National Aeronautics and Space Administration

Langley Research Center • Hampton, Virginia 23681-0001

NASA Technical Paper 3643

Astronaut Protection From Solar Event of

August 4, 1972

John W. Wilson and Francis A. Cucinotta

Langley Research Center • Hampton, Virginia

T. D. Jones

Oak Ridge National Laboratory • Oak Ridge, Tennessee

C. K. Chang

Christopher Newport University • Newport News, Virginia

April 1997
Printed copies available from the following:

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Available electronically at the following URL address: http://techreports.larc.nasa.gov/ltrs/ltrs.html
Abstract

The dose rates in the blood-forming organ of a typical astronaut for four space

shielding conditions are used to study the astronaut health effects of the solar particle

event which began on August 4, 1972. This event was chosen as it was the most hazardous event for which detailed measurements have been made and for which dire

predictions of the potential health effects have at times been suggested. The code used

for health effects is the biological model developed for tactical nuclear weapons warfare survival of young adults in a 1g environment. We find the risks of early lethality

to be very small especially if appropriate medical action (antibiotics and blood transfusions) is taken soon after the exposure. The primary concern would then be for the

development of cancer later in life. Although leukemia could occur relatively soon

after the exposure, the risk of solid tumors might be best controlled by using mature

individuals for the mission, and thereby offset cancer risk by balancing life span

remaining against the long latency periods associated with solid tumors. Use of

genetic selection criteria could further reduce health risks during the mission. A

possible space experiment to evaluate synergistic effects of the microgravity environmental stress and other space-related stress factors is discussed.

Introduction

From the earliest discussions of space exploration,

the problem of protection against space radiations has

been a concern (ref. 1); the possibility of adverse health

effects from a large solar particle event was reinforced by

the occurrence of a very large ground level event indicating arrival of high-energy particles on February 26, 1956

(ref. 2). The hazard posed by a possible large solar particle event was addressed in the Apollo missions, and the

allowable exposures for this high-risk mission of great

national importance were quite large (200 rem for blood

forming organ and ocular lens, 700 rem for skin, and

980 rem for hands and feet where the older unit rem is

equal to 1 cSv) and provided some balance against the

other risks associated with the mission (ref. 3). For these

short 2-week missions, these limits would allow the

return of the astronauts for proper medical treatment.

Although radiation health workers today find these numbers shocking, it was recognized at that time that the

added mechanical complexity associated with providing

added radiation protection from such events would

dramatically increase the mechanical risks associated

with the mission. Indeed, some deaths occurred from

design complexity, but no known deaths from radiological exposure.

The radiations received during the Apollo missions

were mainly from the galactic cosmic ray background,

but on August 4, 1972, between the Apollo 16 and

17 missions, began the most significant solar particle

event (mainly protons with small percentage of other

ions) known even to the present time (refs. 4 and 5). This

event has been studied in the past and many predictions

of the possible health effects have been suggested. Most

of these judgments were based on examination of human

early radiation response data for single exposures and

often based on responses to exposures during radiation

therapy sessions with seriously sick individuals (ref. 6).

Clearly, the interpretation of the event could be quite

different if repair/recovery effects and specific spacerelated factors are taken into account.

As a result of the needs for tactical nuclear warfare

planning, extensive databases of radiation response have

been made for many animals, and models of the cellular

and tissue level dynamics were derived by fitting the

databases. These models are used herein to extrapolate

the available human data to protracted exposures. We

reexamine the August 4, 1972, event by using these

recently published biological models. Clearly, the use of

such models will enhance our understanding of large

solar particle events and allow the development of practical methods for managing the associated risks.

