The Genetic Effects of Radiation

By ISAAC ASIMOV and THEODOSIUS DOBZHANSKY

Contents

THE MACHINERY OF INHERITANCE 1

Introduction 1

Cells and Chromosomes 2

Enzymes and Genes 5

Parents and Offspring 8

MUTATIONS 10

Sudden Change 10

Spontaneous Mutations 13

Genetic Load 16

Mutation Rates 19

RADIATION 22

Ionizing Radiation 22

Background Radiation 27

Man-made Radiation 30

DOSE AND CONSEQUENCE 32

Radiation Sickness 32

Radiation and Mutation 33

Dosage Rates 37

Effects on Mammals 40

Conclusion 43

SUGGESTED REFERENCES 47

THE COVER

THE AUTHORS

The Genetic Effects of Radiation

THE MACHINERY OF INHERITANCE

Introduction

There is nothing new under the sun, says the Bible. Nor is the sun itself new, we might add. As long as life has existed on earth, it has been exposed to radiation from the sun, so that life and radiation are old acquaintances and have learned to live together.

We are accustomed to looking upon sunlight as something good, useful, and desirable, and certainly we could not live long without it. The energy of sunlight warms the earth, produces the winds that tend to equalize earth’s temperatures, evaporates the oceans and produces rain and fresh water. Most important of all, it supplies what is needed for green plants to convert carbon dioxide and water into food and oxygen, making it possible for all animal life (including ourselves) to live.

Yet sunlight has its dangers, too. Lizards avoid the direct rays of the noonday sun on the desert, and we ourselves take precautions against sunburn and sunstroke.

The same division into good and bad is to be found in connection with other forms of radiation—forms of which mankind has only recently become aware. Such radiations, produced by radioactivity in the soil and reaching us from outer space, have also been with us from the beginning of time. They are more energetic than sunlight, however, and can do more damage, and because our senses do not detect them, we have not learned to take precautions against them.

To be sure, energetic radiation is present in nature in only very small amounts and is not, therefore, much of a danger. Man, however, has the capacity of imitating nature. Long ago in dim prehistory, for instance, he learned to manufacture a kind of sunlight by setting wood and other fuels on fire. This involved a new kind of good and bad. A whole new technology became possible, on the one hand, and, on the other, the chance of death by burning was also possible. The good in this case far outweighs the evil.

In our own twentieth century, mankind learned to produce energetic radiation in concentrations far surpassing those we usually encounter in nature. Again, a new technology is resulting and again there is the possibility of death.

The balance in this second instance is less certainly in favor of the good over the evil. To shift the balance clearly in favor of the good, it is necessary for mankind to learn as much as possible about the new dangers in order that we might minimize them and most effectively guard against them.

To see the nature of the danger, let us begin by considering living tissue itself—the living tissue that must withstand the radiation and that can be damaged by it.

Cells and Chromosomes

The average human adult consists of about 50 trillion cells—50 trillion microscopic, more or less self-contained, blobs of life. He begins life, however, as a single cell, the fertilized ovum.

After the fertilized ovum is formed, it divides and becomes two cells. Each daughter cell divides to produce a total of four cells, and each of those divides and so on.

There is a high degree of order and direction to those divisions. When a human fertilized ovum completes its divisions an adult human being is the inevitable result. The fertilized ovum of a giraffe will produce a giraffe, that of a fruit fly will produce a fruit fly, and so on. There are no mistakes, so it is quite clear that the fertilized ovum must carry “instructions” that guide its development in the appropriate direction.

These “instructions” are contained in the cell’s chromosomes, tiny structures that appear most clearly (like stubby bits of tangled spaghetti) when the cell is in the actual process of division. Each species has some characteristic number of chromosomes in its cells, and these chromosomes can be considered in pairs. Human cells, for instance, contain 23 pairs of chromosomes—46 in all.

When a cell is undergoing division (mitosis), the number of chromosomes is temporarily doubled, as each chromosome brings about the formation of a replica of itself. (This process is called replication.) As the cell divides, the chromosomes are evenly shared by the new cells in such a way that if a particular chromosome goes into one daughter cell, its replica goes into the other. In the end, each cell has a complete set of pairs of chromosomes; and the set in each cell is identical with the set in the original cell before division.

