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OCR for page 233
The Medical Implications of Nuclear War, Institute of
Medicine. ~ 1986 by the National Academy of Sciences.
National Academy Press, Washington, D.C.
Acute Radiation Mortality
in a Nuclear War
JOSEPH ROTBLAT, PH.D.
University of London, London, England
OVERVIEW
Estimates of radiation casualties in a nuclear war depend on assumptions
made about the LDso value in humans. In the absence of direct evidence,
this value has been deduced partly from animal data and partly from a
few radiation accidents, many victims of which have been receiving ex-
tensive medical treatment. The LDso value thus deduced was very high,
600-rad bone marrow dose. The largest amount of data for humans the
1945 inhabitants of Hiroshima and Nagasaki has been rejected for a
variety of reasons.
The recent reassessment of the dosimetry in the Japanese cities for long-
term effects has provided an opportunity for the assessment of acute
radiation effects as well. A survey carried out on a large number of people
in Hiroshima, who were inside their houses during the explosion, contains
information about dates of deaths at various distances from the hypocenter.
It is suggested in the paper that this survey is highly suitable material for
an estimate of radiation casualties under wartime conditions.
A detailed analysis of the mortality as a function of time of death and
distance from the hypocenter has been carried out with the aim of proving
that, after the first day, the mortality was due predominantly to radiation
exposure. The distance at which SO percent mortality occurred has been
deduced from this analysis and found to be 892 + 11 meters.
To convert this to an LDso one needs to know the intensity of the
radiation field as a function of distance, the transmission factors for Jap
233
OCR for page 234
234
HEALTH CONSEQUENCES OF NUCLEAR WAR
anese-style houses, and the organ factor. All these quantities have been
the subject of detailed studies by a U.S.-Japan Workshop. Although the
final values are yet to be agreed upon, it is unlikely that they will differ
significantly from those presented so far. Using these data, a probit of
mortality versus bone marrow dose was obtained, which showed that the
bone marrow LDso for the Hiroshima survey was only 154 reds (220 reds
at body surface). The slope of the line is several times smaller for humans
than for animals.
The implications of these findings on the number of radiation casualties
in a nuclear war are discussed.
* * *
In this paper the basis for calculations of casualties from acute effects of
radiation in a nuclear war, which may result in death within 60 days after
exposure, is discussed. The time of death after whole body exposure is a
function of dose; the general trend of this function, compiled mainly from
mammalian data, ~ is shown in Figure 1.
At very high doses death may occur within hours, but with decreasing
dose, the time of death is extended to weeks. Down to a dose of the order
of 1,000 reds mortality is 100 percent. At lower doses, where the hem-
opoietic syndrome is relevant, there is an increasing chance of survival.
In this dose range the probability of death is a sigmoid function of the
dose that reaches the bone marrow, and is best examined by probit analysis
or by using special probability paper (Figure 2) with the dose plotted
logarithmically. (This particular curve is the result of experiments with
SAS/4 mice, carried out over many years by Lindop and Rotblat.2 I will
make frequent use of these results when comparing various effects in mice
with those in humans. ) The sigmoid curve is then transformed into a linear
relation, yielding two characteristic values: the LDso (the dose that causes
50 percent mortality in the population exposed to it) and the slope. The
remarkable steepness of the line means that estimates of radiation casualties
are very sensitive to the LDso. An error of 30 percent in the LDso can
make all the difference between practically 100 percent survival and prac-
tically 100 percent mortality. It will be shown later that for humans the
line is less steep, but the LDso is still the best statistic for an estimate of
casualties.
The problem is that while there are plenty of such data for animals,
there are practically none for humans. Early data from a group of patients
with cancer,3 which indicated an LDso in bone marrow of about 250 reds,
were dismissed as not being applicable to the general population. The
estimate of the LDso in humans is based mainly on the very small number
of people exposed to radiation in accidents. Most of these victims received
OCR for page 235
ACUTE RADIATION MORTALITY IN A NUCLEAR WAR
1000
100
o
-
~ 1 day \
~ 1 1 \
1 1
10
1
-1 month
\1
10 100 1000
DOSE (Gy)
235
FIGURE 1 Time of occurrence of death from acute radiation effects. Note that
both axes have logarithmic scales (1 Gy = 100 red).
intensive medical treatment, including barrier nursing, antibiotics, platelet
and red blood cell concentrates, and bone marrow transplants.4 Although
it is well known that such treatment enables people to survive very high
doses, nevertheless, it is being assumed that this does not affect the LDso.
