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OCR for page 337
The Medical Implications of Nuclear War, Institute of
Medicine. ~ 1986 by the National Academy of Sciences.
National Academy Press, Washington, D.C.
Genetic Consequences of Nuclear War
PER OFTEDAL, PH.D.
University of Oslo, Oslo, Norway
INTRODUCTION
In the aftermath of a nuclear war, genetic effects may appear trivial in
comparison with the enormity of the catastrophic development in the
survivors' health and the environment.) Gross effects are immediately or
subtly demonstrable on the basis of diverse war scenarios. On the other
hand, in a great number of organisms, genetic effects of radiation have
been shown to occur according to a no-threshold dose-effect curve, thus
implying that effects may be found even in situations and population
groups where other direct effects are small. When I tried to quantitate
these effects the first time- in the working papers for the World Health
Organization (WHO) expert committee 3-4 years ago there was also
the possibility that an analysis might uncover unexpected aspects, in ad-
dition to those at least qualitatively obvious.2 The discussions on the effects
of nuclear war have indicated that whatever sector of effects is focused
on, closer examination has, in each case-be it treatment of casualties,
effects on climate, or effects on world trade led to a picture of possible
and often probable catastrophic collapsed
It is not easy to think differently, especially in an analysis that projects
beyond a tragedy for which more and more occluding consequences are
found. This paper is therefore basically a summary of my calculations for
the WHO paper, with marginal additional reflections inspired by views
and information that have appeared during the past 2 years.
337
OCR for page 338
338
HEALTH CONSEQUENCES OF NUCLEAR WAR
RADIATION DOSE TO SURVIVORS
Radiation is the only mutagen considered in this discussion, and doses
of genetic consequence are only those of nonstenlizing magnitude and
absorbed by survivors with present or future reproductive capacity.
Figure 1 shows schematically He elements of the situation to be con-
sidered in the target areas.
With bombs bigger than 10-100 kilotons (kt), the radiation lethal area
may be smaller than the blast and heat lethal areas, as can be seen in
Table 1.4 Transmissible genetic damage is then induced in survivors be-
yond the blast and heat lethal zones as well as the radiation lethal zone.
u'
o
c,
at
o
c,
LD50
\\ Fireball
\ ~ Heat and Blast Effect
Radiation Dose Curve
I GZ /
/ \
DISTANCE
1
RAD I AT ION LE THAL RAD I US
H EAT AND B LAST LETHAL RAD I US
FIGURE 1 Genetically effective exposure to radiation would occur mainly out-
side the radiation lethal area, with dose distribution as determined by the dose-
distance curve.
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GENETIC CONSEQUENCES OF NUCLEAR WAR
TABLE 1 Areas of Lethal Damage from Various Effects (km2)
339
Explosive Yield
Type of Damage ~ kit 10 kt 100 kt 1 Mt10 Mt
Blast 1.5 4.9 22 104480
Heat 1.1 10.5 60 3501,300
Initial radiation 2.9 5.7 11 2254
SOURCE: Based on Rotblat.4
If the blast and heat lethal zones extend beyond the radiation lethal zone,
the mean radiation dose to the survivors will be relatively smaller.
In Hiroshima and Nagasaki, the mean dose to parents of the 19,000
children born to parents of whom one or both had been irradiated is
estimated to be somewhat over 100 rem (subject to ongoing revisions).5 6
I have used this as a measure of the prompt radiation dose received by
the reproducing fraction of a surviving population after an isolated bomb.
If several small bombs are exploded near each other, there will be more
irradiated survivors (because the collective lethal zone perimeter will be
longer), but the mean genetically significant dose may be taken to remain
the same. With bombs bigger than 50 kt, the blast and temperature lethal
areas will to some extent cover the genetically significant irradiated sur-
vivor zone, thus leading to fewer irradiated survivors and to a lower mean
radiation dose in those that do survive.
With low-altitude and groundbursts, exposure to local fallout downwind
from the target will lead to genetically significant doses in the survivors.
Using arguments similar to those applied to the prompt radiation exposure,
one may assume that there is a lethal area in the central portion of the
plume path and survival zones on the periphery.4
To the extent that fallout is massive and fresh and few countermeasures
have been instituted beforehand, one may take the mean genetically sig-
nificant dose to parents to be of the same order of magnitude as for radiation
from the bomb itself (100 rem) and to be of sufficiently high dose rate to
have the same mutagenic efficiency as acute exposures.
