7 AD-fi49 284 BEHAVIOR DEGRADATION DUE TO iiB-RAD PULSED

RADIATION i/EXPOSURE (58:1 NEUTRON/GAMMA RfiTIO)(U) SCHOOL OF

U CL AEROSPACEAMEDICINE BROOKS AFB TX 0 C BROWN ET AL.UNCLSSIFIED OCT 84 US FSRM-TR-84-30 F/6 6/18 NL

EEOMOEEE

11 il 111112.0

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MICROCOPY RESOLUTION TEST CHARTNATIONAL BUREAU OF STANDARDS 1963 A

* USAFSAM-TR-84-30

00 BEHAVIOR DEGRADATION DUE TO 1100-RAD* N

m PULSED RADIATION EXPOSURE

(5.8:1 NEUTRON/GAMMA RATIO)I

G. Carroll Brown, Ph.D.

Michael G. Yochmowitz, Ph.D.

Gene B. Hubbard, D.V.M., M.S.Kenneth A. Hardy, M.S.

David M. Hughes, B.S.

Billy Yarbrough, Senior Airman, USAF

DTICELu.CT*r~JAN 2 198E

October 1984 S

Final Report for Period June - December 1982 .

Approved for public release: distribution is unlimited.* t ii

c.' USAF SCHOOL OF AEROSPACE MEDICINEAerospace Medical Division (AFSC)Brooks Air Force Base, TX 78235-5000 .. 7_ ,F::7-.-

S 84 12 20 003

NOTICES

This final report was submitted by personnel of the Vulnerability Assess-

ment Branch, Radiation Sciences Division, USAF School of Aerospace Medicine,Aerospace Medical Division, AFSC, Brooks Air Force Base, Texas, under job

order 7757-05-50.

When Government drawings, specifications, or other data are used for any

purpose other than in connection with a definitely Government-related procure-ment, the United States Government incurs no responsibility nor any obligationwhatsoever. The fact that the Government may have formulated or in any waysupplied the said drawings, specifications, or other data, is not to be

regarded by implication, or otherwise in any manner construed, as licensingthe holder, or any other person or corporation; or as conveying any rights or .

permission to manufacture, use, or sell any patented invention that may in any 0way be related thereto.

The animals involved in this study were procured, maintained, and used in

accordance with the Animal Welfare Act and the "Guide for the Care and Use ofLaboratory Animals" prepared by the Institute of Laboratory Animal Resources -

National Research Council.

The Office of Public Affairs has reviewed this report, and it is releas-able to the National Technical Information Service, where it will be availableto the general public, including foreign nationals.

This report has been reviewed and is approved for publication. 0

4 , . p,-

G. CARROLL BROWN, Ph.D. DONALD N. FARRER, Ph.D.Project Scientist Supervisor

ROYCE MOSER, Jr.Colonel, USAF, MCCommander

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bhavioral ',rfo'rmance effects of a high-neutron, low-gamma radiation puise exposure (average

1 1 oU rads5 Midlinep t i 5C3ue, 5.8 :1 neutron/gamma rat io) . Eight rhesus monkeys were exposed atthe Wite S;trcs MIissile Range Fast Burst Reactor and tested daily for up to 5 days afterex;'F3uF-. Dr be exposure day, all niht subjects had ignificantly degraded response acc.-

racy, s-v;en hidl increasfed reaction-time scores, seven experienced productive emesis. One day.'r expi p' 1- mos subjects performed near baseline levels except for occasional brief

e r :o s)- At diys, w1 subjects were unable to meaninfully perform the behavioral taskbvl wera p; ah eff. The o six subjects were more variable than on the previous day.Thre sutjects; experinsr, d ' adl tionai emetic episodeq. At f days, only two of the remaining I

four -in ima.l perform.',1 at. any reasonable degree. It is unlikely that any animal could have .'.

performel on tie sixth lay. . . , .,,. -, .. . ,. .

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DD FORM 1,73, 83 APR . C N(LA SSIA8:I E1

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CONTENTS

INTRODUCTION................................ .. .. ...... . ... .. .. .. ....

* METHODS AND PROCEDURES...........................3Subjects................................3

* Task....................................4Equipment................................5Photography...............................5Exposure Procedures...........................5Dosimetry................................5

BEHAVIOR.................................15

PATHOLOGY.....................................26Materials and Methods.........................26Clinical Evaluation..........................26Gross Pathology............................28Histopathology............................30

DISCUSSION................................38Pathology...............................38Behavior................................39

REFERENCES..................................44

*APPENDIX: THREE-MINUTE AVERAGE REACTION TIME AND ACCURACY SCORES . . . . 47

List of Illustrations

F igur

* 1 Animal response panel........................4-2 Fxp >4ure configuration for phantom dosimetric measurements . . .. 7

43 Animal exposure configuration....................9-4 Phantom subject..........................14

5 Baseline accuracy.........................16

6 Accuracy on expostire and postexposure days.............177 Basclin'- reaction Lime for a correct response...........19

React ion tines on ,xposure and postexposure days .......... 204 Y 1east-sc'iaros l ine fitted to 1)asel inc reaction-time data ....... 5

ICurt icomedul 1 .ry area of the kiuney....................................2)

I1 (*Colon ic lumen and focal areas of the scrosal surface ........ 2912 Pancreas..............................3013 n,, !v n I , i I ie...........................31I pc It( foIlI i ..... ... ... ... ... ... .. ... ... ... ... .. ... ... ... ... ... .. ...... 31

* ~15) Rentl con ical tubular epithelium............................I 1, T,,a iedu1 mr,. collect ing tub~ule-..................327 1- ionrcut Ic niecrosis.........................0

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eiu r V 1 77 r _e

18 Loss of colonic mucosal height . .. .. .. .. .. .. .. . .. 34

19 Colonic lumen .. . . . . . . . . . . . . . . . . .4

20 Crypt spaces . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

21 Absorptive surface epithelium . .. .. .. .. .. .. .. . .. 35

22 Bone marrow . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

2"3 Adrenal cortical epithelial necrosis .. .. .. .. .. .. . .. 36

24 Salivary gland acinar epithelium .. .. .. .. .. .. .. . .. 37

List of Tables

Table

I Schedule for testing at White Sands Missile Range . .. .. . .. 6

2Radiation doses measured in test phantom exposure . .. .. . .. 8

3 Radiation doses measured in phantom exposurc w-ith animal group . 10

4 Radiation doses measured in phantom exposure with animal group 2. 11

5 Booth monitor dosimetry data .. .. .. .. .. .. .. .. . .. 12

6 (Performance errors)/(number of trials) for 4-h test period on

each test day . . . . . . . . . . . . . . . . . . . . . . . . . 18

7 Baseline vs exposure-day maximum reaction times .. .. .. . .. 22

8 Exposure-day errors distributed across eight half-hour test

periods . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

9 Comparison f average reaction times .. .. .. .. .. .. . .. 23

10) Clinical signs in monkeys after irradiation .. .. .. .. . .. 27

It Grtoss pathology . . . . . . . . . . . . . . . . . . . . . . . . . 28

12 Radiation effects -- 1100 fads and 600 rads .. ... .. 4i

I3 (Perf,rTance errors) / (number of trials) for 4-1h test periods for

6 7{)- -id study, n/g 5.5:1 . . . . . . . . . . . . . . . . . . . 42

[ AVcesslonl For"

A v ;- . t Codes"

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19i : ° : -Co on c lu . . . . . . . . . . . . . . . . . . . . .... ................... 34

",'- -. 1 21..Absorptive surface • epithelium.-" - .- ...... '... ".... _...... .-... ..'.. ".. . ...- ,...''.,.35

2 B. .•

23 Adrenal crticalepithliob erss...................3

24 alvay lad ciarepiheiu............................3

BEHAVIOR DEGRADATION DUE TO 1100-RAD PULSED RADIATION EXPOSURE

(5.8:1 NEUTRON/GAMMA RATIO)

INTRODUCTIONp

Nuclear weapons produce blast, thermal x-ray, and electromagnetic pulse aswell as alpha, beta, gamma, and neutron irradiation. An aircraft frame protectsthe crew from the blast of an intermediate dose range (100-3000 rads). Thermalcurtains or shields with PLZT flashblindness/retinal-burn protective windowelements can be used to isolate crewmembers from the thermal effects (6). Inthe lower atmosphere, where most manned systems operate, x-rays produced duringdetonation are absorbed by the atmospheric gases in relatively short distancesand are of little concern. Baum et al. (3) reported that the electromagneticpulse environment minimally affects crewmembers even after exposure to 108

pulses of electromagnetic energy with amplitudes of 447,000 volts per meter.Therefore, of the components in the nuclear environment, nuclear radiation isthe most significant contributor to crew effects.

Acute radiation (gamma) exposures spanning a wide range of doses have beendIescribed by Gerstner (12), Zellmer (35), Pickering et al. (25), and Albaneseand Pickering (1). With whole-body sublethal doses--i.e., 100-300 rads gamma(midbody tissue)--human subjects exhibit mild to moderate prodromal reactions oflistlessness, discomfort, weakness, anorexia, and possibly nausea and vomiting. .With doses in the range of 300-800 rads, reactions are characterized by a higherprobability nd more rapid onset of nausea and vomiting, increased fatigue andlethargy, and then diarrhea. Exposure levels beyond 800 rads speed the onset ofthe above effects and may include extended periods of vomiting and prostration.In the intermediate dose range, these effects gradually abate after 10-12 h butmay reappear after 2-3 days. Depending on the time of their onset and duration, . -

some of these symptoms may moderately or severely impair the ability of aircrewsto perform specific tasks.