Interphase

Prophase

Metaphase

Anaphase

Telophase

Interphase

In this way, the fundamental “instructions” that determine the characteristics of a cell are passed on to each new cell. Ideally, all the trillions of cells in a particular human being have identical sets of “instructions”.[1]

Enzymes and Genes

Each cell is a tiny chemical factory in which several thousand different kinds of chemical changes are constantly taking place among the numerous sorts of molecules that move about in its fluid or that are pinned to its solid structures. These chemical changes are guided and controlled by the existence of as many thousands of different enzymes within the cell.

Enzymes possess large molecules built up of some 20 different, but chemically related, units called amino acids. A particular enzyme molecule may contain a single amino acid of one type, five of another, several dozen of still another and so on. All the units are strung together in some specific pattern in one long chain, or in a small number of closely connected chains.

Every different pattern of amino acids forms a molecule with its own set of properties, and there are an enormous number of patterns possible. In an enzyme molecule made up of 500 amino acids, the number of possible patterns can be expressed by a 1 followed by 1100 zeroes (10¹¹⁰⁰).

Every cell has the capacity of choosing among this unimaginable number of possible patterns and selecting those characteristic of itself. It therefore ends with a complement of specific enzymes that guide its own chemical changes and, consequently, its properties and its behavior. The “instructions” that enable a fertilized ovum to develop in the proper manner are essentially “instructions” for choosing a particular set of enzyme patterns out of all those possible.

The differences in the enzyme-guided behavior of the cells making up different species show themselves in differences in body structure. We cannot completely follow the long and intricate chain of cause-and-effect that leads from one set of enzymes to the long neck of a giraffe and from another set of enzymes to the large brain of a man, but we are sure that the chain is there. Even within a species, different individuals will have slight distinctions among their sets of enzymes and this accounts for the fact that no two human beings are exactly alike (leaving identical twins out of consideration).

Each chromosome can be considered as being composed of small sections called genes, usually pictured as being strung along the length of the chromosome. Each gene is considered to be responsible for the formation of a chain of amino acids in a fixed pattern. The formation is guided by the details of the gene’s own structure (which are the “instructions” earlier referred to). This gene structure, which can be translated into an enzyme’s structure, is now called the genetic code.

If a particular enzyme (or group of enzymes) is, for any reason, formed imperfectly or not at all, this may show up as some visible abnormality of the body—an inability to see color, for instance, or the possession of two joints in each finger rather than three. It is much easier to observe physical differences than some delicate change in the enzyme pattern of the cells. Genes are therefore usually referred to by the body change they bring about, and one can, for instance, speak of a “gene for color blindness”.

A gene may exist in two or more varieties, each producing a slightly different enzyme, a situation that is reflected, in turn, in slight changes in body characteristics. Thus, there are genes governing eye color, one of which is sufficiently important to be considered a “gene for blue eyes” and another a “gene for brown eyes”. One or the other, but not both, will be found in a specific place on a specific chromosome.

The two chromosomes of a particular pair govern identical sets of characteristics. Both, for instance, will have a place for genes governing eye color. If we consider only the most important of the varieties involved, those on each chromosome of the pair may be identical; both may be for blue eyes or both may be for brown eyes. In that case, the individual is homozygous for that characteristic and may be referred to as a homozygote. The chromosomes of the pair may carry different varieties: A gene for blue eyes on one chromosome and one for brown eyes on the other. The individual is then heterozygous for that characteristic and may be referred to as a heterozygote. Naturally, particular individuals may be homozygous for some types of characteristics and heterozygous for others.

When an individual is heterozygous for a particular characteristic, it frequently happens that he shows the effect associated with only one of the gene varieties. If he possesses both a gene for brown eyes and one for blue eyes, his eyes are just as brown as though he had carried two genes for brown eyes. The gene for brown eyes is dominant in this case while the gene for blue eyes is recessive.

Parents and Offspring

How does the fertilized ovum obtain its particular set of chromosomes in the first place?

