HIROSHIMA AND NAGASAKI: A COMMENTARY

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• Document Page Count: 7
• Document Creation Date: December 22, 2016
• Document Release Date: June 24, 2010
• Sequence Number: 18
• Publication Date: October 1, 1983
• Content Type: OPEN SOURCE

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South African Journal of Scie* Vol. 79 October 1983 I
Hiroshima and Nagasaki: A Commentary
P. J. D. Lloyd
The Japanese findings on the effects of
nuclear weapons exploded over Hiroshima
and Nagasaki have recently been published
and are reviewed here. First, the physical
events occurring immediately after the ex-
plosions are outlined; then, the short- and
long-term effects upon the environment are
described, as are the short-, intermediate-
and long-term effects upon the populace.
The findings are discussed in the light of the
common wisdom that the major hazard
which arises from nuclear weapons is that of
radioactivity. It is pointed out that by far the
greatest proportion of deaths and injuries
arose from thermal effects; that about 10%
of the short- and intermediate-term mortali-
ty was caused by the effects of massive doses
of radiation; that the long-term effects are
detectable above background, but have con-
tributed little additional to the toll of human
suffering; and that while the effects of
fallout and induced radiation were initially
apparent on close examination, no long-
term effect has been identified, nor has there
or 2U'Pu, ar resse into a critical mass; _
an uncontrolled chain reaction ensues, with
the splitting of each nuclide into at least two
fragments; neutrons are released to sustain
the reaction; some of the mass of the original
nuclide is converted into energy. Each gram
of uranium which splits releases about 8.2 x
1010 J, so that to create the energy equivalent
to about 20 000 tons of TNT
(9 x 1013 J) requires the destruction of
about 1 kg of 2;U.
A point source of 9 x 1013 J will reach
temperatures of the order of 106?C, destroy
its confinement, and begin to dissipate
energy. A fireball is formed, and the thermal
expansion which results gives rise to a shock
wave. Initially, the surface of the fireball
and shock wave are coincident, but after
about 0.1 ms the shock wave separates from
the fireball surface; the fireball then has a
radius of about 15 in and a temperature of
some 300 000?C.
been any contribution mortalit
diseasefrom thissource. t is concluded that
en7c avours to resist nuclear weapons may
befailing because of irrational attacks upon
the long-term radiation effects of these
weapons, rather than upon the chemical and
biological effects which have already been
other types of weapons.
On 6 August 1946, the city of Hiroshima
disappeared at precisely 08h15. A uranium
bomb of some 13 000 tons of TNT
equivalent had exploded at a height of 580 in
over the city centre. Three days later, at
1lh20, a plutonium bomb of some 22 000
tons of TNT equivalent exploded at a height
of 503 in over Nagasaki. Time heals, and
distance brings perspective. After thirty-
four years the Japanese were able to look
with relative dispassion on the months
following that August, and have now
published their findings.' It is the purpose of
this article to review the chronicle of their ex-
periences, because it suggests that we may be
debating the case for and against nuclear
weapons from the wrong position.
Nature of the weapons used at
Hiroshima and Nagasaki
The basic physics of the atomic bomb is
well-known. Fissile nuclides, typically 21JU
near ultraviolet, visible and infrared rays
thereafter. A few seconds after the explo-
sion, buoyancy forces come into play and
the fireball starts to rise, drawing air in
below it, and forming the typical 'mush-
room' cloud within a few minutes. The
unstable, radioactive elements formed in the
fission process tend to be carried up in the
fireball, and are precipitated as 'fallout'
from a height of 1 km or more as moisture
carried into cooler regions condenses.
An energy balance for such an event
shows that the kinetic energy of fission
fragments and neutrons is about 7.45 x 1013
J; that released by prompt photons and the
absorption of excess neutrons is about 0.62
x 1013 J; that from the long-term decay of
fission products about 0.44 x 1013 J; and
about 0.49 x 1013 J is released harmlessly as
neutrinos. Thus, about 8.5 x 1013 J is
available as dissipatible energy. About half
of this energy is dissipated in the shock
wave, which initially travels above the speed
of sound, and slows after about 2 km to the
speed of sound. Air is accelerated by the
passage of the shock wave to velocities of the
order of 500 m/s (1 800 km/h) close to the
event and falls to about 20 m/s at a distance
of 3 km. The blast wave so created has a
duration of about one second and gives rise
to large forces. Pressures as high as 350 kPa
are achieved 500 in from the event, and fall
to about 100 kPa at a distance of I km, to 50
kPa at 1.6 km and to 10 kPa at 3.6 km.