Event of August 4, 1972

The first indication of an important solar event was

the observation of an optical flare at 0621 UT on

August 4, 1972. The associated coronal mass ejection

(ref. 7) resulted in a significant accumulation of particle

fluence by 0700 UT. The particle flux remained high for

the next 11 hours over which the major accumulation of

fluence of energetic particles occurred (fig. 1). Lowenergy particles continued to arrive through 1000 UT on

August 5, 1972. The doses behind a water equivalent

shield of 0.4, 1, 5, and 10 cm were evaluated by Wilson

and Denn (ref. 4) and are shown in figure 2. The shield

thicknesses used in figures 2(a), (b), (c), and (d) correspond approximately to a space suit, pressure vessel,

work area, and storm shelter, respectively. Although the

exposures are known to have large dose gradients within
2

the body, we assume for evaluation of the risk that the

exposures are uniformly distributed within the indicated

organs. The actual risk estimates may be somewhat

lower as a result of the nonuniform distribution within

the organ. In estimating the dose to specific organs, selfshielding factors are included according to the approximations of Wilson and Denn (ref. 4).

In the past, risk was managed for missions following

the Apollo program by setting dose limits to control both

the early response and the cancer risk of the astronaut.

The risk limits used from the Skylab mission through

Shuttle operations saw little change (ref. 8), and maximum allowable exposure limits for career, yearly, and

30-day intervals were as shown in table 1. The 30-day

limitation was specifically to control the early effects of

radiation, since exposure recovery is in about 4 weeks.

For example, the 30-day limitation is the controlling factor in shielding for short-duration space exploration to

near objects like the moon wherein the protection of the

astronaut requires a “storm shelter” of approximately

10 cm of polyethylene (fig. 2(d)). Meeting these limitations assures the control of adverse health risks of the

astronaut but gives us no insight into the health risks of

accidental exposure during future manned space exploration nor the development of a philosophy to appropriately deal with such an accident. These two items are

discussed in the following sections.

Biological Response Models

Exposures at which significant health effects occur

have been summarized from various sources by the

National Council on Radiation Protection and Measurements (NCRP) and are shown in table 2. The dose associated with 50 percent mortality (LD50 value) is affected

by the degree of medical support; intensive medical care

can greatly increase the chances of survival (ref. 8).

Recent practical experience was gained as a result of the

Chernobyl accident where most exposures were characterized as a relative uniform whole-body exposure due to

gamma rays and surface exposure an order of magnitude

larger from beta emitters (ref. 9), which is somewhat

similar to space exposure distributions (ref. 4). There

were no deaths among those whose whole-body exposure

was less than 2 Gy. All patients of exposures to the marrow system of doses greater than 2 Gy were given supportive care including isolation, antibiotics, and in

extreme cases, transfusions and transplants (ref. 9). Only

one death occurred for exposures between 2 and 4 Gy

with intense supportive care.

The diagnostics of the Chernobyl accident relied on

biological and physical dosimetry. The blood elements

within exposed individuals were monitored within

12 hours of the accident and taken as an indication of the

level of exposure. To understand this methodology, we

show the kinetics of the marrow system in figure 3. The

stromal cells reside on the bone surface and provide the

substrate on which long-term stem cell populations normally reside. The stromal cells consist of those populations associated with the yellow marrow. The stromal

cells provide growth factors which are responsible for the

rate of cell propagation among the various stem populations. The long-term repopulating stem cells differentiate

into lymphoid and myeloid stem populations. Humoral

factors added by the stromal cells control the rate of progression of these differentiated stem populations. All

other blood elements are produced by further differentiation among these two stem populations. Radiation injury

to these stem and stromal populations will have its ultimate consequences in the peripheral blood. The time

course of these peripheral blood elements (specifically

the lymphocytes, neutrophils, and platelets) were used to

estimate the level of exposure (ref. 9). Kinetic models of

the stem and stromal populations based on animal studies

are used in the present report to develop the understanding of the anticipated response of the astronaut to solar

particle event exposure.

An analysis of experimental animal survival data

demonstrated that very few animals ever died at 70 percent of their LD50 (lethal dose for 50 percent mortality)

and very few ever survived at 130 percent of their LD50

(ref. 10). Further studies (ref. 11) used a much larger

database and found the ratio of dose at 90 percent mortality to dose at 10 percent mortality (LD90/LD10) to be on

the order of 2.0 or somewhat less for most species. (See

fig. 4.) Thus, the range of exposure from survival to early

death is very narrow.