In areas with uniformly heavy fallout, those in good shelters may sur-
vive. It has been calculated that in the most heavily contaminated areas
of the United States, following a 5,000-megaton (Mt) attack, it might be
necessary to spend some 6-7 weeks totally in shelter, thereafter making
excursions timed so as to limit daily exposures to 3 rem.7 After about
months, it may be possible to spend a full 16-hour day outside the shelter.
Over a period of 20 years, a total external radiation dose of about 1,500
OCR for page 340
340
HEALTH CONSEQUENCES OF NUCLEAR WAR
rem may accumulate.7 Half of this is possibly genetically significant, but
additional exposure will stem from radioactive contamination. So maybe
one can assume a genetically effective dose of i,000 rem absorbed at a
low dose rate and thus probably only one-third as effective a mutagen as
the corresponding acute dose.8 It is highly uncertain how many survivors
would belong to this category. In heavily contaminated areas, the number
would no doubt be large, but the efficiency of shelters; protective actions;
cleanup of local areas; and selective protection of the pregnant, the young,
and the potentially reproductive will all influence the genetically signif-
icant exposure. On the other hand, with large and contiguous areas being
contaminated, the probability of both parents being equally exposed is
higher than that in the Hiroshima/Nagasaki model calculation; thus the
genetically significant dose may be expected to be somewhat higher than
that proposed above.
The rest of the world would be exposed to delayed global fallout, which
would reenter the biosphere after weeks to years in the upper atmosphere.
The United Nations Scientific Committee on Effects of Atomic Radiation
(UNSCEAR) has calculated that the fallout from the atmospheric tests
during 1954-1962 led to dose commitments for the first generation of
about 1 red per megaton of fission yield.9 On the simplified assumption
that a war with a total of 10,000 Mt of fission took place, a total mean
dose of 10 rem to each person in the world would result. Because a large
fraction of the energy would be fusion, not fission, this calculated dose
is probably on the high side, but not by as much as an order of magnitude.
On the other hand, special circumstances-such as direct hits on nuclear
power plants may lead to major contaminations with long-lived radio-
active isotopes, increasing the mean survivor population dose in the less
contaminated areas.3 4 In those localities where the lethal dose or dose
rate is already closely approached, a further increase would lead to more
deaths, but, as expected, it would influence the reproducing survivor dose
to a lesser extent.
It seems to be a significant feature of the situation that the variation in
the genetically effective dose between individuals of the three categories
discussed bomb exposure, local fallout exposure, and global fallout ex-
posure may vary within little more than 2 orders of magnitude, including
mutagenic efficiency variation due to dose rate. This compression of the
range is caused on the upper side by the limits determined by the lethal
effect of radiation and on the lower side by the wide distribution of the
global fallout. Concurrently, there may be 2 orders of magnitude of var-
iation in terms of individual dose and effect, depending on local fallout
conditions and variation in radiation sensitivity.
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GENETIC CONSEQUENCES OF NUCLEAR WAR
GENETIC RADIATION EFFECTS
341
Genetic damage as a result of radiation exposure is generally believed
to consist of the same elements found in so-called spontaneous mutations.
This view may change as knowledge of the molecular mechanisms of
heritable mutations in higher organisms develops.
Effects to be expected after a given dose may be calculated by a doubling
dose method or by a direct method. With the doubling dose method,
estimates of effects in humans are based on the spontaneous mutation rate
seen in humans and in an experimental animal (usually the laboratory
mouse) and on the dose needed to double the rate in the experimental
animal. in ~ Difficulties are due mainly to the paucity of knowledge about
the normal situation in human populations and to the problems involved
in drawing parallels between two different biological species. The direct
method is based on the observed sensitivity of certain types of genes in
the experimental animal (e.g., those having to do with normal skeletal
development or with cataracts) and an estimate of the corresponding num-
ber of genes in humans. Subsequently, the calculation is extended to
encompass all known conditions in humans with similar genetic mecha-
nisms. The principal difficulties are again the transition from one species
to another and the extension of the estimates from one type of anomaly
to the whole spectrum of damage.