Approximatr hreaka,av
I
J
-, r
2 4 7 2 4 7 2 4; 2
lo-1 to 2 to '
Time after explilsiom (srowmds)
The shock wave spreads and heats the air
in its path. The air becomes luminous, and
effectively shields the fireball. However,
after about 15 ms, the shock wave has
travelled so far and dissipated so much
energy that it can no longer heat the air to
luminous temperatures. The fireball then
becomes visible from outside. This is refer-
red to as the'breakaway' point. The fireball
continues to expand and reaches it max-
imum size of about 220 in one second after
the explosion. The growth of the fireball is
shown in Fig. 1, and the observed surface
temperature of the ball in Fig. 2. The
minimum in the observed temperature at the
breakaway point is caused by the pre-
dominance of high-energy ultraviolet rays
during the first 15 ms, and the increase in the
Fig. I. The growth of the fireball for
a 20 kt weapon.
Shock effects are magnified by the Mach
effect. If the bomb explodes in the air, the
primary shock wave is reflected from the
ground and the reflected wave interferes
constructively with the primary wave. Ther-
mal energy in the infrared region comprises
about 35% of the total energy released,
which, fora fireball of the order of 100 in in
diameter, at an average temperature of
about 5 000 K and with an emissivity of
about 0.6, would imply a peak emission at
about I nm and a total dissipation in the
ultraviolet to far infrared portion of the
The author is director of the Metallurgical
Laboratory, Chamber of Mines Research
Org zation, P.O. Box 91230, Auckland Park
2000th Africa.
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2 4 7 2 4 7 2 4 7 2 4 7 2 4 7
In 1)) ' 10 2 lt) t 1 10
Time after explosion (seconds)
Fig. 2. Change in apparent fireball surface
temperature with time, for a 20 kt weapon.
spectrum of about 45% of the total energy.
Some energy is released as prompt gamma
rays and neutrons. It appears that this is
about 3% of the total energy, but varies
significantly with the construction of the
weapon. The remaining energy is dissipated
largely by delayed beta and gamma X rays
from the fission products.
To summarize, therefore, a nuclear bomb
of 20 000 tons of TNT equivalent dissipates
its energy approximately as follows:
Blast propagated by the shock wave 4.2 x 1012)
Thermal, visible and near UV
electromagnetic energy 3.6 x 1012 J
Prompt gammas and neutrons 0.3 x 10" J
Fission product decay 0.4 x 1013 J
Neutrinos 0.5 x 1013.1
Total 9.0 x 10" J
Short-term effects of energy released upon
the environment
Close to the hypocentre, blast effects are
largely vertical; further away, the total ef-
fect is reduced but the effects are increasing-
ly in the horizontal direction. The results
may be summarized as follows:
Distance from
hypocentre
(km) Damage
0.5 Most buildings almost totally
destroyed.
0.8 Reinforced-concrete, earth-
quake-proof buildings begin to
remain structurally repairable.
1.6 Multistorey brick buildings
destroyed almost completely.
2.6 All buildings require repair
before use; wooden buildings
structurally unsound.
3.2 Wooden buildings begin to be
structurally repairable.
3.6 All windows broken; moderate
plaster damage.
South African Journal *ience Vol. 79
hypocentre is evident from Fig. 3, which
shows the ruins of the Hiroshima Gas Com-
pany's building, which had a reinforced-
concrete frame and brick curtain-walling
some 250 m from the hypocentre.
The thermal energy is attenuated with
distance for two reasons, the familiar
inverse-square relationship, and the absorp-
tion and scattering of electromagnetic radia-
tion in the atmosphere. On the day the bot
was dropped, the sky was clear ov
Hiroshima, and visibility was greater the
20 km, so the second effect was limited.
Assuming that the visibility was exactly 20
km, the following are the thermal energy
fluxes which would have been experienced.