The prompt-dose LD50 of each animal experiment

depends on a host of conditions including strain,

sex, age, diet, food supplements, cage care, bacterial

environment, cage mates. In addition, each investigatorlaboratory combination produces a distinct LD50 value

even if all players attempt to replicate exactly the same

experiment. To predict doses that will not kill any animals and doses that will have no survivors would be

easy. However, poor accuracy would result from

attempts to predict graded mortality over the short-dose

range between the LD90 and the LD10 in one species of

mouse from an LD50 and standard deviation (σ) from

another species of mouse. A very small change in biological and physical factors can easily change a condition of

total survival to total mortality. The specific conditions

of the space environment is expected to play an important role in addition to the specific genetic makeup.

The animal database has been used to estimate a

prompt-dose LD50 and probit slope (σ) within each
3

experiment (ref. 12). Mortality for protracted exposures

within the same animal colony can then be analyzed or

predicted on this common scale defined by stem and

stromal cell kinetics provided that the only variables are

related to the physical radiation environment, such as

dose, dose rate, radiation quality, dose fractionation. Cell

kinetics models should transfer reasonably well within a

species, but the particular LD50 and probit slope estimates may vary twofold within different healthy strains

of inbred animals—especially when studied by different

investigators at different laboratories. Some mouse

strains have an LD50 of 8 Gy and other strains treated the

same way may have an LD50 of about 4 Gy (ref. 13).

Similar factors are expected to be active in human exposures: the space environment and related space factors.

The human LD50 to marrow seems to be about 3 Gy

for the atomic bomb survivors (ref. 14). But the LD50 for

man can be increased with antibiotics, blood transfusions, and cytokine therapy to about 6 Gy. Intensive

medical care including bone marrow or blood stem cell

transplant could increase survivability to high levels as

shown in table 2, but such medical procedures carry

additional attendant risks (ref. 9) that may be modified

by preconditioning to the space environments. Conversely Morris and Jones (ref. 11) have modeled 13 species of test animals and predicted the LD50 for man to be

only about 1.8 Gy if confined in a cage under nonsterile

conditions similar to that used for test animals. Such

shifts may in fact be typical for space exposure and

would be an important determinate of astronaut health.

The genetic selection of astronauts and their conditioning

may increase their radioresistance but space environmental factors, such as stress of close confinement, stress

from microgravity, cabin atmosphere, may decrease their

radioresistance. Food and water should give a survival

advantage beyond that of the atomic bomb survivors but

microgravity stress, confinement, and so forth may lead

to greater risk. To itemize the various factors and to

explore what the published experimental data say about

the factors taken individually would be useful.

Cancer incidence from radiation exposure in inbred

animals is even more variable than acute radiation injury.

Strains where almost all animals get cancer (without any

exposure) and low-cancer strains exist. Analyzing animal

cancer data in terms of cell kinetics has not been

attempted but would be of great value in understanding

the solar particle exposure effects. Cancer risk estimation

for mice should be predictable in terms of cell kinetics

and a risk coefficient valid for the exposed animals at

risk. Such an analysis could indicate the approximate

degree of risk to man and assess the general degree of

validity to be expected from the model within a mouse’s

lifespan of about 2 years.

Dose Protraction Effects in Risk Management

The primary early radiation syndrome depends on

the exposure level (ref. 6). The expected exposures of

deep organs is a few greys in space exploration, and the

corresponding early biological effects would be dominated by the loss of stem cell populations within the bone

marrow and the associated stroma cells. The initial radiation injury occurs in individual irradiated cells but ultimately shows through the loss of cells from the tissue

system for which intercellular communication (cytokines

or growth control factors, fig. 3) demands increased

replacements to the tissue system. In this respect the

injury to the stromal cells plays an important role as a

primary source of cytokine production for the proliferation of stem cells, their progeny, and control of the

amplifying divisions and differentiation processes in

maturing cells that are progeny of the hematopoietic stem

cells. The ability to replace lost cells depends on the sustained damage to the stem and stroma population. The

repair rates at the cellular level are typically minutes or

hours, whereas the tissue recovery period is typically

days to weeks. For the August 1972 event, the exposure

time is long compared with cellular repair processes but

short compared with the time required for organ recovery. Because the exposure time is long compared with

repair rates, the cellular repair processes are anticipated

to greatly reduce the injury of the exposure anticipated

for this event.