In the United Kingdom an effective LDso of 600 reds to bone marrow-
deduced mainly from the people exposed to radiation in accidents-is
being used to estimate radiation casualties in a nuclear warts
In Hiroshima and Nagasaki a large number of people were exposed to
radiation under wartime conditions, but these data have not been used
because of the alleged difficulty in separating mortalities caused by ra-
diation from those caused by blast or heath However, recent surveys
carried out in Japan in connection with the reassessment of the dosimetry
for long-term effects provided an opportunity for another look at the acute
effects of radiation. The World Health Organization- which carried out
OCR for page 236
236
HEALTH CONSEQUENCES OF NUCLEAR WAR
99
95
90
80
50
CC
o
U)
At:
Ad
LLJ
U)
20
10
5
2
1
o
I I I / L
1 2 5 10
1 1 111 1
20
DOSE (Gy)
FIGURE 2 Probability of death as a function of dose, for SAS/4 mice.
a study of the effects of thermonuclear wary has requested that two
Japanese teams undertake such studies. These are still in progress, but the
team directed by T. Ohkita has produced data which form the basis for
this paper. I should stress that while the data are those of Ohkita and
coworkers, they are not responsible for the analysis that I have carried
out.
The data come from a survey of people in Hiroshima (to my knowledge
no such survey is as yet available for Nagasaki) who were shielded inside
Japanese-style houses during the atom bomb explosion. The houses were
at distances from the hypocenter that varied from less than 600 meters to
1,300 meters. There were a total of 1,216 people in the houses that were
surveyed, of whom 451 died during the first day and 201 (26 percent of
those surviving the first day) died during the following 2 months. The
tabulated data give the number of people that died each day at various
distances, in 100-meter intervals.
OCR for page 237
ACUTE RADIATION MORTALl7~Y IN A NUCLEAR WAR
237
My thesis is that the deaths that occurred after the first day were pre-
dominantly due to radiation exposure and, therefore, that the data obtained
from this survey are suitable for an estimate of the LDso in humans under
conditions of a nuclear war. The evidence for this is based on an analysis
of mortality as a function of time and distance, which shows that the
observed mortality is in much better accord win radiation exposure than
with other causes of death.
First, the time factor will be examined. Figure 3 shows the mortality
in 4-day intervals as a function of time after the explosion. It is expressed
as the percentage of the total number of people in the survey who died
during 2 months, starting from the second day after the explosion. The
histogram shows that there was initially an increase in mortality, which-
after peaking at about 10 days gradually decreased. This is not the result
that would be expected for deaths from blast injures or burns. A survey
by Masuyama~ has shown that after the first day, the cumulative mor-
tality mostly in people caught in the open was increasing according
to an exponential law, with a half-value of 6 days. From Masuyama's
In
J
> 20
U)
Hi:
id
-
J 10
At:
fir
o
0 10 20 30 40 50 60
DAYS AFTE R THE BOMB
FIGURE 3 Percent mortality, in 4-day intervals, as a function of time after the
Hiroshima explosion, starting from the second day.
OCR for page 238
238
HEALTH CONSEQUENCES OF NUCLEAR WAR
curve, it can be calculated how the percent mortality, in 4-day intervals,
would vary with time. As the curve in Figure 4 shows, this variation is
quite different from the findings in the survey of the people in houses
(histogram). By contrast, closer agreement is obtained with radiation ex-
posures. In the absence of data from humans, data from animal expen-
ments must be used. The histogram in Figure 5 shows the percent mortality
observed in mice exposed to a range of doses on both sides of the LDso.
Here the time interval is 2 days instead of 4, because in small mammals
30
G
Z 20
a:
A
-
a:
~10
-l
o
0 1 0 20 30 40 50 60
DAYS AFTER THE BOMB
FIGURE 4 Calculated percent mortality, in 4-day intervals, starting from the
second day, for all victims of the Hiroshima explosion. The histogram is for the
survey group (the same as in Figure 31.