Distance from
hypocentre (km)
Thermal flux
(Mi/m2)
0
4.2
0.5
2.2
1.0
0.9
1.5
0.4
2.0
0.2
3.0
0.1
Such thermal fluxes were sufficient to raise
temperatures at the hypocentre to between
3 000? and 4 000?C. One kilometre from
the hypocentre, roof tiles were vaporized
(Fig. 4), indicating temperatures of over
1800?C. Three kilometres from the
hypocentre, trees and wooden poles were
charred on the surface facing in the direction
of the burst. Widespread conflagration was
another result, and a firestorm grew. From
I1h00 to 15h00 there were local winds of 18
m/s as cold air was drawn in a whirlwind to
the focus of the storm. By I7h00 all fuel
within a 2 km radius of the hypocentre had
been consumed, and the wind died. The
ashes from this fire were drawn up by
buoyancy forces, mixed with the residue of
the explosion, and were precipitated as
`black rain' as the moisture condensed.
The high energy photons (gamma rays)
from the bomb had little immediate effect
upon the environment except to excite
secondary fluorescent X rays. The neutrons,
which were largely fast (with a velocity of
over 106 m/s), interacted with other matter
and gave rise to induced radioactivity. The
approximate dose rates were:
Distance from Gamma-ray Neutron dose
hypocentre (km) dose (rad) (rad)
0
1x106
2x10'
0.5
2x103
4x103
1.0
3 x 102
2 x 102
1.5
2x10'
1x10,
Certain nuclides in particular were ac-
tivated, namelysMn, 14,Na, MSc and J99Co,
as shown in Fig. 5. As late as 1962, PCo
could still be detected in samples of iron col-
lected in the vicinity. Also important in the
short-term dose calculations was JsAI, with a
half-life of only about 2.3 minutes. Im-
mediately after the explosion, the activity
Fig. 3. The three-storey Hiroshima Gas Corr
party's building 250 in from the hypocentre.
one metre above the soil due to 13A1
about 200 times that due to PsMn.
This radiation had, in general, no detec-
table effect upon fauna observed in the im-
mediate vicinity. Bombardier beetles, ear-
wigs, beach fleas, earthworms, tiger beetles,
moths, mosquito larvae, rats, rabbits and
mice showed no effects. Some Drosophila
mutations were observed, but it could not be
concluded these were the direct effect of the
radiation. Many fish died, but this seemed
to be the effect of blast rather than of radia-
tion. Birds suffered from blast and burns. A
number of horses clearly showed both ther-
mal and radiation injuries. The major ef-
fects upon plants were those of blast and
heat. However, the stumps of trees within
700 in of the hypocentre tended not to bud at
first. There was retardation of growth,
fasciation, malformation and variegation of
herbaceous species. These effects disap-
peared within three years after the blast.
Some short-lived chromosomal abnor-
malities were observed.
Fig. 4. A roof tile with clear evidence that its sur-
face temperature exceeded 1800?C during the
0.3-s thermal pulse caused by the explosion.
Long-term effects upon the environment
The longer-term effects of the two nuclear
weapons upon the environment were small,
though detectable. The physical damage
was made good with remarkable speed. By
1948, houses and buildings were rapidly in-
creasing in number so that it became dif-
ficult to study long-term effects upon
vegetation. The primary long-term effect
was that of the longer-lived radionuclides.
Some of these consequences were noted
above (Fig. 5). Ashes and nuclides from the
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Thermal injury was the primary cause of
this disaster. Recall that thermal fluxes of
over 0.9 MJ/m2 occurred within 1 km of the
hypocentre. Such fluxes, acting on bare skin
for 300, ms, will result in charring and car-
bonization. Even fluxes of 0.1 MJ/m2, 3 km
from the hypocentre, will cause erythema of
the skin within 300 ms. Such fluxes are
unusual in thermal injury, and the injuries
are known as 'flash' burns. Shielding is ob-
viously possible, and in fact reduced the
mortality rate at a distance of 2 km by a fac-
tor of about five. The usual thermal radia-
tion phenomena were observed, with light-
coloured materials reflecting the heat and
offering better shielding than dark-coloured
materials.
Another important cause of death was
blast injury. There were primary injuries
due to the blast, but the effects were masked
South African Journal ofScie* Vol. 79 October 1983
explosion were carried over an elliptical
area, 19 km long and up to 11 km wide, to
the north-west of the hypocentre at
Hiroshima. At Nagasaki, rainfall 3 km to
the east of the hypocentre played a major
part in removing activity from the at-
mosphere. The area around the Nishiyama
reservoir was particularly severely con-
taminated.
Two months after the explosions, the
fallout contributed up to 0.05 mrad/h at
Hiroshima and up to 1 mrad/h at Nagasaki.