Risk of early lethality to the astronaut is related

largely to depression of the immunological system and

other blood elements through cell killing of various stem

cell or the stromal cell populations (fig. 3). Because bone

marrow doses are not expected above a few greys, the

primary treatment is to supplement the immunological

system with antibiotics. Clearly, the efficacy of this

action for space-stressed astronauts needs to be understood. In developing such an understanding, we use the

models developed for application to military operations

to study the effects of protracting the dose over a period

of many hours.

We use the model for early lethality as adapted by

Young, Jones, and Morris (ref. 15) to examine the repair/

recovery effects in humans due to rather large exposures.

Figure 5 shows the mortality for a 2-Gy dose to the bone

marrow by 250 kVp X rays (the 250 kVp refers to the

peak voltage of alternating current X-ray machine) delivered as multiple equal fractions 1 hour apart. Each fraction was given in a 15-min exposure. Mortality can be

quite large when received in a single high dose rate

expose. (Note that Jones estimates that the bone marrow

LD50 of 250 kVp X rays is 2.15 Gy, whereas that of 60Co

gamma rays is 2.95 Gy.) Supportive medical treatment is

expected to allow survival as shown in the figure. As the
4

number of fractions is increased, the mortality drops

dramatically to less than 10 percent (even without medical treatment) beyond 15 fractions (or equivalently

15 hours). The stem and stroma cell survival at the end of

each fractionated exposure is shown in figure 6. Stem

cell survival for the single 2-Gy bone marrow dose is

very low (much less than 10 percent). As the number of

fractions is increased, the stem cell survival shows a dramatic increase approaching 40 percent. Likewise, similar

changes in the stromal cell population and repopulation

reduces the mortality for the 20 fractions at 2 Gy to

10 percent. Clearly, cellular repair and repopulation are

effective in reducing the risk when the exposure is highly

fractionated with adequate time between fractions for

repair. The stem and stroma cell populations during and

after exposure to a 2-Gy bone marrow dose given as

20 fractions are shown in figure 7. The recovery period

in this case is about 2 to 4 weeks.

The equivalent dose for the solar event is uncertain

and we have assumed the equivalence to 250 kVp X rays

which may be somewhat conservative. Figure 8 shows

the estimated stem and stroma populations within the

astronaut for the August 4, 1972, exposures with various

shield configurations. Although substantial decreases in

the stem and stroma populations occur for the space suit,

the effects are clearly reduced within the pressure vessel

and further reduced to a small perturbation when

shielded within an equipment area. The value of having a

shelter to further protect the astronaut is not clear from

the present results on early lethality. Figure 9 shows mortality for a 2-Gy exposure as a function of dose rate corresponding to exposure periods of 15 min to 20 hours.

Also shown in figure 9 are the results of the exposures

based on the August 4, 1972, event within a space suit

and pressure vessel at the appropriate average dose rate.

If the astronaut remained in the work area or went to the

storm shelter, then no real threat to the survival of the

astronaut would exist as would be true for the space suit

or pressure vessel if appropriate medical treatment was

given. The corresponding stem cell survival is shown in

figure 10 as a function of the exposure period along with

similar results for exposures at 1 Gy. The corresponding

mortality for the astronaut for a 1-Gy exposure protracted

over several hours or more is very large.

The estimated total cancer risk for young adult males

for the August 4, 1972, event in the case of accidental

exposure shows strong protraction effects as seen in figure 11. The fatal cancer risk would be about a factor of 2

smaller. The much smaller leukemia risk is shown in figure 12. Leukemia would appear in 4 to 10 years after

exposure and would be the most meaningful risk for a

middle-aged adult population. Of lesser importance to a

middle-aged population are the solid tumors which do

not appear for 20 to 30 years.