The International Commission on Radiological Protection (ICRP) takes
genetic damage seen in the first two generations to constitute one-quarter
of the stochastic risk induced, following occupational exposure (age I8-
30) to low-dose, low-dose-rate radiation, with the remaining risk being
various forms of cancer exposure (age 18-651.~3 25 On the assumption of
constant sensitivities, it may be calculated that for population exposures,
the corresponding fractions are about 0.4 for genetic risks (age 0-30) for
each child born and 0.6 for cancer risk (age 0-65) for lifetime cancer.
In Hiroshima/Nagasaki, it has not been possible to demonstrate genetic
effects in children born to parents, one or both of whom were exposed to
bomb radiation. ~4 The question may be discussed whether the effect might
be too small to be registered, or if circumstances limit the possibility of
insight, or if the findings really demonstrate that humans are less sensitive
to genetic harm from radiation than are, for instance, laboratory mice. ~4 ~5
Types and numbers of genetic anomalies expected after exposure to 1
million manrem (which appears to correspond to the genetically significant
dose in Hiroshima/Nagasaki) are shown in Table 2. (All these calculations
are made by the doubling dose method, except for Ehling's, ~6 which uses
a direct method.)
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342
HEALTH CONSEQUENCES OF NUCLEAR WAR
TABLE 2 Genetic Effects of One Million Manrem of Radiation to a
Population of Constant Size: Types and Numbers of Anomalies
Exposure
Acute
Chronic
~~ ~
Unbalanced ~anslocation ~
malformed liveborn 46602330
Tr~som~cs, XO 90903030
Simple dominants 6030020100
Complex dorn~nants,
multifactorial disease
mutationally maintained 4545016160
Multifactonal disease non
mutationally maintained 0000
Recessive mutations (2,400) (900)
Total (excluding recessive) 24090089320
Total UNSCEAR'77 s 63185
Total UNSCEAR'82 9 22144
Ehling 1984~6
Simple dominants 25
Recessives (250)
NOTE: The upper part of this table is based on the material and arguments presented in Oftedal
and Searle.2S
During the next few years, it is expected that improved data on spon-
taneous mutation rates will be available, in particular from Hungary (A.
CzeizI, personal communication). It is also hoped that an international
collaborative effort sponsored by the International Commission for the
Protection Against Environmental Mutagens and Carcinogens (ICPEMC)
and organized in collaboration with John Mulvihil1 from the National
Cancer Institute may yield data on the sensitivity of man's genetic material,
based on mutation rates observed in children born to surviving cancer
patients treated with radiation or cytostatics.~7
POPULATIONS AND EFFECTS
In view of the many uncertainties involved in estimating the genetic
effects, it seems unwarranted to try to differentiate between different
scenarios. However, let us again look at the three categories of exposure:
direct bomb radiation, local fallout, and global fallout.
On the perimeter of one or several smaller bombs, survival conditions
similar to those in Hiroshima and Nagasaki may be expected, and mean
OCR for page 343
GENETIC CONSEQUENCES OF NUCLEAR WAR
343
genetically significant doses of just over 100 red may be experienced. On
the basis of ICRP's sensitivity figures, one would expect about 240 extra
cases of genetic ill health among the 19,000 children born to exposed
parents, but none were found.~3 ~5 If one assumes that the populations
involved are 10 times that of Hiroshima/Nagasaki, about 200,000 children
would be born to exposed parents. Some 2,000-3,000 cases of genetically
determined ill health might appear, in addition to the 10,000-20,000
normally expected. So in this category of population, genetic ill health
might increase by a quarter in the first two generations postexposure,
subsequently decreasing over a period of several generations.
Areas of heavy local fallout would, according to several scenarios,
cover extensive areas and involve large populations. In my WHO paper,
I suggested a total world population of 2 x 108 reproducing survivors in
this category.2 With a mean genetically significant dose of 1,000 rem,
but delivered at a low dose rate, the amount of genetically defective
offspring would be about doubled. Obviously, this estimate is very ten-
tative, there being uncertainties at all levels of calculation, from the bomb-
ing scenario details to the normal incidence of genetic ill health. The
implications of a doubling of the present mutation rate are not easy to
foresee, keeping in mind the speculative nature of our picture of society
in the ravaged areas of large portions of the earth. If the present family
pattern is retained, if generally both parents are exposed, and if the number
of children per couple is elevated in order to compensate for the population
lost in the war, the majority of families would experience one or several
genetically determined cases of ill health.