OCR for page 239
ACUTE RADIATION MORTEM IN A NUCLEI We
30
J
>
Ct:
LU
Z 20
A
~1 0
239
~1
0 1 0 20 30
DAYS AFTE R EXPOSU R E
FIGURE 5 Percent mortality in 2-day intermurals, for SAS/4 mice, exposed to a
range of doses on both sides of the LDso.
death occurs over 30 days, instead of over 60 days as in larger mammals.
The resemblance of the data to those from the Hiroshima survey (Figure
3) is quite good.
Another way of looking at the time distribution is to calculate the mean
survival time of a population exposed to a given dose. As shown in Figure
1, at high doses the time of death depends very much on the dose, but
such dependence albeit smaller also occurs in the LDso region. The
lower line in Figure 6 shows the variation of the mean survival time, in
days, as a function of dose, for mice. In order to compare the data obtained
from mice with those from humans, the dose is expressed as the proportion
of the LDso. The upper line shows this dependence for the Hiroshima
survey. Taking into account the difference in time of death, as explained
above, the similarity between the results is striking.
OCR for page 240
240
40
~30
us
-
.< 20
>
-
10
of
UJ
o
HEALTH CONSEQUENCES OF NUCLEAR WAR
-
-
, ,
Hiroshima Survey
-
~ce
0 1.0 2.0 3.0
DOSE IN TERMS OF THE LD-50
FIGURE 6 Mean survival time as a function of dose expressed in terms of the
LD50. The upper line is for the Hiroshima survey group. (The doses at the relevant
distances were taken from Figure 13.) The lower line is for SAS/4 mice.
Yet another time dependence of interest is the LD50 calculated for a
population surviving a given time. In Figure 7 the distance at which 50
percent of the exposed people died is plotted against the day in August
1945 from which the calculation of the mortality was started. For example,
the first point (50 percent mortality distance = 1,022 meters) was cal-
culated for all 1,216 people in the survey. For the second point, on August
7, the 50 percent mortality distance of 892 meters was obtained from the
765 people who survived after the first day, and so on. The notable feature
of this graph is the very steep drop after the first day, after which the 50
percent mortality distance remains practically steady and then decreases
gradually (indicating a gradual increase in the LDso). The shape of the
curve after the first day is as would be expected for radiation mortality.
Indeed, the top graph, obtained from the data from mice, shows exactly
the same behavior: the LDso, calculated for consecutive days, changes
little initially and then gradually increases.
The second evidence for the suitability of the survey data to calculate
the LDso comes from the analysis of mortality versus distance. In a recent
paper, Ohkita9 presented data (Figure 8) for the whole population in
Hiroshima (both in the open and inside houses during the explosion) in
terms of the daily mortality rate against distance at various time periods
after the explosion. The earlier time periods show a two-component de-
crease, which Ohkita interprets to be due to the difference between ra
OCR for page 241
ACUTE RADIATION MORTALl7~Y lN A NUCLEAR WAR
241
diation and other fatal casualties. The smaller slope must be due to the
latter because the mortality extends beyond the distance at which the
gamma rays from the bomb were significant. In Figure 9, line A is a
reproduction of Ohkita's data for the period from 7 to 14 days after the
bomb. Line B shows the data from the survey group. The notable differ-
ence between the two lines is to be expected, if it is assumed that line B
gives the mortality predominantly due to radiation and that line A rep-
resents deaths from a mixture of radiation and other causes, with the latter
being predominant.
