Nuclear weapons trigger an explosive reaction that shears off destructive energy locked inside the bomb’s atomic materials.
The first atomic weapons, like those dropped by the United States on the Japanese cities of Hiroshima and Nagasaki in World War II, did that with fission: splitting unstable uranium or plutonium atoms so that their subatomic neutrons fly free, smash up more atoms and create a devastating blast.
Before we can get to the bombs, we have to start small, atomically small.
An atom, you’ll remember, is made up of three subatomic particles — protons, neutrons and electrons.
The center of an atom, called the nucleus, is composed of protons and neutrons.
Protons are positively charged, neutrons have no charge at all and electrons are negatively charged.
The proton-to-electron ratio is always one to one, so the atom as a whole has a neutral charge.
For example, a carbon atom has six protons and six electrons.
It’s not that simple though.
An atom’s properties can change considerably based on how many of each particle it has.
If you change the number of protons, you wind up with a different element altogether.
If you alter the number of neutrons in an atom, you wind up with an isotope.
For example, carbon has three isotopes:
1) carbon-12 (six protons + six neutrons), a stable and commonly occurring form of the element,
2) carbon-13 (six protons + seven neutrons), which is stable but rare and
3) carbon-14 (six protons + eight neutrons), which is rare and unstable (or radioactive) to boot.
As we see with carbon, most atomic nuclei are stable, but a few aren’t stable at all.
These nuclei spontaneously emit particles that scientists refer to as radiation.
A nucleus that emits radiation is, of course, radioactive, and the act of emitting particles is known as radioactive decay.
For now, we’ll go over the three types of radioactive decay:
- Alpha decay: A nucleus ejects two protons and two neutrons bound together, known as an alpha particle.
- Beta decay: A neutron becomes a proton, an electron and an antineutrino. The ejected electron is a beta particle.
- Spontaneous fission: A nucleus splits into two pieces. In the process, it can eject neutrons, which can become neutron rays. The nucleus can also emit a burst of electromagnetic energy known as a gamma ray. Gamma rays are the only type of nuclear radiation that comes from energy instead of fast-moving particles.
Remember that fission part especially.
It’s going to keep coming up as we discuss the inner workings of nuclear bombs.
Nuclear bombs involve the forces, strong and weak, that hold the nucleus of an atom together, especially atoms with unstable nuclei.
There are two basic ways that nuclear energy can be released from an atom.
In nuclear fission (pictured), scientists split the nucleus of an atom into two smaller fragments with a neutron.
Nuclear fusion — the process by which the sun produces energy — involves bringing together two smaller atoms to form a larger one.
In either process, fission or fusion, large amounts of heat energy and radiation are given off.
Nuclear Fission
We can attribute the discovery of nuclear fission to the work of Italian physicist Enrico Fermi.
In the 1930s, Fermi demonstrated that elements subjected to neutron bombardment could be transformed into new elements.
This work resulted in the discovery of slow neutrons, as well as new elements not represented on the periodic table.
Soon after Fermi’s discovery, German scientists Otto Hahn and Fritz Strassman bombarded uranium with neutrons, which produced a radioactive barium isotope.
They concluded that the low-speed neutrons caused the uranium nucleus to fission, or break apart, into two smaller pieces.
Their work sparked intense activity in research labs all over the world.
At Princeton University, Niels Bohr worked with John Wheeler to develop a hypothetical model of the fission process.
They speculated that it was the uranium isotope uranium-235, not uranium-238, undergoing fission.
At about the same time, other scientists discovered that the fission process resulted in even more neutrons being produced.
This led Bohr and Wheeler to ask a momentous question:
Could the free neutrons created in fission start a chain reaction that would release an enormous amount of energy?
If so, it might be possible to build a weapon of unimagined power.
And it was.
In a fission bomb, the fuel must be kept in separate subcritical masses, which will not support fission, to prevent premature detonation.
Critical mass is the minimum mass of fissionable material required to sustain a nuclear fission reaction.
Keeping the fuel in separate subcritical masses leads to design challenges that must be solved for a fission bomb to function properly.
The first challenge, of course, is bringing the subcritical masses together to form a supercritical mass, which will provide more than enough neutrons to sustain a fission reaction at the time of detonation.
Bomb designers came up with two solutions, which we’ll cover in the next section.
Next, free neutrons must be introduced into the supercritical mass to start the fission. Neutrons are introduced by making a neutron generator.
This generator is a small pellet of polonium and beryllium, separated by foil within the fissionable fuel core.
In this generator:
- The foil is broken when the subcritical masses come together and polonium spontaneously emits alpha particles.
- These alpha particles then collide with beryllium-9 to produce beryllium-8 and free neutrons.