The third element discussed global fallout would imply that the
genetically determined ill health would be increased by a small fraction.2
Calculations can be performed to show that the absolute numbers may
become very large, but it would probably take a refined epidemiologic
analysis to prove that the increase had in reality taken place. 14 l~ However,
due to regional differences in climatic conditions, quite significant vari-
ations in amounts of fallout would occur, with a corresponding variation
in exposure.~9
OTHER EFFECTS ON FUTURE GENERATIONS
Two other aspects deserve to be mentioned in order to make the picture
complete.
In experimental work with the mouse it has been demonstrated that
recessive mutations may be induced by radiation about seven times more
frequently than dominant mutations.20 In an outbreeding large population,
recessive mutations are ordinarily expressed only in the distant future and
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344
HEALTH CONSEQUENCES OF NUCLEAR WAR
with low predictability. They are therefore generally disregarded in esti-
mating harmful genetic effects of radiation. However, in small, isolated,
and inbreeding populations, recessive mutations might come to expression
earlier and in significant numbers and add to the detriment resulting from
radiation exposure. It is conceivable that situations of this type might
develop after a nuclear war, if small bands of survivors were to live in
isolation for several generations. Modern man probably experienced this
kind of breeding pattern in his early history, and many racial characteristics
may have become established in this way.
Another aspect that concerns the next generation, although not genetic,
is the teratogenic effect of radiation. Some stages of embryogenesis are
particularly sensitive to radiation, but in general the defects lead to spon-
taneous abortion and so may be regarded as a category of limited con-
sequence.2~ 22 However, it has been shown recently in Hiroshima and
Nagasaki that fetuses irradiated during the third and fourth months of
development are particularly prone to brain damage, with a relatively large
frequency of mentally retarded children born in this group.23 In any nor-
mally reproducing population, a small fraction of the population under 30
years of age about 1.0 percent will be pregnant with a child at this
stage of development. Among the children born to survivors some 5-7
months after exposure to bomb radiation, mental retardation may thus be
expected to be a dose-dependent characteristic. To the extent that pro-
tracted irradiation is equally efficient in this respect, even those exposed
to fallout radiation and contamination may show this type of damage. On
the basis of the dose calculations referred to above, a prevalence of some
additional 2-3 percent of retarded children might be the result in the target
areas.
It also appears from the Hiroshima/Nagasaki data that the intelligence
quotient of children exposed during the sensitive fetal period may be
reduced, even if it remains in the normal range (W. J. Schull, personal
communication). The reduction is dose dependent. Generally speaking,
then, fetal exposure may conceivably lead to a lower level of intelligence
in large portions of the generation born during the first years after war.
There is a possibility that material on hand in Norway might give some
information on whether the fallout from atmospheric bomb tests has had,
to a corresponding degree, the same kind of effect. A oroiect to investigate
this is being planned.
r ~D
GENETIC HANDICAPS IN THE POSTWAR WORLD
If, under given circumstances, the radiation and genetic load would
appear to threaten the survival of a group, a number of practices might
OCR for page 345
GENETIC CONSEQUENCES OF NUCLEAR WAR
345
be instituted to reduce the load and to conserve the material resources
available. These practices could range from selective shielding of repro-
ducing individuals, to infanticide and euthanasia, to selective or, indeed,
compulsory breeding by those individuals showing indications of least
genetic damage. In animal husbandry, this principle is known as progeny
testing.
THE WORSE, THE BETTER: A TRAGIC PARADOX
As is apparent from this discussion, the upper limit of the genetically
significant radiation exposure is determined by the lethal and sterilizing
effects of radiation. To the extent that postwar adverse conditions reduce
survival, it may be presumed that those suffering greater radiation insults
will succumb before those that have a lighter radiation load.24 Thus,
adverse conditions, whether societal (e.g., lack of care for the disabled),
physical (e.g., nuclear winter), or biological (e.g., plagues or pests), all
serve to reduce genetic damage by selective mechanisms that are tragically
unspecific, inefficient, and harsh. The wanton and meaningless destruc-
tiveness of the nuclear holocaust is illustrated even in this detail.
NOTES
World Health Organization. 1984. Effects of Nuclear War on Health and Health Services.
Geneva: World Health Organization.
2Oftedal, P. 1984. Genetic damage following nuclear war. Pp 163-174 in Effects of
Nuclear War on Health and Health Services. Geneva: World Health Organization.
World Health Organization. 1985. Effects of Nuclear War on Health and Health Services.