A similar but more direct result is obtained by plowing the probit of
mortality found in the survey group against the distance from the hypo-
center. Figure 10 shows the probit for mortality during day 1, and Figure
'A 1.1
J
1.0
Oo 0.9
G
~ 0.8
>
z
SAS/4 Mice
-
-
-
-
-
-
-
1 1 1 1
0 5 10 15 20
DAYS AFTER EXPOSURE
~ 1000! ~
-
<: Hiroshima Survey
CC
o son ~ ~ ~ ~ T -
lo
~ 800
o
700 _
z
~600 1 1 1 1 1 1 1 1 1
C} 6 8
-
1 T
it'
20 22 24 26
10 12
14 16 18
DATE (August 1945)
FIGURE 7 Lower curve: Distance from the hypocenter at which a 50 percent
mortality occurred in the people from the Hiroshima survey group who were alive
on the date shown on the horizontal scale. Upper curve: Similar plot for SAS/4
mice, but with the vertical scale giving the LDso in terms of its value for the
initial population. Note that the relative dose increases downward.
OCR for page 242
242
HEALTH CONSEQUENCES OF NUCLEAR WAR
10° _
LL
o
~ 10-3
C]
10-4
within 1 day\
1-6 days ~
7-14 days >~ ``
- 15-30 days \~N A,
\
31~0 days `` \\~\\
61-91 days ~_-
- 92-183 days
184-365 days ~~ ~
0 500 1000 1500 2000 2500 3000
D ISTANCE F ROM HYPOCENTER (m)
FIGURE 8 Average daily mortality rates for various periods as a function of
distance from the hypocenter based on a 1946 survey in Hiroshima (data from T.
Ohkita9~.
11 shows the probit for mortality during the subsequent 2 months. The
slope of the latter is 2.2 times greater; therefore, I submit that Figure 11
represents a true regression line for radiation exposure in Hiroshima. The
good fit enables the determination, with great accuracy, of the distance
from the hypocenter at which there was a 50 percent mortality. This
distance is 892 + 11 meters.
The next step is to convert this distance to dose, and here there is a
snag. The necessary parameters for the conversion are: the variation of
OCR for page 243
ACUTE RADIATION MORTALITY IN A NUCLEAR WAR
· \
10-1
-
~:
10-2
\ B
id,
_
~ MA
A: All Victims
B: Shielded Group
\
'\~`
\
hi.
10-3 ~1 1 1 1 1 \ 1 · 1
500 600 700 800 900 1000 1100 1200
\
DISTANCE FROM HYPOCENTER (meters)
FIGURE 9 Line A: Data from Figure 8 for the interval from 7 to 14 days after
the bomb. Line B.: The same data for the group in the Hiroshima survey.
OCR for page 244
244
99
95
90
r
o
~ 50
UJ
He
UJ
' 20
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1
HEALTH CONSEQUENCES OF NUCLEAR WAR
-
~ ~ ~!
-
-
-
o ~1 1 1 1 1 1 1 1
500 600 700 800 900 1000 1100 1200 130
DISTANCE FROM HYPOCENTER (meters)
FIGURE 10 Probability of death as a function of distance from the hypocenter
for the people in the survey group who died on the first day. The bars denote +
1 standard deviation.
tissue kerma in air (a measure of the intensity of a radiation field, in reds)
with distance; the transmission factor for buildings; and the organ factor,
that is, the fraction of the dose that reaches the bone marrow. All these
parameters have undergone considerable revision recently in the U.S.-
Japan Joint Workshop for the Reassessment of Atomic Bomb Radiation
Dosimetry. The last workshop meeting, held in Pasadena, California, in
March 1985, was supposed to come up with final figures, but they will
not be available until the end of 1986. However, the calculations yet to
be made are not likely to bring significant changes. Therefore, I will use
the most recent data available. The data by Kerr et al. in from Oak Ridge
OCR for page 245
ACUTE RADIATION MORTAIIIY IN A NUCT;FAR WAR
245
National Laboratory on tissue kerma are reproduced in Figure 12. It shows
the different gamma-ray components, as well as the neuron component.
The greatly reduced neutron contribution resulted in a large reduction of
the transmission factors for Japanese-style houses.
By applying the appropriate values, one can calculate the contribution
of the various components to the LDso. As is seen from Table 1, the LDso
turns out to be 154 reds. (In this calculation the relative biological effec-
tiveness of neutrons was assumed to be 1.)