Each adult possesses gonads in which sex cells are formed. In the male, sperm cells are formed in the testes; in the female, egg cells are formed in the ovaries.

In the formation of the sperm cells and egg cells there is a key step—meiosis—a cell division in which the chromosomes group into pairs and are then apportioned between the daughter cells, one of each pair to each cell. Such a division, unaccompanied by replication, means that in place of the usual 23 pairs of chromosomes in each other cell, each sex cell has 23 individual chromosomes, a “half-set”, so to speak.

In the process of fertilization, a sperm cell from the father enters and merges with an egg cell from the mother. The fertilized ovum that results now has a full set of 23 pairs of chromosomes, but of each pair, one comes from the father and one from the mother.

In this way, each newborn child is a true individual, with its characteristics based on a random reshuffling of chromosomes. In forming the sex cells, the chromosome pairs can separate in either fashion (a into cell 1 and b into cell 2, or vice versa). If each of 23 pairs does this randomly, nearly 10 million different combinations of chromosomes are possible in the sex cells of a single individual.

Furthermore, one can’t predict which chromosome combination in the sperm cell will end up in combination with which in the egg cell, so that by this reasoning, a single married couple could produce children with any of 100 trillion (100,000,000,000,000) possible chromosome combinations.

It is this that begins to explain the endless variety among living beings, even within a particular species.

It only begins to explain it, because there are other sources of difference, too. A chromosome is capable of exchanging pieces with its pair, producing chromosomes with a brand new pattern of gene varieties. Before such a crossover, one chromosome may have carried a gene for blue eyes and one for wavy hair, while the other chromosome may have carried a gene for brown eyes and one for straight hair. After the crossover, one would carry genes for blue eyes and straight hair, the other for brown eyes and wavy hair.

Interphase

Prophase

Metaphase

Anaphase

Interphase

Metaphase

Interphase

MUTATIONS

Sudden Change

Shifts in chromosome combinations, with or without crossovers, can produce unique organisms with characteristics not quite like any organism that appeared in the past nor likely to appear in the reasonable future. They may even produce novelties in individual characteristics since genes can affect one another, and a gene surrounded by unusual neighbors can produce unexpected effects.

Matters can go further still, however, in the direction of novelty. It is possible for chromosomes to undergo more serious changes, either structural or chemical, so that entirely new characteristics are produced that might not otherwise exist. Such changes are called mutations.

We must be careful how we use this term. A child may possess some characteristics not present in either parent through the mere shuffling of chromosomes and not through mutation.

Suppose, for instance, that a man is heterozygous to eye color, carrying one gene for brown eyes and one for blue eyes. His eyes would, of course, be brown since the gene for brown eyes is dominant over that for blue. Half the sperm cells he produces would carry a single gene for brown eyes in its half set of chromosomes. The other half would carry a single gene for blue eyes. If his wife were similarly heterozygous (and therefore also had brown eyes), half her egg cells would carry the gene for brown eyes and half the gene for blue.

It might follow in this marriage, then, that a sperm carrying the gene for blue eyes might fertilize an egg carrying the gene for blue eyes. The child would then be homozygous, with two genes for blue eyes, and he would definitely be blue-eyed. In this way, two brown-eyed parents might have a blue-eyed child and this would not be a mutation. If the parents’ ancestry were traced further back, blue-eyed individuals would undoubtedly be found on both sides of the family tree.

If, however, there were no record of, say, anything but normal color vision in a child’s ancestry, and he were born color-blind, that could be assumed to be the result of a mutation. Such a mutation could then be passed on by the normal modes of inheritance and a certain proportion of the child’s eventual descendants would be color-blind.

A mutation may be associated with changes in chromosome structure sufficiently drastic to be visible under the microscope. Such chromosome mutations can arise in several ways. Chromosomes may undergo replication without the cell itself dividing. In that way, cells can develop with two, three, or four times the normal complement of chromosomes, and organisms made up of cells displaying such polyploidy can be markedly different from the norm. This situation is found chiefly among plants and among some groups of invertebrates. It does not usually occur in mammals, and when it does it leads to quick death.

