is ime mterval .m 90 percent of those exposed to a s.igmfi-

.d .gr r}.5 of syn)p. I cant, dose of radiation. In general, the earlier the onset, the higher the  %,y.Q.y W, N dose is likely to have been. 3 .J.mt; =::tcM. :.~.

In Group I cases' the .mcidence of vonu.t.mg is negh. .ble at 2 hours2.314815e-5 days <br />5.555556e-4 hours <br />3.306878e-6 weeks <br />7.61e-7 months <br />. &cMQ re9uiri'nC . .

m+v

(

s

> ~

If no vomiting has occurred by 4 hours4.62963e-5 days <br />0.00111 hours <br />6.613757e-6 weeks <br />1.522e-6 months <br />, the patient is most probably gi

%#k =1

• U., *w% ten ;;p"OI@ "<

• mptoriis. .; p the syn-

,osed will-in Group I. .

In Groups II and IIf, the onset begins at one hour or soon thereafter.

Jy).g;4.;jb

-.i.cf

,boratory In Groups IV and V, the timetable of events is accelerated. Early , QQj;y.g onset of d,arrhea, i atax m,ia, disorientation, coma or c.:ardiovascular. col gGekog . H mv ...< p rad and  ?

- . . . ;.. 3 T3;;, ,-

lapse.is of serious prognost.ic importance and will mdicate Group V c.t.,i:,,.1,r i such as cases. The amount of intensive care devoted to these very seriously

...g~7'.y$,.y(

Q adividual man, for injured patients will be determined by the total number of cases at W,

...... ./:1 _r P w" ' -

.tal body risk and the availability of facilitics, i :=3. e 7 -' 7 Six to Eight IIours Post.Errosure: During thi= time the prodromal ,

j gi.J

, apprec .

symptoms reach their maximum intensity. f., k g Z3M m beings Groups III, IV, and V cases show weakness and fatigue, conjune,ti- ;g .y/ y @; @S pposition . .. .

- p.. ..yp.w < 3.n , .j

. hat with v2t.is, sweat.mg and paresthec.ia. ygb .g 4: Q.d.h gj.

Twenty-Four to Forty-Eight Ilo~urs Post-Expoure: .c.m i:talitico l Pk In Group I and II cases, the prodromal syniploms have subsided.

(come 12 In Group III, IV, and V cases there may be a persistence of symp-l j

-j 9 p, %

j. @%

3;teg)) toms with perhaps some gradual tailing oft in Group III. .%C#Yp, In Groups IV and V the clinical picture will be merging into that :M. .; F .u.-G./ .C'i 9.av of the manifest, illness without any intervening latent period. .': 17q JrE.i w . :;-

Thus it can be seen that, provided there are no complicating .g.Q$ p-s hatures such as physical trauma, burns, etc., and no unduc psychologi- i!

. c:n ba '

Cal overlay such as panic, hysteria, etc., it might, be possible during K[.,.ty%gj ,.

p d Tb the first post-incident 24 hours2.777778e-4 days <br />0.00667 hours <br />3.968254e-5 weeks <br />9.132e-6 months <br /> to diagnose provisionally from clinical 9 g. .,.th cxtreme ,

• p j.Qj cev:rity bservation alone the injury group into which the patient, falls.

f'dQ:

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4.5 Cu.NICAI. 8TAGE II (LATEhT PERIOD) ,, .

ss, diar-

. T S W '?

In Group I cases there will be no manifest IIIness and perhaps only i $ir%' M aro kept, ould be minimal prodromal symptoms; therefore there will be no recognizable

<sM, such c, - latent, period. These patients will not need to be hospitalized if such O'MN'I. .

t:x the facilities are limited, although they should avoid excessive physical 9.E d' ;

.s 1.

activity and should be observed carefully and followed if adequate ~

1 l facilities are available.

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i % ." i. U l c.-' 'I. Q8 AfEDICAL ASPECTS OF RADIATION ACCIDENTS

w. .

- 4

.In Group II cases the latent period is normally 2-3 weeks, during r

which time the patient is essentially asymptomatic apart from some tonsillar swellir

, T .' i .

T.. 7 I weakness and fatigue. [ bleeding from t turia and mcle:

f In Groups III and IV the latent period is shorter, perhaps 5-14  :

y.3 n.% : 4

.c.m ,. days. s. .

and mild purp:

t loss, and secon

1. .y yj Group V cases may not have' a discernible latent period. Fever, tract, are apt te W, g profuse sweating, insomnia, headache and skin changes may continue g Forty to fift and intensify after the initial prodromal phase. In addition, other i

%@U.-p symptoms to be described later will appear. j begm to remit

' days.