99
95
90
80
J
At:
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o
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O _ 1 1 1 1 1 1 1 1
500 600 700 800 900 1000 1 t00 1200 1300
_
: _
Y.
i,
i,
i,
I,
DISTANCE E ROM HYPOCENTER (meters)
FIGURE 11 Probability of death as a function of distance from the hypocenter
for people in the Hiroshima survey group who died from day 2 to 2 months after
the explosion.
OCR for page 246
246
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OCR for page 247
ACUTE RADIATION MORTALITY IN A NUCLEAR WAR
TABLE 1 Calculation of the LD50 for a distance of 892
meters
Dose (red)
after
~ . .
1 ransmlsslon
Kerma through Organ
Radiation (red) Buildings Dose (rad)a
Delayed gamma rays 294 106 74
Prompt gamma rays 200 92 74
Primary gamma rays 9 4 3
Neutrons 33 12 3
aTotal, 154 red.
247
Similar calculations for other distances establish the relationship be-
tween dose and distance (Figure 131. It fits excellently a straight line on
a logarithmic scale of dose. By using this graph, the regression line can
be redrawn to give the probit as a function of dose (Figure 14~.
Apart from the very low LD,o, another interesting feature is the small
slope of the line obtained for humans, compared with that obtained for
mice (Figure 21. The coefficient of variation, i.e., the ratio of the gradient
of the probit line to the LDso value, is nearly 5 times smaller for humans
than for mice. This coefficient depends on several factors, including the
homogeneity of the population. A smaller coefficient is to be expected
when a highly homogeneous population, like the purebred strain of mice,
is compared with a highly heterogeneous population, like humans.
Before the LDso can be applied to an estimate of radiation casualties
in a nuclear war, two more points must be considered. One is that the
exposure to radiation in Hiroshima was practically instantaneous, while
that from fallout is spread out over hours or days. Since there are no
directly relevant data from humans, data from animal experiments must
be used. From data presented in the literatures it can be inferred that, in
larger mammals, if the same dose were delivered at a constant dose rate
over 24 hours, the LDso would be increased by about 40 percent. However,
in the case of fallout the dose rate is not constant; it decreases rapidly.
Calculations show that for a fallout dose received in 24 hours, the LDso
would be increased by about 10 percent.
The second point is that in fallout calculations, the dose at the surface
of the body and not to the bone marrow is usually calculated, as was the
LDso of 154 reds presented above. Therefore, this value must be divided
by the organ factor, which probably lies between 0.75 and 0.8. This would
give an LDso at the surface of the body of about 220 reds.
OCR for page 248
248
HEALTH CONSEQUENCES OF NUCLEAR WAR
1 000
500
200
Cat
to
o
1 00
fir
o
50
20
10
1 1 1 1 1 1 1 1
500 600 700 800 900 1000 1 100 1200 1300
DISTANCE FROM HYPOCENTER (meters)
FIGURE 13 Bone marrow dose versus distance from hypocenter in the Hiro-
shima survey group.
How many radiation casualties would result from such a low LDso? In
a recent paper, Lindop et alto investigated the sensitivity of radiation
casualty estimates to the assumed value of the LDso. For a single 1-megaton
bomb over London, the number of fatalities was calculated for LDso's
that varied from 300 to 800 reds and for protection factors (the ratios of
the doses received in the open to those received inside buildings or in
shelters) between 1 and 20. Although these calculations covered a large
range of doses, the number of fatalities (N) can be expressed by the
following simple empirical formula: N = 4 x 106(PD)-2'3, where P is
the protection factor and D is the LDso. According to this formula, a
reduction of the LDso from 600 reds to 150 reds would increase the number
OCR for page 249
ACUTE RADlATlON MORTALITY IN A NUCLEAR WAR
249
of fatalities by a factor of 2.5. At an average protection factor of 5, this
would mean an increase in the number of radiation deaths by more than
half a million just from one bomb.
However, as we pointed out in that paper,~3 under wartime conditions,
even exposure to sublethal doses could give rise to fatalities, because the
suppression of the immune system would reduce the chance of recovery
from other normally nonlethal injuries; indeed, the interactions may be
synergistic. It has been suggested that any exposure above 100 reds
should be considered a radiation injury. This would make the total fatal-
ities, direct and indirect, less dependent on the LDso.