The integrated dose over 35 years, from one
hour after the explosion to 1980, in the air
one metre above the ground, amounted to a
maximum of between 4 and 40 rad at
Hiroshima and between 50 and 150 rad at
Nagasaki. It should be recalled that the max-
imum permissible dose for members of the
general public should not exceed 5 rad/yr.
or 175 rad over 35 years, for those of 18 years
of age and older. The ALARA ('as low as
reasonably achievable') principle should ob-
viously apply, but it is interesting that the in-
tegrated dose from fallout after such
devastating events should only approach the
'tolerable' level.
Short-term effects upon the populace
It was difficult to assess the short-term ef-
fects of the explosions on people. The total
destruction of the cities made accuracy im-
possible. Figure 6 illustrates the acute
casualty and mortality levels at Hiroshima
and Nagasaki, and Fig. 7 indicates that in
both cities the death rate was halved every
six days after the explosions. Within forty
days most of the acute effects had passed.
After a year, the casualties at Hiroshima
were as shown in Table 1.
a
00
'0 tell
a
U t))
w
?
by the thermal injuries. Primary visceral in-
juries typical of conventional blasts were
relatively rare, and the incidence of blast in-
jury was higher in those who had been in-
doors rather than outdoors. This suggests
that secondary injuries from materials ac-
celerated by the blast were the main cause of
fatalities. The survivors hospitalized after
the blast on 13 August showed the following
injuries: thermal burns, 50.2%; trauma,
33.3%; both thermal burns and trauma,
16.5%. The traumas were mainly contu-
sions (54%) and wounds due to glass
fragments (35%). The latter were particular-
ly distressing, as they were often the result of
a myriad of glass splinters embedded in the
body.
Finally, there were the immediate deaths
caused by high-energy radiation. It will be
recalled that about 0.3 x 1013 J was
dissipated as prompt gamma rays and
neutrons, which resulted in in-air doses of
greater than 300 rad of gamma radiation
and 200 rad of neutrons within I km of the
hypocentre. At the hypocentre, the doses
were 10 000 rad of gamma rays and 20 000
rad of neutrons. A whole-body dose of 10
rad has a barely detectable effect; one of 100
rad causes mild acute symptoms, with some
diminution of the white cell counts; one of
1 000 rad depresses blood cell and platelet
formation, damages the intestine, and
usually leads to death within 30 days; a
whole-body dose of 10 000 rad leads to im-
mediate signs of damage to the central ner-
vous system, with death within a few hours.
Table 1. Total casualties at Hiroshima, 6 August 1945 to 10 August 1946
(military personnel excluded).
Distance from
hypocentre
Severely
Slightly
Not
(km)
Killed
injured
injured
Missing
injured
Total
Under 0.5
19 329
478
338
593
924
21 662
0.5-1.0
42 271
3046
1
919
1
366
4 434
53 036
1.0-1.5
37 689
7 732
9
522
1
188
9 140
65 271
1.5-2.0
13 422
7 627
11
516
227
11 698
44 490
2.0-2.5
4 513
7 830
14
149
98
26096
52686
2.5-3.0
1 139
2 923
6
795
32
19907
30 796
3.0-3.5
117
474
1
934
2
10 250
12 777
3.5-4.0
100
295
1
768
3
13 513
15 679
4.0-4.5
8
64
373
4 260
4 705
4.5-5.0
31
36
156
1
6 593
6 817
Over 5.0
42
19
136
167
11 798
12 162
Total
118661
30 524
48
606
3
677
118 613
320 081
O\ ?t 60
\0%%? 40
N
?\ ? a 20
1.0 2.0 3.0 4.0 5.0 06 1.0
Distance from hypocentre (km)
Fig. 5. Change in dose rate with time, one metre above the
ground at the hypocentre, Hiroshima.
Fig. 6. Variation of acute mortality (9-*)
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p (II ,rvrd value tII roshimal
? Obl erved value (Nagasaki)
- Calculated value
4 8 12 16 20 24 28 32 3? 40
Days after detonation
In the vicinity of the hypocentre, there
were clear signs of people having suffered
massive radiation doses. Over 3007o of the
eventual survivors and 16076 of those who
soon died were highly nauseous within a few
hours, and many suffered diarrhoea often
accompanied by internal haemorrhage
within a few days. Deaths among otherwise
only mildly injured victims occurred seven
to 10 days after the explosion, usually with
signs of cerebral damage. Autopsies were
carefully performed on 25 who died during
this acute phase; of these, 19 died primarily
from thermal injuries. There was, however,
evidence of radiation damage in most cases.