- The neutrons then initiate fission.
Finally, the design must allow as much of the material as possible to be fissioned before the bomb explodes.
This is accomplished by confining the fission reaction within a dense material called a tamper, which is usually made of uranium-238.
The tamper gets heated and expanded by the fission core.
This expansion of the tamper exerts pressure back on the fission core and slows the core’s expansion.
The tamper also reflects neutrons back into the fission core, increasing the efficiency of the fission reaction.
Fission Bomb Triggers
The simplest way to bring the subcritical masses together is to make a gun that fires one mass into the other.
A sphere of U-235 is made around the neutron generator and a small bullet of U-235 is removed.
The bullet is placed at the one end of a long tube with explosives behind it, while the sphere is placed at the other end.
A barometric-pressure sensor determines the appropriate altitude for detonation and triggers the following sequence of events:
- The explosives fire and propel the bullet down the barrel.
- The bullet strikes the sphere and generator, initiating the fission reaction.
- The fission reaction begins.
- The bomb explodes.
The second way to create a supercritical mass requires compressing the subcritical masses together into a sphere by implosion.
Fat Man, the bomb dropped on Nagasaki, was one of these so-called implosion-triggered bombs.
It wasn’t easy to build.
Early bomb designers faced several problems, particularly how to control and direct the shock wave uniformly across the sphere.
Their solution was to create an implosion device consisting of a sphere of U-235 to act as the tamper and a plutonium-239 core surrounded by high explosives.
When the bomb was detonated, it had a 23-kiloton yield with an efficiency of 17 percent. This is what happened:
- The explosives fired, creating a shock wave.
- The shock wave compressed the core.
- The fission reaction began.
- The bomb exploded.
Designers were able to improve the basic implosion-triggered design.
In 1943, American physicist Edward Teller invented the concept of boosting.
Boosting refers to a process whereby fusion reactions are used to create neutrons, which are then used to induce fission reactions at a higher rate.
It took another eight years before the first test confirmed the validity of boosting, but once the proof came, it became a popular design.
In the years that followed, almost 90 percent of nuclear bombs built in America used the boost design.
Of course, fusion reactions can be used as the primary source of energy in a nuclear weapon, too. In the next section, we’ll look at the inner workings of fusion bombs.
Little Boy, the bomb dropped on Hiroshima, was this type of bomb and had a 14.5-kiloton yield (equal to 14,500 tons of TNT) with an efficiency of about 1.5 percent.
That is, 1.5 percent of the material was fissioned before the explosion carried the material away.
Fission bombs worked, but they weren’t very efficient.
It didn’t take scientists long to wonder if the opposite nuclear process — fusion — might work better.
Fusion occurs when the nuclei of two atoms combine to form a single heavier atom.
At extremely high temperatures, the nuclei of hydrogen isotopes deuterium and tritium can readily fuse, releasing enormous amounts of energy in the process. Weapons that take advantage of this process are known as fusion bombs, thermonuclear bombs or hydrogen bombs.
Fusion bombs have higher kiloton yields and greater efficiencies than fission bombs, but they present some problems that must be solved:
- Deuterium and tritium, the fuels for fusion, are both gases, which are hard to store.
- Tritium is in short supply and has a short half-life.
- Fuel in the bomb has to be continuously replenished.
- Deuterium or tritium has to be highly compressed at high temperature to initiate the fusion reaction.
Scientists overcome the first problem by using lithium-deuterate, a solid compound that doesn’t undergo radioactive decay at normal temperature, as the principal thermonuclear material.
To overcome the tritium problem, bomb designers rely on a fission reaction to produce tritium from lithium.
The fission reaction also solves the final problem.
The majority of radiation given off in a fission reaction is X-rays, and these X-rays provide the high temperatures and pressures necessary to initiate fusion.
So, a fusion bomb has a two-stage design — a primary fission or boosted-fission component and a secondary fusion component.
To understand this bomb design, imagine that within a bomb casing you have an implosion fission bomb and a cylinder casing of uranium-238 (tamper).
Within the tamper is the lithium deuteride (fuel) and a hollow rod of plutonium-239 in the center of the cylinder.
Separating the cylinder from the implosion bomb is a shield of uranium-238 and plastic foam that fills the remaining spaces in the bomb casing.
Detonation of the bomb causes the following sequence of events:
- The fission bomb implodes, giving off X-rays.
- These X-rays heat the interior of the bomb and the tamper; the shield prevents premature detonation of the fuel.
- The heat causes the tamper to expand and burn away, exerting pressure inward against the lithium deuterate.
- The lithium deuterate is squeezed by about 30-fold.