$3p.;d Clinical reco-f.V g 4.6 CuMcAt. SrAcEs III Asr, IV (MAMFEsT ILLNESS AND REcovEny)

"s . m months, althou,

- - -M Group I Cases:

& Group III Case

. '.t . W These cases, as previously stated, show no symptoms attributable

y. ll to radiation. They should be diligently followed, however, so that This group l significant changes in the laboratory findings will not escape detection manifestations

.Ib !' in individuals in whom overt prodromal symptoms might not have  ! dence of gastr <

I appeared. Certain of these patients might develop anxiety symptoms .

at: Indicated, a l'

f difTicult to differentiate from those due to the radiation syndrome.

IIere, reassurance from the attending physician will be of great Twelve to foi is heralded by 0 importance. ulceration may i bleeding from t'

+ .< Group II Cases: At 16-18 de u

• j.' ;, Q These patients show a mild to moderate " hematopoietic form" of rapidly. At ab f,a , ; ! $ ' the Acute Radiation Syndrome. and occult bloo Seventeen to twenty days post-exposure there may be epilation, ' persist and dur 1.' ' : h.;

ipg/

3v perhnps preceded by scalp tenderness for 1-2 days. The distribution of the epilation will depend on the orientation of the body in respect to the direction of the radiation. IIowever, hair loss may be most i

Marked pancyt may show almo q During the foi o

4 marked in areas of the head in contact with the pillow. Clinical lethargic and'i

[' h experience in radintion therapy has shown that epilation rarely occurs and diarrhea be y with single doses of less than 350 rad and that complete epilation from the bowel

} .g occprs readily with single doses of 450-600 rad. IIowever, the skin pain or cramps 1; doses may vary with the type and energy level of the radiation a,nd and, in females thus the occurrence of epilation could give only an extremely rough g Between 25

{ '

idea of the minimum dose that the patient may have received. Epi-3 parental fluios f,i lation may involve areas of the trunk and extremitics and observation g measures' deatik

. p of the pattern of epilation may serve to indicate the geometry of the original accident situation. It can also be caused by beta radintion, . Croup IV Cases p? the effect of which is confined to the skin. (See sec. 4.8.)

s

. f At about the same time (18-21 days) various other clinical mani. These patient h festations begin. Chills, fatigue, fever, headache, exertional dyspnea their total clini<

,k and sore throat may occur. The patient's general condition deteri. gastrointestinal orates, requiring confinement to bed. Mucosal reddening and times the total E f1 l hematological fi

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• SECTION 4 69 s.ge.@D y 4 -

. .r D weeks, during [ n.

.j,.lg..Q,e tonsillar swelling may be seen in the orophary'nx and some days later gart from some .

bleeding from the gums may occur after brushing the teeth. IIema '),,4  ; . q q. . - 3

[ turia and melena may occur or may be detected by laboratory tests

h c- .. .6 *

, perhaps 5-14 ,

. . .t. !

]

8 and mild purpura may be seen. There is usually a gradual weight loss, and secondary infections, most often involving upper respiratory y . , ,.

peri:d. Fever, . K; 2 7 ,.;

2 may continue tract, are apt to occur. 1 " i.

g Forty to fifty days after the exposure the clinical manifestations cddition, other l

i.

begin to remit and convalescence usually begins between 60 and 90 n . . f, 7 .

days.

. o e Clin ca recovery should be apparently complete within about 6 [* f W

.o:k jc'OVERY) g M.;' i months, although some weakness may persist longer. .y.: y,-

at,/:m i' Group III Cases: .:$v(i:1; ms attributable This group shows an accelerated version of the hematopoietic h $,;'.

awever, so that manifestations of the Acute Radiation Syndrome, and definite evi- , y'. ' . , .

scape detection

. night not have i dence of gastrointestinal changes. Vigorous therapeutic measures l $ * ^- *( <

xiety synaptoms ,

are indicated, although the prognosis is poor. '

Twelve to fourteen days after the exposure the onset of symptoms _=

. tion syndrome. l 111 b3 of great is heralded by fever and sore throat. Afarked pharyngitis with ' '

ulceration may be seen. Within a few days there is hyperemia and blceding from the gums and loosening of the teeth.  :@.. 5 At 16-18 days post-exposure, epilation begins and progresses h ;i ^d 7 ~

.I

>oletic form" of rapidly. At about this time purpura of the skin and mouth are seen ' -' ' -

~-

and occult blood can be founTin the stools. These manifestations 57 YP ation, il 8 persist and during the subsequent week large ecchymoses develop. bM  % '..i Af arked pancytopenia is evident by this time and'Ihe bon'e marrow

%.g.' ' I Pb3Mribution 3 3: N.y

. body in respect may shopv~ almost'c'Ernplete acellularity. % 3 echcovf- bc.go f _