A38/Inf. DOC/5 Thirty-Eighth World Health Assembly. Geneva: World Health Organi-
zation.
4Rotblat, J. 1984. Physical effects of nuclear weapons. Pp. 41-64 in Effects of Nuclear
War on Health and Health Services. Geneva: World Health Organization.
5United Nations Scientific Committee on the Effects of Atomic Radiation. 1977. Sources
and Effects of Ionizing Radiation. New York: United Nations.
6Loewe, W. E., and E. Mendelsohn. 1981. Revised dose estimates at Hiroshima and
Nagasaki. Health Phys. 41 :663-666.
7Gant, K. S., and C. V. Chester. 1981. Minimizing excess radiogenic cancer deaths after
a nuclear attack. Health Phys. 41:455-463.
~Russell, W. L. 1972. The genetic effects of radiation. Pp. 487-500 in Peaceful Uses
of Atomic Energy, Vol. 13. Vienna: International Atomic Energy Agency.
9United Nations Scientific Committee on the Effects of Atomic Radiation. 1982. Ionizing
Radiation: Sources and Biological Effects. New York: United Nations.
10Luning, K. G., and A. G. Searle. 1971. Estimates of genetic risks from ionizing ra-
diation. Mutat. Res. 12:291-304.
~ ~Searle, A. G. 1974. Mutation induction in mice. Pp. 131-207 in Advances in Radiation
Biology, Vol. 4, J. T. Lett, H. I. Adler, and M. Zelle, eds. New York: Academic Press.
OCR for page 346
346
HEALTH CONSEQUENCES OF NUCLEAR WAR
t2Ehling, U. H. 1984. Methods to estimate the genetic risk. Pp. 292-318 in Mutations
in Man, G. Obe, ed. Berlin: Spnnger.
i3International Commission on Radiological Protection. 1977. Recommendations of the
International Commission on Radiological Protection. ICRP Publication 26. Oxford: Per-
gamon.
~4Schull, W. J., M. Otake, and J. V. Neel. 1981. Genetic effects of the atomic bombs:
A reappraisal. Science 213: 1220-1227.
~5Oftedal, P. 1984. On the lack of genetic damage in Hiroshima and Nagasaki. Or, is
the mouse a good model for man? Health Phys. 46:1152-1154.
~6Ehling, U. H. 1984. Quantifizierung des genetischen Risikos. Pp. 103-104 in Jahres-
berifht 1983 Gesellschaft fur Strahlen- und Umweltsforschung, Munchen. 8042 Ober-
schleissheim: Gesellschaft fur Strahlen- und Umweltsforschung.
i70ftedal, P., and J. Mulvihill. In press. Possible genetic effects of cancer therapy, seen
in surviving cancer patients' offspring. Fourth International Conference on Environmental
Mutagens, Stockholm, 1985. New York: Alan R. Liss.
International Commission for the Protection Against Environmental Mutagens and Car-
cinogens. 1984. Mutation Epidemiology: Review and Recommendations. Committee 5
Reports. Amsterdam: Elsevier.
i9Oftedal, P., and E. Lund. 1983. Cancer of the thyroid and ~3~I fallout in Norway.
Pp. 231-239 in Biological Effects of Low-Level Radiation. Vienna: International Atomic
Energy Agency.
20Ehling, U. H., and J. Favor. 1984. Recessive and dominant mutations in mice. Pp. 389-
428 in Mutation, Cancer and Malformation, E. H. Y. Chu and W. M. Generoso, eds. New
York: Plenum.
2~Russell, L. B. 1954. The effects of radiation on mammalian prenatal development.
Pp. 861-918 in Radiation Biology, A. Hoellaender, ed. New York: McGraw-Hill.
22Rugh, R. 1958. X-irradiation effects on the human fetus. J. Pediatrics 52:521-538.
23Otake, M., and W. J. Schull. 1984. In utero exposure to A-bomb radiation and mental
retardation: A reassessment. Br. J. Radiology 57:409-416.
24Lechat, M. F. 1984. Short term and medium term health effects of thermonuclear
weapons and war on individuals and health services. Pp. 77-100 in Effects of Nuclear
War on Health and Health Services. Geneva: World Health Organization.
25Oftedal, P., and A. G. Searle. 1980. An overall genetic risk assessment for radiological
protection purposes. J. Med. Genetics 17:15-20.
Representative terms from entire chapter:
genetically significant