Operations on the lunar surface would reduce the

accidental exposure levels by at least a factor of 2

because of shielding below the local horizon. Added protection could be found by using a cliff or crater wall. The

probability of early death is probably negligible in these

cases. Furthermore, protection would be gained from the

Martian atmosphere for Mars surface operations.

The present calculations were meant to apply to

healthy adult individuals on future NASA exploration

missions. Because the models are developed for 1g

ground-based data, the specific stress associated with

space travel is not accounted for in the model. It would

seem desirable to compare the model and its associated

database with exposures in space of small mammals as a

means of testing the effects of microgravity and other

space stress factors.

Small Mammal Experiment

Many factors affect the LD50 of human and animal

populations. Some of the factors (genetic, nutrition, general health, bacterial environment) have been tested in

laboratory experiments, but specific space-related stress

factors have not been tested. Such a test could be made

with relative ease because large health risks are involved

and good statistics could be obtained with relatively

small populations. In addition to the relative small number of mice, the duration of the experiment would be

only a few weeks during the recovery period. Follow-up

observations for cancer induction could be made but may

be of little meaning with such a small population.

Concluding Remarks

On the basis of a biological response model for use

in estimating biological effects in young adult males and

the estimated flux spectra of the August 4, 1972, solar

event, repair and recovery play an important role in

determining the early response in solar particle event

exposures. In the present analysis, such events are

unlikely to result in early death in the case of accidental

exposure if adequate supportive medical procedures are

provided. Although the August 4, 1972, event is the largest event for which detailed observations are available,

some uncertainty still exists of the size of the event the

astronaut may ultimately encounter. Indeed, a reevaluation of the flux spectra of the August 4, 1972, event has

been suggested because the satellite data may exhibit

some saturation and the spectral shape above 60 MeV

was not measured. Even if a larger event is indicated, the

reduction of dose on the lunar surface is likely not to

change these conclusions for lunar-based operations.

The marrow cell kinetics models that have been

developed are based on uniform marrow doses and
5

conventional sources of X/gamma photons and fission/

fusion neutrons. Hematopoietic stem cells circulate

freely within the body and are usually treated as having

random distribution within hematopoietic marrow. In

contrast, marrow stroma is typically described as the

cytokine-producing yellow marrow that serves as a necessary and sufficient substrate upon which the hematopoietic stem cells can proliferate. Highly nonuniform

exposures to marrow of the body would seem to ensure

that sparred stromal tissues could serve as a favorable

microenvironment upon which circulating stem cells

could attach and proliferate. Because several studies

have indicated that restoration of normal myelopoiesis/

hematopoiesis can be monoclonal, it seems that nonuniform marrow irradiations could, in principle, greatly

amplify the probability of survival beyond that expected

from molecular repair and compensatory repopulation

associated with protracted irradiations. Published experimental data on nonuniform marrow irradiation should be

analyzed in terms of cell kinetics. The result should serve

to either realistically model nonuniform exposures or to

design a minimum set of simple mouse experiments that

will elucidate the process adequately.

Another source of uncertainty has been the use of

existing model coefficients evaluated from conventional

therapeutic and environmental sources for applications to

space radiation environments. Because the rate constants

in the cell kinetics models have been specified, evaluated, and validated in terms of target size and hit effectiveness considerations such as DNA per cell and

electron track density associated with radiation tissue

interactions, it is desirable to use published biophysical

data to develop more realistic cellular rate constants for

cell injury. These two refinements may change current

conclusions in a consistent direction or they may tend to

offset each other, depending upon the way that existing

calculations are applied to space missions. Clearly, the

importance of space missions, the value placed on human

life, the visibility of space endeavors, and the need to

optimize protection, shielding, and survival all mandate

that continued emphasis should be placed on development of more realistic models of injury and response.