More data about man's ability to operate after exposure to high-neutron/low-gamma environments is needed. The only large body of data for neutrons andnontherapeutic human exposure is the followup on the Hiroshima and Nagasakisurvivors, and the relative value of that data has diminished with recent evalu-

* ation and revisions. The end point has been death rates from various types ofcancers. Leukemia mortality rates appeared to be higher in Hiroshima than inNagasaki. Based on tentative 1965 dose estimates, the differences were attrib-uted to a much higher neutron component at Hiroshima (8). In 1980, William Loewe

and Edgar Mendelson (19) sharply revised those bomb dosimetry estimates. Theirproposed leukemia mortality dose-response curves show no difference between thetwo cities. They believe the neutron element was so low in both cities that .2only very limited conclusions can be drawn about the relative biological effec-

tiveness of neutron and gamma radiation. The debate, however, is by no meanssettled.

IO

- . . , ,". " - ,- " . -

The capability of Air Force systems to withstand exposure to a nuclearenvironment without losing their mission-completion capability is termed "sys-tems nuclear survivability." Because man is a crucial part of Air Force sys-tems, the identification of "sure safe" and "mission failure" radiation doses,with effects of time considereu, is essential. Within limits, the aircraftframe and additional safety devices can provide protection from many nuclear-weapon effects but not from nuclear radiation. An enhanced-weapon's dispersiondistances are considered to be significantly larger than those of currentweapons, yield for yield. If a weapon is released from a low altitude, thecrewmembers who drop the device may receive partial exposure from it. There-

fore, we must understand the operational significance of behavioral-performancedegradation; i.e., 1) the onset and duratiun of early transient incapacitationand performance decrement, and 2) immediate permanent incapacitation, althoughthis would not be expected to occur at doses considered in this report.

Flying requires highly complex tasks that must be performed for extended

period of time. Normal aircraft operation involves many stressors includingtask complexity, workload, fatigue, and physical and psychological stress. Howmuch stress small amounts of radiation add and its effect on mission completionmust be assessed. Even with a protracted exposure, a total dose of 300 rads(gamma) has been shown to impair performance and increase reaction times (4,

34). Less is known about the behaviorL- effect of neutron doses; the equivalentnumber of rads (neutrons) apparently does not produce equivalent exposure ef-fects. Examples of studies that compare gamma and neutron exposure effects arethose by George et al. (11) and Thorp and Young (29).

The study by George et al. investigated the relative effectiveness of fis-sion neutrons for performance decrement in the miniature pig. The incidentneutron/gamma (n/g) ratio was 10:1; the dose rate was 2000 rads/min; and mid-brain doses ranged from 1500 to 36,000 rads. The task for the pigs was totraverse on cue a two-chambered shuttlebox. Their response to supralethal dosesfrom the neutron field was distinctly different than to similar doses from thegamma field. Early performance decrement, early transient incapacitation, and

immediate permanent incapacitation all occurred at much lower doses from thegamma exposure than from the neutron. With early performance decrement anddeath within 48 h as end points and with the gamma exposure as the referencepoint, the relative effectiveness of the neutron field was 0.23.

Thorp and Young (29) evaluated the relative effectiveness of neutrons forcausing early transient incapacitation in 58 monkeys (Macaca mulatta). The neu-

tron/gamma ratio was 10:1; the dose rate was 2000 rads/minute; and the midbraindoses ranged from 2200 to 4400 radz. The task for the monkeys was a visual-liscrimination two-choice problem, between a square and a circle. The subjecthad to press a lighted symbol displaying the square. Significantly higher neu-tron doses than gamma doses were required to elicit early transient incapacita-tion. The ED5 0 for the gamma field was 2186 rads (midbrain tissue dose); forthe neutron field, 3215 rads. The difference was signiftcant. The relative ef-fectiveness for the neutron field in the study was 0.68 when compared to similar

gamma exposures.

For early transient incapacitation, the relative effectiveness of similarneutron exposures was much lower for miniature pigs (0.23) than for monkeys(0.W ). Also in the studies by George at al. (11) and Thorp and Young (29), theTidtnurax dose was higher for the gamma field than for the neutron, but the

0 - • . °,

difference was less in the study using monkeys (29). This could be an importantfactor in reported differences for relative effectiveness. Dose-rate differenceshave been considered as a variable in relative biological effectiveness (RBE)type studies, but dose-rate effects are generally attributed to rates less than1000 rads/min. The rates used by George et al. and Thorp and Young were beyondthe general area of dose-rate concern. Other factors responsible for the RBEdifference include the different tasks or animal species used. However, theconclusions of the above studies are still in the same direction--gamma expo-sures produce greater postirradiation performance decrements generally attrib-uted to central nervous system disturbances than do similar neutron exposures.

The purpose of this study was 1) to examine the effect of neutrons in orderto better define dose levels and effects that might impact specific Air Forcesorties, specifically at 24 and 48 h after exposure (although our data collec--tion continued for 120 h), and 2) to document the gross and microscopic pathol-ogy induced by high-neutron/low-gamma exposure. A review of the results fromgamma-exposure studies led us to anticipate that the dose level selected forthis study would produce moderate radiation effects as related to mission com-pletion. The task and schedule arrangement 1) contained periods of moderatelyheavy workload (a correct response every 2 s), 2) had an uncomplicated arrange-ment between stimulus and required response, 3) allowed each subject to estab-lish his own pace in operating the task, 4) permitted a significant shift in thepace (faster or slower) but with a response that could still be classified ascorrect, 5) had a moderately undesirable consequence (shock) for an incorrectresponse, and 6) had task length sufficient to produce mild fatigue (as a func-tion of duration and workload).

METHODS AND PROCEDURES

Subjects

Eight male American-born rhesus (Macaca mulatta), ranging between 2.9 and3.3 kg, were randomly selected from the USAF School of Aerospace Medicine(USAFSAM) colony and trained to operate the three-lever Multiple Avoidance Pro-gram (MAP) described later.

Clinical evaluation and chemistries were used to ensure that the monkeyswere in good health prior to exposure. The animals were necropsied to ensurethat clinical impressions and data obtained prior to exposure were not biased bydisease undetected by conventional methods.

Training. Each subject was Individually hand trained by standard shapingtechniques until performance was sufficiently stable for training by laboratoryprogramming equipment. Initially each subject was trained for about 1 h perday. The shock level was approximately 3.0 mA for 0.3 s duration. Once avoid-

ance was consistent (95%) on the center lever, the other two levers were phasedin. Training sessions were gradually increased up to 4 h (to match 4-h testsessions). Subjects were trained in 12-min work periods followed by 3-min restperiods. This cycle continued throughout training and testing conditions.

I

3 I--

.. I. - . .

Diet Control. At the beginning of each work period, each animal received amonkey biscuit and a small piece of fruit. This facilitated catching and re-straining; it also simulated a subject with a small amount (snack) of food inthe stomach. When returned to the home cage, each subject was fed a normalfood ration (8-10 biscuits and 1 whole orange). Feeding times were constant tofacilitate observation for emesis during exposure.

Task

The MAP panel (Fig. 1) was located directly in front of the animal. When

one of the red lights was lighted, the subject was allowed 2 s to press thelever directly below that light to extinguish it. Failure to press within 2 sor pressing one of the two incorrect levers resulted in a small shock (2.0-3.0mA) to the feet of the subject for 0.3 s. At the end of the 2-s response inter-val or when the subject pressed a lever, the lighted lamp was extinguished imme-diately and one of the other two was lighted. Thus, a stimulus cue lamp neverrepeated, and the speed of presentation was established by the animal as long as

a response occurred within 2 s. Some subjects established work rates (set theirown pace) of almost twice that of some other subjects.

_.'

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Equipment

Each subject was placed in an individual cubicle (2'x3'x4') to minimizeexternal distractions. The booth was power ventilated, and a small amount oflight entered near the top-opening door.

All programming was done with Digibit equipment manufactured by BRS/LVE.The order of stimulus presentation was randomized in six balanced blocks of 24trials per block, determined individually for each subject by a punched-paper-tape reader. This allowed each animal to work at his own pace.

Complete data was summarized each minute and dumped to punched papertapefor backup. Identical data was simultaneously transmitted to a DEC MINC (11/23computer) for recording on RX02 floppy disks. Collecting the data in machinereadable format saved time in subsequent analysis. The MINC also permitteddisplay of the data in real time. This immediate feedback was useful in moni-toring performance and helped in detecting equipment problems during the coursein testing.

Photography

All photography and video recording were by White Sands Missile Range(WSMR) personnel. Before leaving the exposur( ll at the end of each worksession, the animals were still-photographed as P g--up. As soon as they wereback in their individual holding cages, a 3-min , recording was made ofeach animal. For some typical animals, the edited video recordings have beenpaired with the subject's performance for each day. The purpose was to comparethe general appearance of the animal (which may be poor) with his performancescores (which may be near baseline levels).

Exposure Procedures

The eight subjects were always tested in two groups of four. Each group

(morning or afternoon) was fed 1 h before its work period started. See Table 1for an account of daily activities.