At this acute stage, it showed itself primarily
in the haematopoietic organs, particularly
the spleen, where lymphocytes were almost
entirely absent. About two weeks after the
blast, the acute phase of injury drew to a
close. About 9007o of the eventually fatal
cases had died by this stage, and about 90016
of the survivors who received medical treat-
ment during this phase complained of ther-
mal injury.
Intermediate-term effects upon the
populace
From the beginning of the third week
after the explosions to the end of the eighth
week, the effects of radiation took their toll,
and a further 10016 of the ultimate total of
fatal cases died during this period. The first
sign of the effects of radiation was usually
the loss of hair, or epilation, the degree of
which varied with distance from the hypo-
centre and with shielding. At Hiroshima,
7601o of those exposed within 1 km of the
blast, who were either outside or in wooden
buildings, suffered epilation. The onset was
17 days after the explosion, on average, and
continued for one to two weeks. Hair
regeneration then started after 8 to 10
weeks.
The second sign was subsurface haemor-
rhage, which showed itself as purplish spots
or patches. The incidence among those ex-
posed within I km was about 50074. There
were related oropharyngeal lesions, the in-
South African Journal of ctence Vol. 79 October 1983
cidence of which was highly correlated with
epilation to about 1.5 km from the hypocen-
tre; at greater distances, the lesions were
more common, and were as high as 10% at
4.5 km. Other haemorrhages were common,
particularly nasal and uterine. Ocular
haemorrhage was also prevalent. All these
signs were often aggravated by fever, which
rose as each new symptom appeared and
continued until death intervened.
Haematological examination showed
that damage to the bone marrow had reduc-
ed the regeneration of blood cells, par-
ticularly white cells. Red cell counts were
typically 8017o of normal, haemoglobin 50%
of normal, and white cells about 5% of nor-
mal, in those exposed to 450 to 600 rad and
who died within 14 days. In less severe cases,
about half the population died within 40
days; their white cell count was never less
than about 10% of normal. A third group
had a minimum in their white cell count
after about four weeks, at about 2501o of the
normal count; about 10076 of this group
died, usually more than 40 days after the ex-
plosion and of complications rather than
from direct injury due to radiation.
There were those who were potentially af-
fected by secondary radiation, i.e. by the
radiation from neutron-induced radioiso-
topes in the air and soil, and by fallout.
Those entering Hiroshima an hour after the
explosion and staying near the hypocentre
for five hours would have received about 20
rad; the next day they would have received
less than 10 rad in eight hours. In such
populations, about one-third had less than
8001o of the normal white cell count. Those
exposed to fallout experienced marked
malaise, headache and abnormal menstrua-
tion soon after the event. In the longer term
there was a marked increase in the white
blood cells, particularly leukocytes, with
counts over five times the normal in extreme
cases, 50 to 80 days after the explosion. This
effect occurred and disappeared most rapid-
ly in children. Eight years after the explosion
the white cell count was almost normal in the
population living in the areas most affected
by fallout.
Long-term effects
A primary effect was the formation of
scar tissue at the site of thermal injury,
which led to deformity or functional distur-
bance. Particularly distressing was the for-
mation of `keloids', or the overgrowth of
scar tissue during regeneration, forming ir-
regular protrusions like the shell of a crab.
This occurred in about two-thirds of all ther-
mal burns, usually within 150 days of injury
and gradually disappeared over the next
decade or so.
The blood disorders so characteristic of
radiation injury persisted for several years.
A year after the explosion, there was a high
incidence of general malaise and dizziness
associated with some reduction in the red
and white cell counts. After two and three
years these symptoms persisted, but to an
ever smaller degree. After eight years
anaemia was a statistically significant ex-
perience, and this persisted, while declining,
for up to 15 years.
The formation of cataracts in the eye was
common. Those exposed while infants and
examined 14 years later had a greater than
50% incidence if exposed within 1 km of the
hypocentre, and a greater than 1007o in-
cidence if exposed within 1.4 to 1.6 km,
although in only 13% of all cases was the size
of the cataract moderate (no marked or
severe cases were found).
Amenorrhea was common (greater than
50% incidence) after the explosion and
typically continued for five to six months.
The majority of women over 45 went into
menopause. Exposure to radiation did not
appear to affect the age of menarche in
teenage girls. There was no evidence for an
increase in sterility due to exposure, but
there was a statistically lower conception
potential in exposed women from
Hiroshima than in those from Nagasaki.