A further uncertainty in the present model is the

effects of space-related stress factors, especially microgravity. Changes in the biological response due to shifts

in LD50 value are noted in animal experiments from various factors such as strain, sex, age, diet, food supplements, general care, social factors. The microgravity

environment is known to cause perturbations in the blood

system that would undoubtedly result in increased radiosensitivity but the effects of such pertinent factors are

not yet quantified by space experiments. A small mammal experiment with limited numbers of animals could

provide valuable information on the space-related stress

factors.

The outcome of an improved understanding of the

early response to solar event exposures may reduce the

corresponding shielding requirements because repair and

recovery of the blood-forming organ appear unlikely to

result in any serious early response for this organ. The

primary protection concern may then be cancer induction. Such an outcome could have an impact on the

shielding requirements in future deep-space missions and

potentially reduce the mission cost.

NASA Langley Research Center

Hampton, VA 23681-0001

December 10, 1996
6

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no. 3, 1989, pp. 445–461.

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Cell Kinetics Model of Radiation-Induced Myelopoiesis—

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7

a

Varies with gender and age at initial exposure.

Table 1. Ionizing Radiation Exposure Limits

[From NCRP 98 (ref. 8)]

Dose equivalent, Sv, for—

Exposure interval Skin Ocular lens Bone marrow

30 days 1.5 1 0.25

Annual 3 2 0.50

Career 6 4 a

1–4

Table 2. Exposure Levels for Single High-Dose Rate Exposure at Which Health Effects Appear in Healthy Adults

[From NCRP 98 (ref. 8)]

Health effect

Dose, X or gamma

radiation, Gy

Blood count changes in population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0.15–0.25

Blood count changes in individual . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0.5

Vomiting, effective threshold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.0

Mortality, effective threshold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.5

LD50 with minimal supportive care. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2–3.6

LD50with supportive medical treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.8–5.4

LD50 with autologous bone marrow or blood stem cell transplant . . . . . . . . . . . . . . . . . . . . 11.0
8

Figure 1. Fluence from August 1972 solar event as function of time and energy.

1011

1010

109

108

107

106

100 101 102

Energy, E, MeV

103

Fluence > 

E, protons/cm2

Aug. 5, 1992 1000

2200

2000

1800

1600

1400

Aug. 4,


1992 

1200

1000

800

700

UT
9

(a) Shield of 0.4 g/cm2 polyethylene. (b) Shield of 1 g/cm2

 polyethylene.

(c) Shield of 5 g/cm2 polyethylene. (d) Shield of 10 g/cm2 polyethylene.

Figure 2. Dose to shielded astronaut for August 1972 event.

Skin


Bone marrow

104

103

102

101

100

Dose, cGy

August 3 August 4 August 5

Skin


Bone marrow

104

103

102

101

100

Dose, cGy

August 3 August 4 August 5

Skin


Bone marrow

104

103

102

101

100

Dose, cGy

August 3 August 4 August 5

Skin


Bone marrow

104

103

102

101

100

Dose, cGy

August 3 August 4 August 5
10

Figure 3. Cell populations and humoral factors controlling peripheral blood elements.

Stromal


cell Growth


factors

Long-term


repopulating


stem cell

Lymphoid


stem cell

Lymphocytes,


lymphomas,


etc.

Erythrocytic


cells

Neutrophils Platelets

Macrophages,


leukemias, etc.

Humoral


factors

Myeloid


stem cell

Thrombocytic


cells

Granulocytic


cells
11

Figure 4. Mortality as function of bone marrow dose for various test animals (ref. 10). where

(A = 98.62, B = 5.09 × 107, and C = 17.93);

Figure 5. Mortality for hourly fractionated 2-Gy bone marrow dose as function of number of fractions.

100

80

60

40

20

0

Mortality, 

M, percent

.51 .63 .75 .87 .99 1.11 1.23 1.35

x

M A

1 B e–cx +

= -------------------------

x

D

LD50

= ------------.

40

30

20

10

0 5 15 10

Number of 15-min dose fractions

20

Mortality, 

M, percent

Untreated


Medical treatment
12

Figure 6. Stem and stroma cell survival at end of exposure period for a fractionated 2-Gy total bone marrow dose.