The exposures occurred 30 min after the start of the work period, so 90 minnad elapsed since the snack (e.g., 1 biscuit and 1 orange slice) had been con-sumed. The small amount of food in an animal's stomach at the time of exposurewas significantly less than his normal ration of 8-10 biscuits and I wholeorange.

Dosimetry p

The exposure parameters required to deliver an 1100-rad pulsed midline dose(neutron + gamma) to a 3.0-kg primate exposed in a training booth to the FastBurst Reactor (FBR) were determined via dosimetric measurements in Aldersonneutron-tissu3-equivalent primate phantoms approximating the size of the animalto be used in the experiment. The phantom exposures were conducted in trainingbooths identical with the ones used by the animals. Free-field measurementswere also conducted.

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On the basis of phantom dosimetric measurements, the required core-tempera-

ture size (AT3 ) of 2500 C and exposure distance of 541" were established. To cor-

roborate the programmed exposures, dosimetered phantoms and monitor dosimeterswere exposed with each group of animals.

From a free-field dose value at 54"1 of 7 rads per oC of reactor core-tem-perature change (AT3 ) and a midline/free-field dose ratio of 0.7 obtained fromdosimetry measurements in May and July 1981 (5), we established that a midlinedose of approximately 1200 rads could be attained with a reactor core tempera-

ture of 2500 C. For corroboration, a dosimetry primate phantom was exposed on3 August 1982 (Op 9612). The phantom was exposed P-A in the primate booth at amidline-to-reactor-center distance of 514" (137 cm). Figure 2 illustrates thedosimeter exposure configuration used in the phantom exposures. The results ofthe phantom measurements for this operation are listed in Table 2. The averagetotal midline dose was 1247 rads, with an average midline neutron/gamma doseratio of 5.8:1. We considered this adequate for the experimental requirements,and the reactor operators were instructed to try to duplicate this pulse in the

animal exposure.

INSTRUMENT PANEL

0.063 IN. (1.6mm)ALUMINUM 1BACK PLATE

ALUMINUMTRAINING E

CHAIRF K

50 IN. (127cm) K

DISTANCE TO REACTORCORE CENTER H

BOOTH MONITOR L

C

Figure 2. Exposture (onfigtirition for plh int om dosirietric 11llmlreiiitet si t 'Ji

FBR, 3 August 1982.

7 5

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['A3LE 2. RADIATION DOSES MEASURED IN TEST PHANTOM EXPOSURE (WSMR FBR,3 AUG 82, OP 9612, AT3 = 276 0c)

3S

Gamma Neutron TotalDosimeter dose dose dose N/G Doseposition (rads) (rads) (rads) ratio

PosteriorA 209.2 1548.9 1758.1 7.4B 229.6 1600.4 1830.0 7.0C 191 .5 1 352.9 1544.4 7.1

Average: 1710.8 7.2

MidlineD 166.1 11814.4 1350.5 7.1F 192.5 11214.1 1336.6 5.9H 139.0 940.6 1129.6 5.07 188.3 984.3 1172.6 5.2

Average: 1247.3 5.8

AnteriorJ 115.2 502.8 618.0 4.4K 136.7 491.7 628.4 3.6L 147.5 553.6 701.1 3.8

Average: 649.2 3.9

Free-fieldat 54" 184.6 1431.0 1615.6 7.8

Boothmonitor 233.8 1R-16.3 2050.1 7.8

Average midline total dose = 4.52 rad/°CAT3

Average midline total dose = 0.61Monitor total dose

Average midline total dose : 0.77Free-field total dose

0

* .1..;... '. . . . , ...

On 6 August 1982 two groups of primates, four animals each, were exposed onthe FBR--one group in the morning (Op 9614) and one in the afternoon (Op 9615).A dosimeter phantom and a free-field monitor were exposed at 54" with eachgroup. In addition, booth monitors were exposed with each animal. Figure 3illustrates the overall exposure configuration. The pulse of 3 August 1982 wasnot replicated. The core temperature sizes actually obtained for the two groupswere 2210 C, and 2310 C, respectively, indicating a delivered dose somewhat lowerthan anticipated. The phantom dosimetry data obtained for these two operationsare listed in Tables 3 and 4. The average midline doses measured in the phan-toms were 1039 and 1108 rads respectively.

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CORE DOSIMETERS

PHANTOM MMONITOR

DOSIMETERS -- 5' . .

2/

\ i FREE-FIELD "N " MONITOR

DOSIMETER

. 7'

Figure 3. Animal exposure configuration for WSMR FBR experiments.

9

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TABLE 3. RADIATION DOSES MEASURED IN PHANTOM EXPOSURE WITH ANIMAL GROUP I

(WSMR FBR, 6 AUG 82, OP 9614, AT3 = 2210C)

Gamma Neutron Total

Dosimeter dose dose dose N/G Dose

position (rads) (rads) (rads) ratio

PosteriorA 165.4 1242.2 1407.6 7.5

B 181.4 1383.5 1564.9 7.6

C 166.2 1247.8 1414.0 7.5Average: 1462.2 7.5

MidlineD 118.9 771.0 889.9 6.5

F 135.4 1026.8 1162.2 7.6

H 158.5 872.8 1031.3 5.5

I 157.4 915.7 1073.1 5.8Average: 1039.1 6.4

Anterior •J 86.3 405.5 491.8 4.7

K 113.3 425.8 539.1 3.8

L 123.7 518.5 642.2 4.2Average: 557.7 4.2

Free-fieldat 514" 164.7 1212.8 1377.5 7.4

Boothmonitor 194.4 1496.7 1691.1 7.7

Average midline total dose = 4.70 rad/ 0CAT3

Average midline total dose = 0.61Monitor total dose

Average midline total dose = 0.75Free-field total dose

.4

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p

,A33 4 RADIAT ...... DOSES MEASURED IN PHANTOM EXPOSURE: WITH ANIMAL GROUP 2( SMR F!R, 6 AUG 82, OP 9615, AT3 = 231 0 c)

T3

Gamma Neutron TotalDosimeter dose dose dose N/G Doseposition (rads) (rads) (rads) ratio

PosteriorA 179.9 * *

B 205.1 1458.1 1663.2 7.1

C 174.8 1200.7 1375.5 7.9Average: 1519.4 7.5

Midline

D 133.4 828.4 961.8 6.2162.0 998.0 1160.0 6.2

H 176.8 912.3 1 089. 1 5.21 166.8 1052.6 1219.4 6.3

Average: 1107.6 6.0

Anterior

J 116.0 * *

K 123.8 506.3 630.1 4.1L 128.2 516.2 644.4 4.0

Average: 637.3 4.1

F ree-fieldat 54" 174.5 1321.5 1496.0 7.6

iooth

. nitor 209.1 1635. 3 18844.4 7.8

z'ar-ige midline total dose 4.79 rad/ 0 C' 3

Avort~e midline total doseMonitor total dose

6 4v'<ruo m.idine total dose .74Fr*,*-. c .. tot: drt

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*' _ - . , - • . . . . . . " . . . . . . ; - , . . . " "

Table 5 lists the results of the individual booth monitors. This data indi-cated average estimated midline doses of 1066 and 1118 rads to the respectivegroups. These were in good agreement with the phantom measurements. This dataalso indicated that all exposures were within ± 4% of the average.

Based on the phantom data, entrance and exit doses are approximately 1.38and 0.55 times the midline dose. For the 1066-rad exposure (Op 9614), the en-trance and exit doses were 1471 and 586 rads; for the 1118-rad exposure (Op 9615),1543 and 615 rads. The average neutron/gamma dose ratios (± SD) based on thephantom data in Tables 2, 3, and 4 were as follows: midline, 6.0 ± 0.8; freefield, 7.6 ± 0.2; entrance, 7.4 ± 0.45; and exit, 4.1 ± 0.4.

The gamma dose component was measured with type 700 LiF thermoluminescent(TL) powder dosimeters (Harshaw Chemical Co. Lot # 1-OL-1), which were read outon a Harshaw Model 2000 thermoluminescence analyzer at USAFSAM. Gamma doses wereassigned by comparison of responses of the dosimeters exposed at the WSMR FBRwith responses of dosimeters (from the same lot) exposed to known doses ofcobalt-60 gamma rays.

TABLE 5. BOOTH MONITOR DOSIMETRY DATA (WSMR FBR, 6 AUG 82)

Operation 9614, AT3 = 221oC

Animal Monitor EstimatedBooth ID (No.) total dose (rads) midline dose (rads)*

1 156Z 1 1684 10272 190Z 2 1729 10553 318D 3 1810 11044 204Z 4 1771 1080

Average:1066 (± 33)

Operation 9615, AT3 = 231C

1 356D 5 1788 10912 348D 6 1801 10993 344D 7 1881 111474 346D 8 1863 1136

Average:1118 (± 27)

* onitor do-e x C.61.

0

12

-

The fast neutron dose component was measured with dl-alpha-alanine, a freeradical dosimeter system. The radiation-induced free radical response of thealanine was measured on a Varian Associates Model E-6 Electron ParamagneticResonance Spectrometer at USAFSAM; the peak amplitude of the free radical spec-trum was used as the response. The dl-alpha-alanine measures both the fastneutron and gamma dose components. To determine the fast neutron dose (DN), theresponse due to the gamma dose component (DG) as determined with the TL dosi-meters had to be subtracted. The DN was determined from the following empiricalrelationship:

DN = N (DA - DG)

Where N = fast neutron dose conversion factor

DA = Co-60 equivalent dose in rads

DG = gamma dose in rads.