- The compression shock waves initiate fission in the plutonium rod.
- The fissioning rod gives off radiation, heat and neutrons.
- The neutrons go into the lithium deuterate, combine with the lithium and make tritium.
- The combination of high temperature and pressure are sufficient for tritium-deuterium and deuterium-deuterium fusion reactions to occur, producing more heat, radiation and neutrons.
- The neutrons from the fusion reactions induce fission in the uranium-238 pieces from the tamper and shield.
- Fission of the tamper and shield pieces produce even more radiation and heat.
- The bomb explodes.
All of these events happen in about 600 billionths of a second (550 billionths of a second for the fission bomb implosion, 50 billionths of a second for the fusion events).
The result is an immense explosion with a 10,000-kiloton yield — 700 times more powerful than the Little Boy explosion.
How is a hydrogen bomb different?
A hydrogen bomb, also called a thermonuclear bomb or an H-bomb, uses a second stage of reactions to magnify the force of an atomic explosion.
That stage is fusion: mashing hydrogen atoms together in the same process that fuels the sun.
When these relatively light atoms join together, they unleash neutrons in a wave of destructive energy.
A hydrogen weapon uses an initial nuclear fission explosion to create a tremendous pulse that compresses and fuses small amounts of deuterium and tritium, kinds of hydrogen, near the heart of the bomb.
Basics of the Teller–Ulam configuration.
The X-rays produced by a directed primary fission explosion at one end of a chamber heat and compress fuel material at the other end, triggering the secondary fusion reaction.
The swarms of neutrons set free can ramp up the explosive chain reaction of a uranium layer wrapped around it, creating a blast far more devastating than uranium fission alone.
The United States tested a hydrogen bomb at Bikini Atoll in 1954 that was over 1,000 times more powerful than the atomic bomb dropped on Hiroshima in 1945.
Britain, China, France and Russia have also created hydrogen bombs.
Consequences and Health Risks of Nuclear Bombs
The detonation of a nuclear weapon unleashes tremendous destruction, but the ruins would contain microscopic evidence of where the bombs’ materials came from.
The detonation of a nuclear bomb over a target such as a populated city causes immense damage.
The degree of damage depends upon the distance from the center of the bomb blast, which is called the hypocenter or ground zero.
The closer you are to the hypocenter, the more severe the damage.
The damage is caused by several things:
- A wave of intense heat from the explosion
- Pressure from the shock wave created by the blast
- Radiation
- Radioactive fallout (clouds of fine radioactive particles of dust and bomb debris that fall back to the ground)
At the hypocenter, everything is immediately vaporized by the high temperature (up to 500 million degrees Fahrenheit or 300 million degrees Celsius).
Outward from the hypocenter, most casualties are caused by burns from the heat, injuries from the flying debris of buildings collapsed by the shock wave and acute exposure to the high radiation.
Beyond the immediate blast area, casualties are caused from the heat, the radiation and the fires spawned from the heat wave.
In the long term, radioactive fallout occurs over a wider area because of prevailing winds.
The radioactive fallout particles enter the water supply and are inhaled and ingested by people at a distance from the blast.
Scientists have studied survivors of the Hiroshima and Nagasaki bombings to understand the short-term and long-term effects of nuclear explosions on human health.
Radiation and radioactive fallout affect those cells in the body that actively divide (hair, intestine, bone marrow, reproductive organs).
Some of the resulting health conditions include:
- Nausea, vomiting and diarrhea
- Cataracts
- Hair loss
- Loss of blood cells
These conditions often increase the risk of leukemia, cancer, infertility and birth defects.
Scientists and physicians are still studying the survivors of the bombs dropped on Japan and expect more results to appear over time.
In the 1980s, scientists assessed the possible effects of nuclear warfare (many nuclear bombs exploding in different parts of the world) and proposed the theory that a nuclear winter could occur.
In the nuclear-winter scenario, the explosion of many bombs would raise great clouds of dust and radioactive material that would travel high into Earth’s atmosphere.
These clouds would block out sunlight.
The reduced level of sunlight would lower the surface temperature of the planet and reduce photosynthesis by plants and bacteria.
The reduction in photosynthesis would disrupt the food chain, causing mass extinction of life (including humans).
This scenario is similar to the asteroid hypothesis that has been proposed to explain the extinction of the dinosaurs.
Proponents of the nuclear-winter scenario pointed to the clouds of dust and debris that traveled far across the planet after the volcanic eruptions of Mount St. Helens in the United States and Mount Pinatubo in the Philippines.
Nuclear weapons have incredible, long-term destructive power that travels far beyond the original target.