The evidence for an increase in the number
of stillbirths with an increase in exposure to
radiation, or changes in sex ratio or birth-
weight, was inconclusive. There was some
evidence for an increase in the incidence of
malformations among those born of expos-
ed women, particularly in the bone, heart
and large vessels, but no malformation was
characteristic, and the increase in incidence
lessened with time.
Exposure in utero led to increased foetal
mortality from about 3016 in the unexposed
to over 20016 in those exposed within 2 km of
the explosions. Neonatal and infant death
rates were about 4016 in the unexposed and
over 25% in those significantly exposed
within 2 km. In a 24-year study of nearly
1 300 children from both Nagasaki and
Hiroshima who had been exposed to some
radiation in utero, there was a significant in-
crease in mortality, particularly up to the age
of seven. At the age of 17, there were signifi-
cant differences in mass, height, and head
and chest circumferences for those exposed
in utero within 1.5 km.
A particular problem has been the
development of microcephaly (a head cir-
cumference more than two standard devia-
tions below the age- and sex-specific mean
size). The normal incidence was about 307e;
among those exposed within 1.5 km, the in-
cidence was about 25% (30 cases, of which
12 were severe). Severe mental retardation
often accompanied this. Microcephaly was
severest in those exposed during the first
trimester.
I turn now to what might be termed the
very long-term effects, as studied in a
population of about 109 000 since 1950. The
population is distributed into various radia-
tion dose categories as shown in Table 2.
The control group matches the exposed
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South African Journal ofScii Vol. 79 October 1983
?
Hiroshima 82 085 20 176
Nagasaki 26 682 6 347
Total 108 767 26 523
Diseases of digestive organs
group as nearly as possible in the distribu-
tion of age and sex. About 2570 of this
population died between October 1950 and
September 1974. A comparison of the
causes of mortality between the unexposed
and the 200+ rad group is made in Fig. 8.
There was a very significant increase in the
incidence of leukemia and a significant in-
crease in non-leukemia cancers and disease
in the exposed sample. However, it is
noteworthy that the greater mortality due to
the increase in cancers was not unduly
severe. Figure 9 gives the excess deaths from
cancers per annum per million of popula-
tion, for those exposed to more than 100
rad. There were about 145 cases of leukemia
amongst survivors who received 100 + rad,
over the period 1946 to 1975. It may also be
noted that early entrants to the radioactive
cities showed no long-term effect due to the
induced radioactivity.
Other cancers which may well exceed the
background level include cancer of the
thyroid, lung, breast (in women) and
salivary glands. Again, however, the
numbers involved must be noted. For in-
stance, in a study of over 10 000 women dur-
ing the period 1958 to 1966, there were 22
definite cases of breast cancer observed
where 22 had been expected. However, in
the control group of nearly 2 500, only two
All causes
Trauma
All diseases
Tuberculosis
All cancers
Leukemia
All cancers except leukemia
Cancer if esophagus
Cancer of stomach
Cancer of lung
Cancer of female breast
Cancer of urinary organs
Benign and unspecified neoplasm,
lascular lesions of central nervous system
Circulatory system disease
Oateaes of blood and blood-forming organs
29 943 13 787 10 707 2 665 1 677 1 460 1 670
4 699 6 705 3 700 1 231 1 229 1 310 1 461
34 642 20 492 14 407 3 896 2 906 2 770 3 131
Other diseases
Diseases except neoplasms
4 5 10 20
Fig. 8. Causes of death of survivors of explosions who were exposed to 200 + rad, compared to
those exposed to normal environmental radiation, in the period 1950 to 1974. Bars represent
809e confidence interval.
but is closely related only to radiation dose'
(p. 319).
There remains the fear that such chromo-
somal aberrations may be transmissible to
children born of irradiated parents. The
possibility of this occurring has been the
subject of the most searching enquiry, but
`genetic surveys undertaken to date have
yielded no positive evidence for a genetic
hazard due to atomic bomb radiation' (p.
326). There may, however, be reasons for
supposing that any effect would show itself
less readily in the human population than it
would amongst laboratory populations of
mammals (where it is readily seen).
Leukemia
All cancer
--- All cancer except
leukemia
0 10 20 3)t 4i0 Est,
Age at time of bum,nng
Fig. 9. Absolute risk of cancer-caused death ac-
cording to age at time of exposure to IM i tad.
Discussion
At this point in the book, the tenor of the
text changes. The full description of the
quantitative findings, summarized above,
comes to an end, and consideration is given
to the sociological consequences of the bom-
bing.