Previously N was determined to be 2.44 (± 0.11 SD) by direct comparisonwith activation foil measurements exposed concurrently to the WSMR FBR spectrum(5). DA was determined by comparison of total dose (neutron + gamma) responsewith a Co-60 gamma calibration set exposed on an Eldorado 78 Co-60 teletherapyunit at USAFSAM. The gamma output of this facility had been measured with ioni-zation chambers having calibration factors directly traceable to the NationalBureau of Standards. DG was determined with type 700 LiF dosimeters.

The primate phantoms were constructed (Alderson Research Laboratories,Inc., 390 Ludlow St., Stamford, CT 06904-1271) of Alderson Plastinaut materialwith an elemental composition approximating soft tissue, especially with regard Sto hydrogen and nitrogen, thereby making this material "tissue equivalent" tofast neutrons. The phantoms (illustrated in Fig. 4) closely approximated inphysical size the animals used in this experiment.

13

~

* *1

I

a

4 0U

S

*

a

S I. B0 t

I -

S

0

3 H NA V 10 R

7a Iabesotd edeach dlay were accuracy (the number of errors) ano~ cor-rei -respornse tim es. Subj~ects were scheduled to perform on 1 2 occasions;: fourbaseline runs; in exposure run; and postexposure followups at 24, 48,7,

: -nd 120 n. The first two baselines were used to test equipment and allow~e.to o d 4ust to t! -ir new surroundings. The other, two basel ines were ue

i a t anc ard a.-,iinst which ?,ioh subject's performance could be judged on expo-suro and postexposure days.

Figures 5 and 6 show the iccuracy for each subject on each tes.,t day. Th epl points represent 12-mmn summaries (given in the Appendix). Subjects goner-

-ally performed with near 100% accuracy on baselines 3 and 4, preceding exposure.Th is is indicated in Figure 17 by the overlapping of points forming a bold plot5ym bol.

On exposaire day, the earliest accuracy decreases were rioted within 12 minafter exposure--in subjects 2, 3, 5, and 7, with respective accuracy scores of33%, 76', 97%, and 80%. (Subject 5's performance had never gone below 98% dur-ing baselines 3 -and 4. ) Within 42, 57, 72, and 117 min, subjects 1, 4, 6, and3excerienced their first performance decreases--with respective scores of 93%,

95%, 75%, and 97%. The earliest decreases for four subjects (1, 2, 4, and 7)coicided with their lowest accuracy scores. Subjects 3, 5, 6, and 8 had their

*lowest scores--22%), 921, 2%, and 69% respectively--at 42, 207, 162, and 1921 minafter exposure.

On postexp-osure day 1, subjects 1 and 6 had perfect scores; and subjects 3,57,nra d near-perfect scores. Subject 2's diminished accuracy began

anc~ Cmin inito teruni and lasted about 50 min, with scores ranging from 87% p

.1 t~lop0ostexpcsa,,re day, subject C continued to give perfect per-fc r' mrce sub, 3, a nd 7 continued with near-perfect performance; and

S reP Ur-,, t) neair-perfect performasice. Subject 5's performance ranged* e~ n I r'1 )! subject 4'Is, from 0 to 1 3%; and subjiect 8 could not work

an 4iis:mov-'c f rom the experiment.

Dy the I~nir~. postexposure day, subjects 1 1 2, 6, and "~ gave near-perfect*pmrt'an while subjects 3 and ') had variel performance. During his last 2 h

of r ane ect S's accura-:cy ranged from 95)% to 99, in contrast to hisneir-perf t Ini ines. o)ubJect 3's accuracy di,! not diminish until his last

* ~ ~ ~ o r--C r~-~P~ orm~tnce, when it -anged from )3% to) 971.

'tn- f'oh ly, subjects 1 , 3, 5, and 6 give- near-perfect performances.l ii not. Durir g the first half-hour, subjeo-t 2's accuraciy fellI

rr 0 t: -Its :3econd half-hour yield1ed no performance, so he warf; with-lr ~ ~ ~ 1 i-r ho re Iy. SUbjc 7 '1 wei incl 1i iar trI ftr, haiv ing, scorer

* in '~~- f 41." r .~n 1) 'rin, 'n~u~' a~it,, 35%1 during tho next hour.

1, n 1 ti~ W ; cel rr:T1

I-, 'r ' r " In tl' w,,nt r. no i r w i th nPa r er otn'' ~~' iu 1 *ira hetween _ n:. ,"ubj~rt he-p

i wn nI ate ' , C' rom cQ%1 to 71 ;lbi(ot Ps CuO" were

Y .~1"I a tr'

BASELINE 1 BASELINE 2

0.75 0.75

-.-.

S0.5 0.5

Li Li

0.2S 0.25

a+ 0

0 so 160 240 0 60 160 240

MIINUITES MIINurTES

BASELINE 3 BASELINE 4

1 g * I i g g! i g i * g g e * g, I * e , * I! g * g * e g l l I -

0.75 0.75

cr-

0.5 0.5

C-,-

cc

C0.25 0.25

-" *0 24o 0 60 ISO 240

M INUTE5 MINJTES

-- +

*Figiire 5. Bisel in' J-ni Si t ;ire numbe11)red L threu( 8, ;nld thles rlare trp Iil ver I 1 2-r i i i ( i t bi -s ( C i i

rest per inds ) 1-urk spot.,s I ad i Cat C whe re sub c: t s per formancesoverlIa p.

tI '0.507

- - -.

EXPCS IRE P.E. DfRY I

I, r O

88 8I 8O.

, Cr

i a:

90 16 240 so 160 240

iIN JTES MINUTES

P._. DRY 2 P.F. DR 3 S

0 • 5 0.75

7- 7- 0cr (r

ce 0.5 or, 0.5S-D

CC-

C- Ib

3--_ .- * ,A .a. LA__ ----- ____- o _______________

F I0 160 240 0 60 163 240

M, I N jTrES rITNJTES

P.E. ORI, 4 P.E. DRY 5

roo 6 o9 * l o 9 o9I!|l :, I :,77

7. 15 0.75

, ,.b -w 0.5 'C- -

7 C-

I~ L:

0 .6' 240 00 160 240

MTN JTES

Ii triir e. .AcCIr;lCV OT1 exposLiire :ind pnstexposure (P.d.) cays. Subjects are

tumbt'red 1 through 8, and scores are computed over 12-min intervals

(l loed 3in rest periods). Dark spots indicate where sub- 0

ject,;' per tormanes ovrlap. The neutron pulse occurred at 30 min

or cxposlurt, d;iV.

17

... . : .. .0

- ,,. ,,,... .'MI in- ;.:m'sr i a> rE tot i I riuber t-rro. ;ui1

I -'s ~ V VY'21

': !. in a th liii Ifni! to )' 1 .4 ;1 <rpi n I

he- . .... ~ .. r .: r -'o t, 11w);. .'t

q iM post axp)iui'" 1-t; a -urn- 410rin 51V n prPseri.t nw

in :c -J--, i ran, P 1) j-.

-. ~17 , - *.v;fl, tho 3u;o w wo~.<re .57217 tniine>1 anA ItK'in i

v ir 'l .,ia . '1 m ; -2 1- prior 5 tK:'- 5it'c;s M. The 3 31 wrrr

fina o .3 inwn* .m5 iv tne' flus-t' af errors this subtject ma- I-

a. ;-w to -s n ia--l subtr ntii1 -Wna in performs- ±@u. For thiz rn :5w .

* ~ .* I -tow t.-s; !q3y by me no of tho number of errors made on each test

23 iKV /kNUMBPH OF Tti LA u>) FOR 4-1i OO

-'9 1. C ON OACH TOM DAY

0 <is s-E mX.'t' Postexposure daysO n0--: 3 4 d iI 1 2 3 '4 5

'K 1 17 51 1 1 50 57 93 3314

2 1W. I 1_ 130 135 53 59 236a DO

1> 7"? Oi s'. 53 '9764 3333 "593 583

2 . 62 150 67 6 9 3b4-S 75 1 03 &Y-) 71314 2603

Iro 315 0II W

3F 1 F,, 13 72 31'4

03A. A.