This is why the world’s governments are trying to control the spread of nuclear-bomb-making technology and materials and reduce the arsenal of nuclear weapons deployed during the Cold War.
It’s also why nuclear tests conducted by North Korea and other countries draw such a strong response from the international community.
The Hiroshima and Nagasaki bombings may be many decades past, but the horrible images of that fateful August morning burn as clear and bright as ever.
Genetic Consequences of Nuclear War
Radiation Dose To Survivors
University of Oslo, Oslo, Norway.
Radiation is the only mutagen considered in this discussion, and doses of genetic consequence are only those of nonsterilizing magnitude and absorbed by survivors with present or future reproductive capacity.
Figure 1 shows schematically the elements of the situation to be considered in the target areas.
Figure 1
Genetically effective exposure to radiation would occur mainly outside the radiation lethal area, with dose distribution as determined by the dose-distance curve.
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.
Transmissible genetic damage is then induced in survivors beyond the blast and heat lethal zones as well as the radiation lethal zone.
Table 1Areas of Lethal Damage from Various Effects (km2)
| Explosive Yield | |||||
|---|---|---|---|---|---|
| Type of Damage | 1 kt | 10 kt | 100 kt | 1 Mt | 10 Mt |
| Blast | 1.5 | 4.9 | 22 | 104 | 480 |
| Heat | 1.1 | 10.5 | 60 | 350 | 1,300 |
| Initial radiation | 2.9 | 5.7 | 11 | 22 | 54 |
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Source: Based on Rotblat.
Table 1
Areas of Lethal Damage from Various Effects (km).
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).
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 survivor 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.
To the extent that fallout is massive and fresh and few countermeasures have been instituted beforehand, one may take the mean genetically significant 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 survive.
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.
After about 8 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 rem may accumulate.
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 1,000 rem absorbed at a low dose rate and thus probably only one-third as effective a mutagen as the corresponding acute dose.
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 significant 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 rad per megaton of fission yield.
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 radioactive isotopes, increasing the mean survivor population dose in the less contaminated areas.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 exposure—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 variation in terms of individual dose and effect, depending on local fallout conditions and variation in radiation sensitivity.
Genetic Radiation Effects
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.
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 number of genes in humans.
Subsequently, the calculation is extended to encompass all known conditions in humans with similar genetic mechanisms.
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 18-30) to low-dose, low-dose-rate radiation, with the remaining risk being various forms of cancer exposure (age 18-65).
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.
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.
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,16 which uses a direct method.)
Table 2
Genetic Effects of One Million Manrem of Radiation to a Population of Constant Size: Types and Numbers of Anomalies
| Exposure | ||||
|---|---|---|---|---|
| Acute | Chronic | |||
| Damage Category | First Generation | Equilibrium | First Generation | Equilibrium |
Unbalanced translocation  malformed liveborn |
46 | 60 | 23 | 30 |
| Trisomics, XO | 90 | 90 | 30 | 30 |
| Simple dominants | 60 | 300 | 20 | 100 |
| Complex dominants, multifactorial disease mutationally maintained | 45 | 450 | 16 | 160 |
| Multifactorial disease nonmutationally maintained | 0 | 0 | 0 | 0 |
| Recessive mutations | (2,400) | (900) | ||
| Total (excluding recessive) | 240 | 900 | 89 | 320 |
| Total UNSCEAR’775 | 63 | 185 | ||
| Total UNSCEAR’829 | 22 | 144 | ||
| Ehling 198416 | ||||
| Simple dominants | 25 | |||
| Recessives | (250) | |||
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NOTE: The upper part of this table is based on the material and arguments presented in Oftedal and Searle.2
Genetic Effects of One Million Manrem of Radiation to a Population of Constant Size: Types and Numbers of Anomalies.
During the next few years, it is expected that improved data on spontaneous mutation rates will be available, in particular from Hungary (A. Czeizl, 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 Mulvihill 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.17
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 genetically significant doses of just over 100 rad 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.
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 × 10 reproducing survivors in this category.
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 tentative, there being uncertainties at all levels of calculation, from the bombing 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.
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.
However, due to regional differences in climatic conditions, quite significant variations in amounts of fallout would occur, with a corresponding variation in exposure.
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.
In an outbreeding large population, recessive mutations are ordinarily expressed only in the distant future and with low predictability.
They are therefore generally disregarded in estimating 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 spontaneous abortion and so may be regarded as a category of limited consequence.
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.
In any normally 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 protracted 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 project to investigate this is being planned.
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 be instituted to reduce the load and to conserve the material resources available.
These practices could range from selective shielding of reproducing 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.
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 destructiveness of the nuclear holocaust is illustrated even in this detail.