In another paper presented in this volume, Greer and Rifkin listed
several conditions that may impair the immune response. Apart from
exposure to radiation, they include physical trauma, burns, and malnu-
t~ition. This last condition may explain the low LD50 in Hiroshima, since
there is evidence that the people in Hiroshima were undernourished both
99 _
95 _ i//
so iL
~0
-
o
50
i
cat
20
10 _
5 _
2
1
o
10 20 50 100 200 500 1000
/
/
/
1
_/
I 1 1
DOSE (cGy)
FIGURE 14 Percent mortality versus bone marrow dose in the Hiroshima survey
group.
OCR for page 250
250
HEALTH CONSEQUENCES OF NUCLEAR WAR
before and after the bomb.~4 By the same token, the other conditions
mentioned by Greer and Rifkin if confirmed would reduce the LDso
in wartime, even without the malnutrition factor.
In conclusion, it must be stressed that although it is now fairly certain
that the LDso in humans is considerably lower than was thought before,
at least under wartime conditions, the actual values, and therefore the
estimates of radiation casualties in a nuclear war, are still uncertain. While
final calculations must be deferred until the new dosime~y has been firmly
established, it is fair to conclude that estimates of radiation casualties
previously thought to lie at the upper end of the range have now shifted
to the region of probable.
NOTES
~Bond, V. P., T. M. Fliedner, and J. O. Archambeau. 1965. Mammalian Radiation
Lethality: A Disturbance in Cellular Kinetics. New York: Academic Press.
2Lindop, P. J., and J. Rotblat. 1960. Protection against acute effects of radiation by
hypoxia. Nature 185:593-594 (and unpublished data from subsequent experiments).
3Lushbaugh, C. C. 1974. Human radiation tolerance. Pp. 475-522 in Space Radiation
Biology and Related Topics, C. A. Tobias and P. Todd, eds. New York: Academic Press.
4Hubner, K. F., and S. A. Fry. 1980. The Medical Basis for Radiation Accident Pre-
paredness. New York: Elsevier.
Martin, J. H. 1983. Human survival-radiation exposure levels. J. Soc. Radiol. Prot.
3: 15-23.
6Adams, G. E. 1984. Lethality from acute and protracted radiation exposure in man. Int.
J. Rad. Biol. 46:209-217.
7World Health Organization. 1984. Effects of Nuclear War on Health and Health Services.
Geneva: World Health Organization.
~Masuyama, M. 1953. Statistical study of human casualties of the atomic bomb, especially
of the death rate in the acute stage (quoted by T. Ohkita in Immediate Effects, 1985,
Hiroshima ENUWAR Workshop).
9Ohkita, T. 1985. Immediate Effects, in Lessons from Hiroshima and Nagasaki. Hiro-
shima ENUWAR Workshop.
Kerr, G. D., J. V. Pace, and W. H. Scott. 1983. Tissue kerma vs. distance relationship
for initial nuclear radiation from the atomic bombs Hiroshima and Nagasaki. Pp. 57-103
in U.S.-Japan Joint Workshop for Reassessment of Atomic Bomb Radiation Dosimetry in
Hiroshima and Nagasaki. Radiation Effects Research Foundation. February 1983.
t~Ellett, W. H., and T. Marayama. 1983. Shielding and organ dosimetry. Pp. 83-101
in U.S.-Japan Joint Workshop for Reassessment of Atomic Bomb Radiation Dosimetry in
Hiroshima and Nagasaki. Radiation Effects Research Foundation. November 1983.
seepage, N. P. 1968. The effect of dose-protraction on radiation lethality of large animals.
Pp. 12.1-12.23 in Proceedings of a Symposium on Dose Rate in Mammalian Radiation
Biology. USAEC CONE 680410.
~3Lindop, P. J., J. Rotblat, and P. Webber. 1985. Radiation casualties in a nuclear war.
Nature 313:345-346.
i4Committee for the Compilation of Materials on Damage Caused by the Bombs in
Hiroshima and Nagasaki. 1981. Hiroshima and Nagasaki: The Physical, Medical and Social
Effects of the Atomic Bombing. Hutchinson: London.
Representative terms from entire chapter:
percent mortality