- ..-.. > [1' ~ . -

1 .4, . . * .Id

g u! t 5iO o :r eati ~ t I e3frao eo.r:,p Dna~cotans~ar~I t ia ,xommar'y. There is generally more- var'iahili '.y in ~'

r, tri ; ea o a ,.- n sob). -,c re.,-aonds it his . own p~ioo w ith in- the ro!.4 *o tIndc- basel m n1t.irs(Fig. 7)' overall roaict ion t imes2 rainged f'r-rm

* .0 S; i"h s3Ub oD rett~ ~ne;e lp-ill y j ilt? Ia ,I,!<o la 4- .s the a Ioies t ronae ob t ,, a he fas3tc!t .

b bbb b b

01C160 24'

L B2P L' 1 N 4

II

0 -- .. . . ,

S - - *c4 N J' ~ ~

*v I-

EXPOSJRL P.E .pp4o I

2 r}

7 b

SC, 60 240 5 80 16, 240MIN jTLS r TN JTL,

0

.L. PqY L P.L. 9, .j

4

b~ b b~ bO

II

0 160 -40 s 160 240

rTfN J TE £ MINJTES

P.L. DAY 4 P.E. nqY'

I 200

0 80 10 240n 80 160 240rINJTL ]' irNirTLS

.6 ~ 2 "' 1T24

" igr-8.Racin ims nexosr --.d..stexour days S-ub.ects.are

- --_ . -_-. . . _-

During the 30-min preexposure period on exposure day, the subjects' response

patterns were generally similar to the preceding baselines. In particular, thescores were within the same range (.5-1.0 s); they were linear; they were flat;and the fastest subjects (2, 4, 6, 8) maintained their ranking. After the neu-tron pulse, reaction times slowly rose in all subjects except number 8, whosereaction times remained flat. Variability increased in all subjects, and new

maximum reaction times were reached. Subjects 2, 3, and 4 were the first toexceed their maximum baseline reaction times, by 27 min after exposure; laterthat day their respective maximums became 1.03, 1.28, and .98 s, yielding netincreases of .21, .40, and .28 s over their maximum baseline scores. Subjects 1,

5, and 7 were next, exceeding their baseline maximums at 42 min after exposure;their new highs were 1.27, 1.35, and 1.04 s, for net maximum increases of .42,.37, and .21 s. Subjects 6 and 8 were among the fastest baseline responders andamong the last to exceed their baseline maximum reaction times; 57 min afterexposure, their new maximums were 1.5 and .72 s, for net increases of .58 and.05 s. These results are summarized in Table 7, with the percent of time thatexposure-day maximums exceeded baseline maximums. Statistically, by a sign test,the increase in maximum reaction times in 8 of 8 subjects is a significant event.

At 24 hours after exposure, responses were returning to baseline patterns.Subjects 2, 4, and 8 were still considered to be among the fastest responders,and 5 the slowest. For all subjects response times were considerably less vari-able than on exposure day; they were generally linear, flat, and ranged from .5to 1.0 s.

By the second postexposure day, quick-responding subject 8 was unable toperform and was removed from the experiment. Subject 4, another quick responder,exhibited variable response times ranging from .5 to 2.0 s and was withdrawn fromthe study. Subjects 2 and 6 had the quickest responses, but with greater varia-bility than on previous days. Subject 5 maintained his position of having theconsistently slowest responses, with times generally in excess of 1.0 s. The

responses of the other subjects, more variable than before, continued to rangebetween .5 and 1.0 s.

On the third postexposure day, subjects 1, 2, 3, and 5 were consistentlytaking ! or more s to respond; subject 5 was still the slowest. Subjects 6 and7, whose responses were the fastest, ranged between .75 and 1.0 s.

During the fourth postexposure day, subject 2 had to be withdrawn since he

could not complete the sessions. Subjects 1, 3, and 5 continued to take morethan 1 s to respond, and subjects 6 and 7 responded as they had on the previousday.

By postexposure day 5, four subjects remained for testing. Subject 3 couldnot complete the 4-h performance period and was withdrawn. The remaining subjects(1, 5, and 6) each took more than 1.0 s to respond on the average during a 12-mintrial. Their range (at baseline, .5-1.0 s) now stood between 1.0 and 1.5 s, i.e.,

an approximately 50-100% increase in correct response times.

21 •

............................... ......................

I t.i itl *. - - -. -, -..-- -. - _* -- .

TABLE 7. BASEL INE VS EXPOSURE-DAY MAXIMUM REACTION' TIMlE.-

Baseline Net increase Time (mnin)* % Time 0Subect(s)Exposure ()baseline is over

No. -- ID b3 b day (s) over baseline 1st exceeded baseline

1.85, .(7 1.27 .42 42 752, 6 1. -21 27 19

3 318 .68, .86 1 .28 .14o 27 81.7.69 .98 .28273

5 ' 5b .98, .88 1 .35 .37 42 752, .73 1 .50 .585,'6

3L,' .33, .81 1 .0~4 .21 42 '5.)3, .607 .7 2 .05573

* ~ ~ i, L, T~ible 6 and ranking within subjects, a multiple comparison peru

l ')on Fr iedman ranK sums (1 6)* detected significant differe nces5 at th,l ,onra~stinO, t"ne errors on all the test days against tkl" lat, ba'-r-,'"(

7xpos,-ur;e Jay and postexposure days 3, 14, and 5 had signifi(cantly or,-S Ve, 4-.s tes t periY1ds) than the last basel ine. Tabl')e sio

*,, errr s o- istribateod over eig~ht hal f-hour performance pe oen exposIr. 1 J. '

'y~s. 7r 7, ,roco ._ire and a-eethe to.a njr of err-orZ a ma 1 inst the sevcenth half-hour after expos-ure 4er,: sigii

* in- a~ b ~r af erra)rs -ommitted durin ' the 'a es~.

~n t rse f !' he 4-, test :rl on (..ch ts i

Sa n-

u r-, 5-i uson '-ri r~ nik,r), me t -45 u ) 5' 'X '~j' r

'''

* - P> o0:4.-4

*Li

TAL*.BSLN SEPSREDYMXMMRATO IE

*i

• . . . S - = .. _v - --. -.

T U5 L F. EXPOrSURE-DAY ERRORS DISTRI3UTED ACROSS EIGHT HALF-HOUR TEST

PE RI O1);

Half-Hour Performance Periods -

NObj ID Postexposure TotalXo. -- ID Preexposure 1 2 3 4 5 6 7 errors .

15% 1 1 36 6 4 2 1 0 51 9190 0 98 1 3 0 3 2 6 130311 C 101 393 207 45 14 10 13 783204 0 11 31 8 3 1 8 1 63

3353 0 14 36 72 41 34 53 104 3541 0 12 199 253 600 372 8 1445

Q7 11 11 16 14 10 14 174

3 6 6 23 9 8 451 508

" )t 1 er'rors 5 325* 543* 512* 385* 677* 464 597* 3508

T difffirence from preexposure period: 0 = .05, by equation 20,

.5 Hollander and Wolfe (16).

TABLE 9. COMPARISON OF AVERAGE REACTION TIMES

(a) Times (s) for 4-h Test Periods

Ese ines Exposure Postexposure days-- 4 b4 cay 1 2 3 4 5

970 .8 .78 1 .00 1.29 1.07 1.29-. .75 .76 .92 1 .04 1. 4 WD - "

- . - .79 1 .00 1.10 1.09 1.13

.67 .97 W1 W D W

1- c' 1 .95 1 .47 1 .19 1.12 1.30.77 .79 .88 .93

.8S 98 .92 1 .00 WD". u6 WD WD WD WD

: 2 ...'" Tn r,. v.-r B:3se1 inc (4; b4"~ Reactio -l

- , ,,-Fx c ur, Postexposure days".__ - __ : _-_ . lay 1 _o4 h'

YS-- " .4. '4'' 44 7

4).c

" • .... 10 31 ,33 29 5

--- " 1 9 9 ") f9,•1.4*; .! £ -"; ? 4 W- S

" :11 2>' WX W C

* f 1". 1 - I.

"-"" .. .. . " - ,- " " " " " " I • I I I " - I

.4 ..

Each subject's reaction times were examined individually for radiation ef-* fects. The benefit of this approach is that it eliminates the "averaging out"

of effects between subjects due to subject variability when reaction times mightchange. It also prevents averaging out effects within a given subject due totemporary excursions from his baseline behavior. We first fit baseline behaviorwith a least-squares line and then constructed the p = 0.95, a = 0.05 tolerancelimits of Lieberman and Miller (18) to identify a band of normal behavior aboutthis line. Brown et al. (4) first applied this approach to reaction-timeexperiments. The method requires time-independent data. The Durbin-Watson test(24) indicated four instances that were correlated. Figure 9 shows the validresults. The least-squares line was fit to the baseline (3 and 4) data points.The upper and lower limits correspond to the p = 0.95, a = 0.05 criterion. Scoresabove the upper limit represent reaction times significantly longer by this cri-terion; similarly, reaction times below the lower limit would be judged signifi-cantly shorter.

By this criterion subjects had increased reaction times as follows: onexposure day--subjects 1, 2, 3, and 5; on postexposure day 1--subject 2; post-exposure days 2-4--subjects 1, 2, 3, and 5; and postexposure day 5--subjects1, 3, and 5. Subjects 4, 6, 7, and 8 (eliminated from this analysis because ofthe significance of the Durbin-Watson test) exceeded their maximum baseline

4 scores on test days as follows: subject 4 (withdrawn on postexposure day 3), on

all test days; subject 6, on exposure day and postexposure days 3-5; subject 7(withdrawn on postexposure day 5), on all test days; and subject 8 (withdrawn onpostexposure day 2), on postexposure day 1.

We conclude that of the eight subjects, seven had increased reaction timeson exposure day, and four on postexposure day 1. Allowing for withdrawals due toinability to perform, we found that six of seven subjects had increased reactiontimes on postexposure day 2, six of six on postexposure days 3 and 4, and four of

four on postexposure day 5. All increases in reaction time on exposure dayoccurred after the pulse.

00

24

24"

6' . - • . . - ; ; . T " i" " -" " "

SBET16)SUBJECT 190(2)

2

LjF F FF F F1.

F F F F f, F F . E E00 0

i 0.5 44

0.5

0 s0 160 240 MINUTES 24

MINUTESMIUE

SUBJECT 318(3) SUBJECT 356(5)

22

F 1.5LiJ

F ~FF pA F~~D F ___

cE ELLI _ _ _ _ _ _ _ LI

0 so I0S15 240 0 so 160 240

MINUTES MINUTES

* Fiure9. Least-squares lines fitted to baseline reaction-time data.