Figure 7. Surviving fraction of stem cell population for 20 hourly fractions of 2-Gy total bone marrow dose showing

recovery period.

10–1

100

0 5 15 10

Number of 15-min fractions

20

Cell survival

Stem


Stroma

0 5 10 15 20 25 30

Days

Surviving fraction of cells

Stem


Stroma

10–1

100
13

Figure 8. Bone marrow cell populations for August 4, 1972, exposures.

0

Time, days

10 20 30 0

Time, days

Space suit Pressure vessel

Equipment room Shelter

10 20 30

0

Time, days

10 0 20 30

Time, days

10 20 30

Stem


Stroma

Stem


Stroma

Stem


Stroma

Stem


Stroma

100

10–1

Surviving fraction of cells

100

10–1

Surviving fraction of cells

100

10–1

Surviving fraction of cells

100

10–1

Surviving fraction of cells
14

Figure 9. Mortality following 2-Gy bone marrow dose as function of dose rate. Exposures to August 4, 1972, event in

space suit and pressure vessel at event average dose rate also shown.

Figure 10. Stem cell surviving fraction for 1- and 2-Gy bone marrow doses as function of exposure period. Results for

August 4, 1972, event for several shield configurations also shown.

Untreated


Medical treatment


August 4, 1972


Space suit (untreated)


Pressure vessel (untreated)

40

30

20

10

0 1 2 3 4

Dose rate, Gy/hr

5 6 7 8

Mortality, 

M, percent

10–1

100

0 5 15 10

Exposure period, hr

20

Stem cell survival

2


1


Dose, Gy

Space suit


Pressure vessel


Work area

August 4, 1972
15

Figure 11. Cancer risk for 1- and 2-Gy bone marrow doses as function of exposure period. Risk from August 4, 1972,

event for various shield configurations also shown.

Figure 12. Risk for leukemia from 2-Gy bone marrow dose as function of exposure period. Risk for August 4, 1972,

event for several shield configuration also shown.

0

.20

.15

.10

.05

5 15 10

Exposure period, hr

20

Risk of cancer

2


1


Dose, Gy

Space suit


Pressure vessel


Work area

August 4, 1972

0

.03

.02

.01

5 15 10

Exposure period, hr

20

Risk of leukemia

Space suit


Pressure vessel


Work area

August 4, 1972

2

Dose, Gy


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April 1997 Technical Paper

Astronaut Protection From Solar Event of August 4, 1972 WU 199-45-16-11

John W. Wilson, Francis A. Cucinotta, T. D. Jones, and C. K. Chang

L-17590

NASA TP-3643

Wilson and Cucinotta: Langley Research Center, Hampton, VA; Jones: Oak Ridge National Laboratory, Oak

Ridge, TN; Chang: Christopher Newport University, Newport News, VA.

The dose rates in the blood-forming organ of a typical astronaut for four space shielding conditions are used to

study the astronaut health effects of the solar particle event which began on August 4, 1972. This event was chosen

as it was the most hazardous event for which detailed measurements have been made and for which dire predictions

of the potential health effects have at times been suggested. The code used for health effects is the biological model

developed for tactical nuclear weapons warfare survival of young adults in a 1g environment. We find the risks of

early lethality to be very small especially if appropriate medical action (antibiotics and blood transfusions) is taken

soon after the exposure. The primary concern would then be for the development of cancer later in life. Although

leukemia could occur relatively soon after the exposure, the risk of solid tumors might be best controlled by using

mature individuals for the mission, and thereby offset cancer risk by balancing life span remaining against the long

latency periods associated with solid tumors. Use of genetic selection criteria could further reduce health risks during the mission. A possible space experiment to evaluate synergistic effects of the microgravity environmental

stress and other space-related stress factors is discussed.

Solar-particle event; Dose rates; Biological response models; Shielding 16

A03

NASA Langley Research Center

Hampton, VA 23681-0001

National Aeronautics and Space Administration

Washington, DC 20546-0001

Unclassified–Unlimited

Subject Category 52

Availability: NASA CASI (301) 621-0390

Unclassified Unclassified Unclassified