Similarly, this review must now change
from a bald presentation of the facts to a
personal interpretation of their significance.
Of course, even the summary has been
somewhat subjective - some pieces of
evidence have been more strongly accented
than others. Equally, this happened in the
original - it would not be possible to con-
dense some 800 primary references without
a degree of subjective selection. However,
the reader should be warned that in what
follows, the interpretation is personal and
based upon the selection of evidence
presented in the previous sections.
I suggest that the common wisdom
assesses the hazard of nuclear weapons as
being that of 'radiation' - specifically,
high-energy electromagnetic radiation.
There is a widespread belief in reproductive
sterility being one consequence of their use,
and where that does not occur, in the pro-
duction of malformed offspring. There is
also a common belief in a consequential
massive increase in cancers and a host of
other ill-defined illnesses. Many people con-
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were observed whereas 5.4 had been ex-
pected; and in the group of nearly 1 000 who
had been exposed to 200+ rad, five were
observed whereas two had been expected in
the absence of any radiation effect. The
possibility that there is also an `observer' ef-
fect due to the intensity of study cannot be
ruled out. However, in another study of
over 1 000 women exposed to 100 + rad bet-
ween the ages of 10 and 19, there were 10
cases of breast cancer up to 1969, whereas
the expected number in another control
group of the same age distribution and over
the same period was only 1.4. It thus seems
likely that there is a correlation between the
degree of exposure and the incidence of
breast cancer.
While the evidence linking a particular
cancer and exposure to massive doses of
radiation may be equivocal, there is no
doubt that chromosomal changes occur.
Moreover, the number of aberrations is
directly related to radiation dose, although
at Hiroshima the relationship was linear and
at Nagasaki it was quadratic. Furthermore,
symmetric aberrations and dicentric/acen-
tric aberrations have persisted from the time
of exposure to the present. However, there is
no evidence for a link between chromosome
aberration and disease: `Chromosome aber-
ration exists as if it were unrelated to health
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?
South African Journal ooience Vol. 79 October 1983
cider that the whole face of the world will be
changed by invisible radiation, and much of
the attack upon the use of nuclear weapons
is based upon this. (The production of elec-
trical energy by controlled nuclear fission is
perceived by some as subject to a similar
hazard, and is vigorously opposed for this
reason.)
This is not the place to summarize the
evidence for these points of view. It suffices
to say that they exist and are a major element
in opposition to the use of nuclear weapons
on the one hand, and obstacle to the growth
of the nuclear energy industry on the other. I
submit that the attack upon the use of
nuclear weapons would be far more suc-
cessful. d far more soundly based if the
parallels between these weapons andthose
whic soce v ready finds intolerable were
raven. Specifically, there is a consensus that
chemical warfare is intolerable. Chemicals
are known which could cause devastation on
a scale similar to that which occurred at
Hiroshima and Nagasaki. Seven years after
a slight industrial accident at Seveso, in nor-
thern Italy, the surrounding countryside is
uninhabitable, and attempts to dump con-
taminated soil became a major political issue
in the European Economic Community
earlier this year. But what could cause
greater distress than the chemical changes
which occur when the human body is expos-
ed to thermal fluxes of over 0.1 MJ/m2? At
both Hiroshima and Nagasaki, these
chemical changes were responsible for the
deaths of about one hundred thousand peo-
ple within a few days. And these were
civilians in a well-nigh defeated country, not
combatants locked in a Somme salient.
Fortunately, mankind has perceived the
problem of heat damage to civilians. The
events of the Vietnam war, and the
disastrous effects of the indiscriminate use
of napalm there, are fairly clear. The defini-
tion of chemical weaponry is slowly being
extended to cover this awful weapon, too.
However, the thermal flux from nuclear
weapons has been overlooked, even though
it is far more terrible in its effect than a few
hundred megajoules of naplam.
Similarly, mankind has generally reacted
against the use of bullets which expand on
contact. Even the preparation of a 'dum-
dum' bullet can be treated as a criminal act.
Yet there appears to be no realization that
nuclear weapons can accelerate many
strange shapes to bullet-like velocities, with
results equivalent to those of the worst shape
of bullet.
Then there are the short-term effects of
massive doses of radiation, which, at much
over 1 000 rad, act upon the central nervous
system as terminally as the most potent of
the banned nerve gases, and which, at much
over a few hundred rad, lead to effects upon
the body as pernicious as the worst of the
forbidden biological weapons. It is a most
challenging question, why one weapon can
be rejected and yet another, with an
equivalent or greater effect, can continue to
be considered for possible use.