3 and 4 = baseline Scores (reaction times) on days preceding

exposure day.*A =exposure day (neutron pulse occurred at 30 Min).

B, C7, 1), E, F =postexposure days 1, 2, 3, 4, 5 respectively.

A least-squares line was fit to the baseline scores computed over12-mmn intervals, and surrounded by p = .95, (x = .05 simultan-eous tolerance limits. By this criterion, scores above the

uipper limits are judge(] to be longer than baseline reaction times.

25

00

P AT Ho LOG Y

Materials and Methods

e o)nqeys were euthanatized with 13 ml of T-61R -ntravenou~y via theright siphenous vein. Complete postmortem examinations were darie. immediately

after 4uthanasia. All tissues were fixed in 10% buffered formalin, processed

routinely, and stained with hematoxylin and eosin.

Clinical Evaluation

P-r4or to radiation exposure, the eight monkeys were alert, active, and

.aiillv normal. When first seen, approximately 4 h after exposure, the major

, igns were vomition, anxiety, and cachexia (Table 10). These signs were

e.;serti.'Iy the same in all subjects, except for one that apparently did not S;emit. Several subjects had loose stools with perianal pasting of feces. The"no y e ealth declined steadily for the remaining test periods, with cachexia,

_,re×a, iril -Jehydration becoming more pronounced each day. Vomition was essen-LUi. y e-.e't on postirradiation day 1; but reoccurred on day 2 in three of the

0 -non,-y; t4o of these also had melena and muscle tremors, one with intermitt,,nt

" ._e monkeys with convulsions and one with severe debility wer._inn d ay -. One monkey began taking minimal amounts of food and water

. .iri1iorn -lay 3, while the others were essentially anorectic. On day !X,

-ney developed epistaxis and gingival hemorrhages and was euthanatized duex. extrem Ielity. All remaining monkeys were euthanatized on postirradiation

:iay -,; ar n< .d lrpel d epistaxis, three had me lena, and four had gingival

0

S:' .. .5

0 i

St

- - - -~ * ~ C~ThJ' 7';. NV~ -~'%. -. x-. ~-. *. -

* S

S2 -

-~2 '. - .22-N. -- -- N

N.2 N N N N -. N N ~ >0222 22 22 - 2

22 22>. 22>. .0 N02> .2OWN 00 00202 >2 -c .3>2Z 2.> 22.0 ''38 ~N

N-

9 2

N >13.2 >0.2

NN2 NN2 NN2 N

2.0W 22WzH W N 2 2- - -. 0-.-- 0.2

222 022.2)13.0 0.3.0

.3 N

2 022.-N 2 2 2 20

02.2 >0.2-- 0 -'--.0 ---. 2.2220 N N 2 N N 2 N N 2 N 0 22 2. 2.) .2 22>

'3.-. "2-' 2 >22.'

2 22 2 N

'3 N '30

.0 "2.0 N

N 2

- W>E S

* 0

N'02 2

* S

* S

* 0

2

Gross Pathology

With a few notable exceptions, the eight monkeys had essentially the samegross lesions (Table 11). These lesions were recognized over time, with indi-vidual variations. The most notable and earliest gross lesion occurred in the 0two monkeys that were euthanatized first. They both developed hydrothorax, andtheir chest cavities were approximately half filled with a clear, dark-yellowfluid. The third monkey euthanatized due to general debility had moderate fluiddistention of the pericardial sac. All eight monkeys when euthanatized were inprogressive stages of emaciation and dehydration. Externally, seven of theeight had indications of clotting defects exhibiting one or all of the following:melena, epistaxis, and/or gingival hemorrhage. Internally, the most commonchanges were loss of body fat and dark reddening of lymph nodes, renal medullas,and gastrointestinal mucosas and contents (Figs. 10 and 11). Two subjects hadmarked reddening of the pancreata and surrounding tissues (Fig. 12).

L

TABLE 11. GROSS PATHOLOGY

Postexposure day

euthanatized Monkey # Lesions

Day 2 204 (4) dehydration; hemorrhage: kidney, lymph nodes,pancreas; hydrothorax; melena

346 (8) dehydration; emaciation; hemorrhage: 0

pancreas, kidney, lymph nodes; hydrothorax;congestion of gastric mucosa

Day 4 190 (2) dehydration; melena; hemorrhage: gingiva,myocardium, kidney, stomach, cecum; hydroperi-cardium

Day 5 156 (1) dehydration; emaciation; hemorrhage: gingiva,lymph node, rectum; congestion: rectum

318 (3) dehydration; melena; hemorrhage: gingiva,

lymph node, stomach, large intestine, pancreas .

344 (7) dehydration; emaciation; hemorrhage: gingiva,

small and large intestine

348 (6) dehydration; melena; hemorrhage: lymph node,kidney, small and large intestine

356 (5) dehydration; emaciation; hemorrhage: gingiva,kidney, small and large intestine; melena

28

F 2*)

1t. .no io~ o I ell anld 1) 1a c kti ' tind e roe-Itvcr hemorhage,

H isto pathal ogy

All! eight monkeyi3 had essentially the same microscopic lesions with vani-oc f a expression. The primary microscopic changes were necrosis, con-

...,m~i, and hemorrhage. Lymphoid necrosis and hypocellularity of bonemir-ow 4 recognized in all subjects (Figs. 13 and 1)4). The lymphoid necrosis

. ~ ~ " c'Y-or n yphoid tissue, throughout the body. Individual cellular necrosis-1 tV pr KX 'r5i: of cell damaige in the salivary glands, adrenal glands,

"a~i , ~a~ran tsti/iltracts, and kidneys. Ne crosis was espe-- .. th- .<i liheys aind in two subjects' pancreata.

r,, -n -~ 7fF*ion were most evident in the lungs, gastrointestinal sub-0Yrp- Phnls xtravasated erythrocytes were usually associated with

~ g ~ in-nd e dema . Marked hemosiderosis in the liver, lymphne ',a r- 'i nd a. renal glands was noted in one subject; minima 1 i to moderate

4r- r0'Mrniri in two othors. The most severe and l ife- threaten Ing* were recoigniz-1 Jn th- kidneys, lymphoid tissues, inte-stine:3,

-n r i , a nd b on e mar r ows .

Tm.r~of* a 1 1-subj ects h,-d d iffuse severe ne crosis of renal tubulalrI lIT. h o' lmf-ns containco deeply eosinophilic proteinaceous

oc-P -lhol '11 cells3, -in minerailized necrotic debris. The* ifl.,a w-r rc. Thb avaueis 1 of' the < idneys were congested, and

'-iaov~sinto-1 thfe I n' erst i t inmas, was mi imal to severe (Figs .

~ ~rr ~n-roa-i3 in six of the, monke ys was minimol with scatte-red mndi-Ii xc " ,rn- in I 'ndocrinoe epi thel iai cl is uindergoing degenerative change,

* "''a '~'I y K-arvarr loxi.-, cytoplasmic swelling, and hyperobromicity of nuleIi.w a autV at wit a od:Im in thei pncreata ad dfuse severe necrosis' and

wer- tho first to Do cuthanat izpd.

ItsV

4-

AV

-or j~ '

(ircI l1Tmph noclotol i i i- I1Vc'orel ulr with lo's, of I \nlpho',\VtoS inh(ce i'n 01 ctLerr-; mottI, ind nirdullo rv cordi - The ihoi Ir

i1 dl- iii cIt cd. HlE 270

Vr W

Z IV

414

~ * -r

;0'~ ''*~s

2~1~ +C 0:.1IVA

*o

1:11K-irc 15. Renal cortical tubhular epithelium - diffuse necros-is with hemor-rhlge and protinceous material in tubular lumens and in thei it k2r st i tiur.-. HE 93X.

00 q0

F igUre 16 . Rcn.'I)) 1'hdl, I]., t-. (,(, lect ing tu h u I e,, cont a in slIoughed renal14 cort IcaI t uiiI iar e p itheI. ;ilI (-(,I Is occ Iid i ng thle Iltme ns. H& 15 5X .

q 320

-. 7-7.- . V7.. - .

fi0

F'i gtire 1 7. Dif fus52 severe panc rea tic nec ro-,is-hemorrhage, congest ion, andmoderate interlobular ede'MatOus chan1ge. H&E 230X.

":istrointestinal changes were severe and diffuse throughout the length ofthe tract. The mucosas, submucosas, and occasional subserosal foci were edema-rou3 ind often had collections of extravasated erythocytes within the edematous

i.s.Thc muicosal architecture was irregular with a marked decrease in cryptf. ,.dft ion of crypts, necrosis3, and regeneration of epithelial cells. The4e~ro hypocelluilar with noticeable reduction of lymphoid cell populations

~ naroiswas recogni'.ed( by loss of cells in the lymph nodes,-'a Vf>x~5,tonsils, lamninae proprias, and mucosas of the body. The loss

elswas not1 uniforvi among subjects, and in three it was minimal.iecrasein the smal1- lymphocyte population and a moderate loss of

ys.The germinal centers were essentially devoid of lymphocytes.m-iar cells did not have any remarkable changes. The loss of lympho

ncreas-edl hypocellularity of the glands and edamratous change. Inalypopiilated by scattered populations of lymphoid cells, there

pa yof cells3. Free erythrocytes and erythrophagocytsis ,ere:3iubjec ts' lymph nodes.