During the fourth post-exposure week the patient becomes prostrate,

", S a may be most Cllow. Ch,mcal lethargic and' intermittently disoriented. Oliguria may be noted powd .i.e

. .'. ~;* * '

>n r .r:ly occurs and diarrhea begins, sometimes accompaniedlySn2ive hemorrhageevUt adpf nplete epilation ,

from the bowel. There is often severe and progressive abdominal -

w;ver, the skm pain or cramps and sometimes ileus. IIematemasis and hematuria o r:diati:n and and, in females, vaginal bleeding, occur. ' Vo jlg (fy ;d [<

Between 25 and 40 days, in spite of v}$flous therapy including " $ .

xtrernely rough i receiv:d. Ept- parental fluids, nutrients, blood transfusions and other supportive tnd observation measures, death ruay occur, preceded by profound shock and coma.

teometry of the betn radiation, j Group IV Cases:

, 8.8.)

l These patients have received an overwhehhing dose of radiation and '

l r clinical mani- their total clinical course is abbreviated to about 15-30 days. The l rtionnl dyspnea gastrointestinal manifestations of the disease predominate and some- I f ondition deteri- times the total survival may be too brief for many of the characteristic reddening and  !

I hematological findings to be observed. Sometimes, however, there 4

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-,m 4

! li 70 . MEmCAL ASTECTS OF R ADIA' TION ACCIDENTS -

3 \'

U may be a rapid development, of pancytopenia within 7-10 days, 4.7 Acurs Ecs 71 together xith a hemorrhagic gastroenteritis.

,t! After a shortened latent period, of perhaps 5-8 days, during which The Acute R:

fatigue and low grade fever occur, the manifest illness begins with large gamma at

' :' ;y nausen, vomiting, diarrhea, high fever and pancytopenia. There is possible that sii

~

gradual progression of these symptoms over the next several days and of a large part n

f later there may be blood in the stool or vomitus. Extreme prostration ) electron beam, h al Wotu o( and episodes of shock and cyanosis ator* is usually 1 l1-e .-m indicate a downhill course unin-

.:,., fluenced by resuscitative measures which leads to the demisc of the . tissue in humai

} (Q; M patient, usually 15-30 days after the exposure.

about thirty mil sNd i Gmp V Cases:

at most,10 cm.

3y,, gy, y,,

These patients received such massive irradiation that survival is for tions of the efic a period of hours or peihaps a few days. There has been one well . body, perhaps t

~.

studied and well documented case of a man who, as a result of a biological effects critieniity ncenient, rcccived an acute dose of about 10,400 rad to the  ; the effects of gn head and 12,000 rad to the upper abdomen (fast neutrons plus gamma tration may be <

j With very lar

rays). The description which follows is based on observations i recorded on this patient [1]. .

3 of the exposure.

2 .

A person who has received this order of exposure will show immediate with crythema disorientation, ataxia and mentn] incapacitation progressing rapidly to Skin sensation d semi-consciousness and severe prostration. Ile may complain of and later of pai

= necrosis.

severe burning sensations in the first few post-exposure minutes. ,

After 20-30 minutes, severe cardiovascular shock appears and the Together witiq patient may seem to be almost moribund. IIe may be incoherent, reaction (analag p retching, vomiting and byperventilating. The skin may appear bowever, this syj Acute Radiatiod

'U, dusky, reddish-violet, but may be cold. The mucous membrancs appear cyanotic and the conjunctivae hyperemic. This paradoxical 1 With lower dd

1. g# less severe'and <

.1 picture of sh~6c'k'in association with skin'hypgemia.is due to the early MM

~

!.' appearance of the erythema which was causedTay the massive dose of ,N X-irradiation as i irradiation. sues will depend w The shock is manifested by a rapid, hardly perceptible pulse and by the first 2 or 3 d a precipitously falling blood pressure. as far as the ac y[

Watery diarrhea and vomiting occur in the first hour or two and long-term effecta S anurin persists throughcut the clinical course. i effects are beyor

[I Some coherence may return to the patient, during which time he may compInin of cramps. Physical examination is likely to reveal nothing 4.8 R Amnios g

( abnormal apart frorn the features already described. The high . Epilat. ion has .

o' . temperature may be ma.m ta.med for several hours and then fall. ..

• . of radiat. ion mju

& Lymphopem.a and marrow destruct. ion may be observed with.m hours Beta-ray . .mjurp

, I of the accident. '

Ir The illness terminntes fatally following increasingly severe resticss- E*"""""" "

l more extrem I

3 ness, mcoherence, abdonu.nal pa.m and swent.mg; the pat.ient finally a . Radiat. ion der a subsid.ing mto collapse and coma.

l f radiat. ion. Bets r.'

3 i,.

ll

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