One thing is certain. It is that
e firs ew days after the atomic bombs
were used against them, 60 000 Japanese
died, primarily of thermal burns; a further
60 000 died over the next few weeks, largely
from burns and partially from massive
radiation doses. Thereafter, all the delayed
effects, all the old wounds aggravating old
age, all the cancers, all the tragedies of the
exposed unborn, may have accounted for
only a further 2 000 deaths. There are no
longer any signs of these events in the bodies
of those in the path of the fallout, nor any
evidence that those who entered the inferno
shortly after the explosion were significantly
injured. However, though we have moved
more than half a lifetime from the most ig-
noble of experiments, the harrowing
memory of its devastation has permanently
scarred our minds. Irrational or not, the ter-
ror of the invisible, of radiation, remains.
To light a star on earth is to incinerate, to im-
molate, and to irradiate. Of these, the last is
to be the least feared.
1. Hiroshima and Nagasaki; The phvstcal, enedical and
social cif fecc.c o f the atomic bombings. Conan it i cc for
compilation of materials on damage caused by the
atomic bombs in Hiroshima and Nagasaki. Hutchin-
son, London; 1981.
Towards the Production and Maintenance of Disease-free Laboratory Animals
Animal studies are
variability in the response o
perimental treatments. This
er relation
terferes greatly with the int p
predictability of results. It can arise from a
wide variety of factors such as genetic
background, nutrition, animal care, en-
vironmental effects and disease. An increas-
ing awareness of the importance of these
sources of variability in animal studies over
the last decade, has led to the establishment
of several modern laboratory animal
facilities in South Africa. One of their main
functions is to produce genetically defined,
specified pathogen free (SPF) animals and
maintain them under standardised condi-
tions. A major challenge in this endeavour is
the production by hysterectomy of SPF
rodents and rabbits under barrier condi-
tions.
Conventional laboratory animals main-
tained in non-barrier buildings harbour a
wide range of pathogens, including ecto and
endo-parasites, fungi, protozoa, bacteria
and viruses, which can either singly or in
concert interfere with experimental results
by causing clinical or sub-clinical disease in
animal colonies. Laboratory animals can be
freed of these pathogens by the removal of
full-term foetuses from an infected animal The course reviewed the historical
by hysterectomy and transfer to the pro- developments of isolator technology from
tected environment of flexible, clear plastic its beginnings in 1895, when von Nuttal and
film isolators for rearing either by hand Theirfelder were successful in challenging
feeding or foster mothers. Louis Pasteur's belief that animal life could
merest in isolator technology for the not be sustained without bacteria by pro-
estab ' ment of pathogen-free animals has ducing and maintaining a germ-free rat in an
grown ra ' ly in South Africa over the last unwieldy and complicated isolator system.
two years amd isolator units have been It examined the wide range of isolator ap-
established by the universities of Stellen- plications for protecting animals and pa
bosch, Pretoria, CaTown, and the Wit- tients from harmful infective gents. Prac-
watersrand, and the State Vaccine Institute tical exercises were carried out with positive
at Pinelands in the Cape. ~., and negative-pressure isolators, which in-
With the commissioning owe new volved the preparation of isolator com-
Medical School Animal Unit at the l7'r- ponents, setting up and leakage testing,
sity of the Witwatersrand and installation o s,,,; sterilization of equipment and supplies,
isolator equipment, a workshop on isolator hsfer procedures for supplying food and
technology with practical exercises was held watelI" and removing animal wastes, and
under the auspices of the South African microbioteyical screening. Techniques for
Association for Laboratory Animal Science obtaining getq-free animals by hysterec-
on 23 - 24 February this year. The work- tomy and caesairt section in surgical
shop was run by Mr J. von Stenglin of the isolators linked to ani'tnal isolators were also
Metal-Plastic company. It was attended by demonstrated and discuss .
delegates from university animal units, the The course, the first of it find in this
South African Institute for Medical country, has provided a sound dation
Research, South African Medical Research for the establishment and developm t of
Council, the National Institute for animals reared in isolators in South Afri
Virology, the Animal and Dairy Science which is the key to providing disease-free
Research Institute and the Technikon RSA. animals for teaching and research. J. Austin
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mplicated by
imals to ex-
'N5' ity fin-
d