.4Qrwswre hypoel'lular in all subjects.A aredpesin f0 i;01 -ti' ampoonn accentuated the fat cells and vessels. Pyknotic

r->a)n. lmma, lre anhlast c ells were rare (Fig. 2)) .

n t flI n cro:3 3s wat3 reco,-gnized] a3 individual epithelial Cell necrosis in~~LV'i .3OJr . 5fur, th- nscr'ozs i was- nulti focal to diffuse ind se.(vere, with

l-ca~s eyinoeti xtraivisation (Fig. 23). The necros3is, wajs essentiall1y

)r~ex.

4*4e

i,, :li 5id e t a a tin o

& t~e~ f

CjA71

44

0 bFi ~uto 20. Crypts ,ire I ied with metajlast it epithlium. Note, the s1igliednec rotit, cellIs in the diiteds crypt li&E 340X.

Ir 1,I~li" IiI n ;Irke I m M ; I . SI -

ilrI1 r I ] ) '1 d i]i kI. .7 0

3min

Aw AN:

Figure 2.Bone marrow is markedly hypocellular with prominent fat cells.

Note the paucity of blast cells. H&E 390X.

AS

F:ig'Irt 2 1. Severe1~ d Iffiise ;idrkona cort irAn upithe] lal necrosis withi hemorrhnigo

anHd congest ion. IIV I 185x.

*3

-. -* . 4

The lung changes included minimal to moderate congestion with accumulationof proteinaceous material in alveolar spaces. Minimal to moderate septal thick-ening, due to proteinaceous material, macrophages, and atelectasis, was occa-sionally recognized.

The salivary glands and testicles had similar changes, with individual cel-lular necrosis (Fig. 24). There was karyorrhexis, swelling of epithelial cell "cytoplasms, and occasional pyknotic nuclei. No inflammatory cells were associ-ated with necrosis in any of the organs.

Pyknotic nuclei were recognized in the cerebrums, cerebellums, and livers; 0these organs had no detectable necrosis, hemorrhage, or edema.

Focal myocardial necrosis wrs recognized in one subject. The focus wasapproximately one-half diameter of the ventricular wall, with discrete marginsand no inflammatory cell infiltrates. The individual myocardial fibers werelightly eosinophilic and vacuolated and had no cross striations. Another sub- Sject had multifocal to diffuse myocardial hemorrhage but no detectable necrosisof myocardial tissue.

Marked hemosilerosis was recognized in one subject with accumulation in theliver, spleen, bone marrow, and adrenal and lymph nodes. Minimal to moderatehemosiderosis was recognized in two other subjects. S

Additional lesions recognized in the monkeys were considered to be unre-lsted to the irradiation damage. The most significant were adrenal minerali-zation and accumulation of inhaled exogenous pigments in the lungs.

O

iwr. ~. mInd i,'idi,'il cellulnr n(,'rflsi. of the salivarv gland acinar epithelium.Note the karvorrhexis and rvtoplasmic swelling. This individualellLiar necrnsis wis commoniv recognized in salivarv glands, testicles,jd rna M, A Tn pan' rea t a . FH&E 700X.

37O

PathLology

Even thouqh the pathorenes is of ion ig radiat icn is unknown, thr, n~-Icn. well1 docuimented in mnnry species (71, 1 1, 3A. The lco,

Laor eight subjects arm~ of interest because of the essentially pure neut~ron ra'ii-tion , the Jos" ra te and tnc s inrgle exposure. Additionally, -, direct extroipa-Untn to tho riit ion c ffeots on humans exposed to comnnarab] e radiat ion canr1 t

* a~de .itn few a rva ions.

T- _renrt uncerstinding of ti scuo dama go by radi atiorn has led to tne won:-:ui'n th-u the most important factor is that of cll killi ng (10, 26, 33).i.,is is cr Wiinly the most notable cllular change recognized in thESe' test,

robjects, a-th the neorosis varying from focal to diffuse and minimal to severe!- -o r organs. Necrosis was recognized in the panoreata, gastrointestinal

tricts bone marrows, lymphoid tissues, kidneys, adrenals, salivary glands, and-Sl-1S. N-es~is in most of these organs has been well documonted by ethrr==Q 10, 13, 23, 26, 3?, 33). Edema and hemorrhage were Eenerally na.:-

40-t with nrotic tissues; and altnough vascular hiotopathologiy wsnetrocgriunthre is little doubt that it occurred. Not being at e to oee acute

0~: w~~ith low levels of radiation is not unusual. :e'.'r A1 author--,- . so' thel iai damage is the~ morst likely cueof tho edema and h'-)T

,::nt ost seriouslIy Af'fra' :hyL radiat0,ion , and tne first r'-n* Lr or i, hot h deoeloped ae v, rn nydrth :ri. Thy toti hy n emrrr .

v n r 1'evo r 0k K5 V, Y~ . enA! diffusu, <( '.f.': r I i'* - . j. Anoither so -,i the tnird to be nt~ ivn

!rern~rim Se-~ ow r ament on pulmonary d7,p-nni t 1 Aqrn fusonn- but 's or SP-iially discuas 4yrrnrxn,

ir- -r m rcP and therapy, in a nutron radit i Un rnv!"n-:

in al aYV~ sbjrts, and predic~tably h Win

zi W ism iCed. Kidne y patholog y, while quite contr1vcrs 1 11

iii !, t ( "'n d r (niA i1nPc, si n-'ah (7, 20,2' ?3 N7,

"Ts i - r" l r'' a n tel; severe par or ea t i c r0 . n c'a 'm'' t neutron radioi nhan- ~ . ~

-,,Ic s porl Warntd (1 ); it is indicated l. ap'' Mr oi !-an d.naag (- in Pr r.!

n . a,.:: -v-r , n'iC hrnq

n ~.. . . . . . . . .. . . . . . . . . . . .

Tht racai.Ierosis seen in one subject was probably due to rapid uptake andS.<nvrsion at' crythrocytic elements (32). This monkey had severe intestinal hem-0 crrlae. No direct documentation of postirradiation hemosiderosis was found.

*PyKnotiC nuclei in the brain and liver are documented, even though theSicanca is extremely difficult, if not impossible, to identify as a real morpho-logic change. The brain cells damaged by the radiation were nost likely oligo-Jendraglia. !Iepatocytes were damaged in the liver. Radiation necrosis is welldocamented in the brain and liver (2, 9, 10, 30) but at much greater dosages thanthose used in this study.

The clinical picture that the monkeys presented was typical of ionizingradiation exposure in mammals, although the signs were apparently more markedthan could possibly have been expected at the relatively low dosage (30). Thesevere lesions in the subjects would have no doubt been fatal and would haveoccurred even with supportive therapy. Since the monkeys were euthanatized,determining how long they could have lived is not possible; but it is unlikelytney would have survived past 10 days, with the majority dying within 7 days.

Behavior

N Xutron exposures at dose levels of 1050-1100 rads (5.8:1 n/g ratio) will* cst likely impair performance accuracy and cause a concomitant slowing in reac-tirL time. The task in this study was rapidly paced, demanded periods of high

-rtct, n wa mentally fatiguing; however, all baseline performance excreded 99%~'A:''r ,'y (Tabl. 6).

....... ... ( n the t;ask loading of this study and operational aircrewto ,.,ntify. Many operational situations require bursts of

y r-d. ,d work rates or short rest periods. An increase of. op- Ar't normal (acceptaible) error rate would likely have a

.. *,'v , cn rt , m'(i-,In performance. Table 6 indicates that at least.,-",*r',j if errors occurred for all subjects on exposure day and for

...... .... X ur d:ys 2-. Mission-essential suttasks have vairying.Jr,.i" un( for faiilure. Low-level and high-level cruise have

'.rit r job perforra-nce. Landing an aircraft on landi ion3 i. quit, di ff-rent than landing on an aircraft carrier in

' , ::onlit ion;. I; oe job. '-an tolerte limited errors, and some.r'; ' fueling, for example, is a task where errors (break-

'.' :v r. :, .'.r, -i t i; a . i t-. Teo :rany br&iknaways, however, cxtend

, , r- r.fu,,Iin r an i ri i Ltimtely lead to mission failure.

.. an t.i. .;t~iy or iini y performed tneir task at a high iev1,. r ,, ,xpoaarC, perfor m,ne accuracy s igni f icantly decreased for

. ,, ,. ia- a nL',c a, iy at the :i-mr, time (seo Table 1). Is.", ,wAi, t, p ' ,r ,Ce of thea eight subjects were appar-

v:. ;, " " , t -ppared t,) be unaf'feetad. Arc, L-., :, y. ,,M) thuii h dependent upon the

. - : .r' .. , . .: A .:t in i m er". r

0 S

i . . , . . ' .:. . . .. ., : - _ , .. ,-,, .. . ". . . . ..S : . -. - . _ / - " - ": ':-

After the 1100-rad neutron exposure, response rate was significantly de-layed. One feature of the task was that an animal could change his responserate up to 2 s (most averaged under 1.0 s). If the response came after 2 s, thesubject received a shock. Seven of the eight subjects had significantly in-creased reaction times on exposure day, four of eight at postexposure day 1, six 0of seven at day 2, six of six at days 3 and 4, and four of four at day 5. Thisshift to slower responding can be seen in Table 9b. On exposure day, reactiontime increased by 11-32% over an average of the previous two baselines. Althoughthe reaction time ranged from a 2% decrease to an 18% increase on postexposure

* day 1, it had a 40-73% increase for the four subjects performing on day 5.

A shift in the range for reaction times demonstrates that a subject is nolonger responding in an expected manner. Many of the changes to slower respond-ing were large. The subjects' ability had been degraded, although the "best"postexposure performance was seen on postexposure day 1.

Productive emesis was another variable of interest. The animals were moni- S

tored at the end of the 4-h postexposure work period. When removed from the workcubicle on exposure day, seven of the eight subjects in the 1100-rad group hadvomitus on their fur, and two animals experienced an additional emetic episodelater that day. At postexposure day 2, three subjects experienced additionalemetic episodes. Most of the animals would uninterestingly consume small amountsof food 1 day after exposur-" but by the third day, most were ingesting almost nomonkey biscuits, fresh oranges, Tang orange drink, or water. Depending on physi-cal condition or termination of the study, the animals were euthanatized at thetimes indicated in Table 12.

To permit easy comparison of data, Table 12 summarizes the performance accu-

racy, reaction time, and emesis effects after radiation exposure for (a) presentstudy--1100 rads and a 2-s response window, and (b) earlier study (5)--600 radsand a 3-s window. The most obvious comparison is that in the 1100-rad study, twoanimals were unable to perform meaningfully on the second postexposure day and sowere euthanatized; in the 600-rad study, all eight animals were performing on the

third day.

The 600-rad exposure generally resulted in moderate performance changes. Inthe 600-rad group, subjects were performing relatively well at postexposure day 3;the number of errors and subject loss are clearly greater for the 1100-rad group(contrast Table 13 with Table 6). It is quite likely that the subjects who re-ceived 600 rads could have worked reasonably well for up to 5 days because theywere still consuming some food; however, only two of the four subjects in the1100-rad group that started postexposure day 5 performed to any appropriate de-gree. Visual inspection of the animals, combined with virtually zero food orwater intake (see Pathology section for possible reasons), made it doubtful thatany animal could have performed to any meaningful degree on day 6.

40

40

TABLE 12. RADIATION EFFECTS

(a) 1100 rads, f/g 5.8:1(behavioral response window 2 s)

Postexposure daysSubject ExposureNo.--ID day 1 2 3 14 5

1 156 A +A + + A + A + S 02 190 A +E A + A +E A + A +*S3 318 A +E A +E A + + A +*S4 20'4 A +E A + A +E S

5 356 A +E A A + A + A A+ S6 348 A +E + + A + 57 3244 A +E A + A + A + A + S

8 3'46 A E A + S

(b) 600 rads, n/g 5.5:1 (Ref. 5)(behavioral response window 3 s)

Postexposure daysSubject ExposureNo. -- ID day 12 3

1 176 A +2 178 A +E A + A +A3 180 A E24 1324 A +E +

5 1524 + E + +

6 160 +

7 L624 A +E A A A8 1724 + E +

A = Decreased accuracy defined by the presence of more errors on exposure andpostexposure days than on either of the two control baselines.

+ = Increased rraction-tirne scores by simultaneous tolerance limits orexceeling both baseline maximums.=Emesis occurrence (productivr).

*= Wi thdrawn durinr . ' -it:~iIllY to successfully perform.

41

I'ABI 13. (PI;RFORIMANCE EIRRORS)/(NUMBER OF TRIALS) FOR 4-Hl TEST PERIODS FOR600-RAD STUDY, N/C 5.5:1

Subject Exposure Postexposure days .0No. -- ID Baselines day 1 2 3

1 176 16 27 12 9 97526 7537 8615 8111 8303

2 118 47 142 69 230 2866656 6110 6675 5091 5167

3 180 27 48 11 25 17

6910 6907 8207 6407 6956

4 134 7 26 7 7 4 0

7126 6743 7018 6089 5832

5 154 39 26 7 15 14

8512 7589 7125 6926 6883

6 160 26 10 13 5 2 69307 9223 9992 8598 9028

7 L64 30 136 37 62 347237 6358 7554 6918 7123

3 174 16 12 7 16 2 084'3 7867 8291 6953 8204

An element of risk always exists when we take animal data, regardless ofhow good we believe it to be, and make generalizations to human operationalt s s. These data can, however, suggest some guidelines. Below are some Sevaluations of the 1100-rad (current) and 600-rad (previous) exposure groups.

Previous Study (5) Current Study600 rads, 5.5:1 n/g 1100 rads, 5.8:1 n/g

1. Exposure will impact both perform- 1. Exposure will have a marked im-ince accur;icy and reaction time. pact upon both performance accuracy

and reaction time.

*-. Fwr , itheit i 'w m:ira7in of 7. Performance will be able to con-er Jr , p'fr":nie <ir prchsi ly .-orl tire within the first 4 h, although 0tinue f'or <,:',:r<i I o . there will be periods (20-30 min) of

poor perfurmarice.

42

0i

-. . .-b - . - . . -

0i

3. For a task with a critically low 3. For a task with a critically low

tolerance for error, performance may tolerance for error, performancebe significantly compromised. Air- will be significantly compromised.

" craft-carrier-based flying personnel Aircraft-carrier-based flying per-would be apt to perform below safe sonnel would probably perform below

standards; landing on a carrier (15-45 safe standards within the firstmin after exposure) could very well be hour; landing on a carrier would be .

beyond an acceptable risk. Safety in dangerously questionable for aboutland-based aircraft operations might 50% of the personnel. An additionalbe compromised, even in a normal take- 20% could be expected to performoff procedure, at 15-30 min after crew poorly, and at times unacceptably,

exposure. for up to 4 h, regardless of risk.

4. By 24 h after exposure, personnel 4. By 24 h after exposure, most

would likely be available for reuse; personnel would be available forbut at 48 h, their speed of response reuse although time-stressed tasksfor time-critical events would still would suffer some degradation; by 48be affected. h, response rate would be distinctly

slowed, but accuracy would be onlyslightly worse than at 24 h. Moresignificantly, there could be an ap-proximate 20-25% total loss of usa-ble personnel by this time.

5. Loitering should be possible for 5. Loitering should be possible for

an extended period of time after expo- an extended period of time, with

sure, with minimal or perhaps no crew personnel surviving up to 96 h. Atredundance. 120 h, approximately only 20-25% of

exposed personnel would be able to

do their jobs.

6. Tasks required for penetration are 6. Skill levels required for pene-* very demanding and woild be marginally tration would be compromised for

affected 24 h after expoosre. After several hours after exposure, but48 h, responses rP'3iin< apeel would marginally affected 24 h after expo-likely be jeopii sure. At 48 h, tasks requiring rapid

response would definitely be jeo-pardized and 20-25% of personnel

joull be unavailable (medical casu-t1ty) or useless.

7. RefueIisg i ,' 4:- '. of'ueling would be seriouslycessful if an r,: .. . prmised within the first hourwere possible. AdI , . ........- , . pro inly successful withinwould likely occur Al '.'' ' ,-30 h, particularly if an increasedpr-o>dure. Activity at 4 n , time element were possible. By 48 h

, ould experience the least after exposure, the surviving per-, ; -fer 7? h, refueling sonnel (75-80%) would continue to be

, : , . : -. ,r , difficult, successful with additional time,]]though br( k!i'iys would unques-t i)lky increase. By 72 h, perform-c.-', 1 li.l ly bf- plagued with

o " -j

'he cruise phase of missions would 8. The cruise phase of missionssuffer the least radiation-related would be minimally affected by

problems. Because of lowered work radiation-related problems. Becauserates, crews should accomplish tasks of lowered work rates, survivingwith limited difficulty. The opportu- crewmembers should accomplish tasks

nity to spread activity out in time with limited difficulty within 72 hsomewhat should increase the expected after exposure. The opportunity to

success rate, but this may not be spread activity out in time would 4

possible in a tactical situation where increase the expected success rate.activity is at a continuous high After 120 h, however, it is unlikelylevel. that any operational crewmembers

would be available. J

9. As noted in Table 12, emetic ac- 9. As noted in Table 12, emesis

tivity, increased reaction time, and/ appears up to 2 days after exposure.

or decreased accuracy may not coincide For this sample, increased reactionnor occur equally in all subjects. time and/or decreased accuracy gen-

erally occurred together (not true

for the 600-rad group).

For the 600-rad data, behavior of the neutron-exposed animals was gener-

4 ally similar to that of animals exposed primarily to gamma radiation. In thecurrent study, a more rapid death rate is easily associated with neutron expo-

sures. Whereas gamma exposures generally result in an early performance

cecrement (EPD) for the dose levels discussed here, recovery time from the EPDappears to be longer for neutron exposures. To further identify the neutron/gamma relationship, it would be advisable to expose an additional group at

1100 rads, all gamma. The 1100-rad neutron exposures for this study defi-nitely exceeded "threshold" dose. An all-gamma exposure would address the

neutron RBE question as presented by the work of George et al. (11). Although

their studies were good, they used different behavioral techniques and differ-ent species. The RBE question becomes increasingly important with the morerecent shift in the types of nuclear weapons being considered (25).

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Arie, I. M. The effect of single massive doses of roentgen radiation

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0 S]

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ell rmer, R. W. Human ability to perfaorm after acute sublethal radiation.ilit Med 126:631-687 (1961).

4640

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