Less extreme changes take place, too, as when a particular chromosome breaks and fails to reunite, or when several break and then reunite incorrectly. Under such conditions, the mechanism by which chromosomes are distributed among the daughter cells is not likely to work correctly. Sex cells may then be produced with a piece of chromosome (or a whole one) missing, or with an extra piece (or whole chromosome) present.

In 1959, such a situation was found to exist in the case of persons suffering from a long-known disease called Down’s syndrome.[2] Each person so afflicted has 47 chromosomes in place of the normal 46. It turned out that the 21st pair of chromosomes (using a convention whereby the chromosome pairs are numbered in order of decreasing size) consists of three individuals rather than two. The existence of this chromosome abnormality clearly demonstrated what had previously been strongly suspected—that Down’s syndrome originates as a mutation and is inborn (see the figure on the next page).

Most mutations, however, are not associated with any noticeable change in chromosome structure. There are, instead, more subtle changes in the chemical structure of the genes that make up the chromosome. Then we have gene mutations.

The process by which a gene produces its own replica is complicated and, while it rarely goes wrong, it does misfire on occasion. Then, too, even when a gene molecule is replicated perfectly, it may undergo change afterward through the action upon it of some chemical or other environmental influence. In either case, a new variety of a particular gene is produced and, if present in a sex cell, it may be passed on to descendants through an indefinite number of generations.

Of course, chromosome or gene mutations may take place in ordinary cells rather than in sex cells. Such changes in ordinary cells are somatic mutations. When mutated body cells divide, new cells with changed characteristics are produced. These changes may be trivial, or they may be serious. It is often suggested, for instance, that cancer may result from a somatic mutation in which certain cells lose the capacity to regulate their growth properly. Since somatic mutations do not involve the sex cells, they are confined to the individual and are not passed on to the offspring.

Spontaneous Mutations

Mutations that take place in the ordinary course of nature, without man’s interference, are spontaneous mutations. Most of these arise out of the very nature of the complicated mechanism of gene replication. Copies of genes are formed out of a large number of small units that must be lined up in just the right pattern to form one particular gene and no other.

Ideally, matters are so arranged within the cell that the necessary changes giving rise to the desired pattern are just those that have a maximum probability. Other changes are less likely to happen but are not absolutely excluded. Sometimes through the accidental jostling of molecules a wrong turn may be taken, and the result is a spontaneous mutation.

We might consider a mutation to be either “good” or “bad” in the sense that any change that helps a creature live more easily and comfortably is good and that the reverse is bad.

It seems reasonable that random changes in the gene pattern are almost sure to be bad. Consider that any creature, including man, is the product of millions of years of evolution. In every generation those individuals with a gene pattern that fit them better for their environment won out over those with less effective patterns—won out in the race for food, for mates, and for safety. The “more fit” had more offspring and crowded out the “less fit”.

By now, then, the set of genes with which we are normally equipped is the end product of long ages of such natural selection. A random change cannot be expected to improve it any more than random changes would improve any very complex, intricate, and delicate structure.

Pleistocene and Recent

Pliocene

Miocene

Oligocene

Eocene

Yet over the eons, creatures have indeed changed, largely through the effects of mutation. If mutations are almost always for the worse, how can one explain that evolution seems to progress toward the better and that out of a primitive form as simple as an amoeba, for instance, there eventually emerged man?

In the first place, environment is not fixed. Climate changes, conditions change, the food supply may change, the nature of living enemies may change. A gene pattern that is very useful under one set of conditions may be less useful under another.

Suppose, for instance, that man had lived in tropical areas for thousands of years and had developed a heavily pigmented skin as a protection against sunburn. Any child who, through a mutation, found himself incapable of forming much pigment, would be at a severe disadvantage in the outdoor activities engaged in by his tribe. He would not do well and such a mutated gene would never establish itself for long.

If a number of these men migrated to northern Europe, however, children with dark skin would absorb insufficient sunlight during the long winter when the sun was low in the sky, and visible for brief periods only. Dark-skinned children would, under such conditions, tend to suffer from rickets.

Mutant children with pale skin would absorb more of what weak sunlight there was and would suffer less. There would be little danger of sunburn so there would be no penalty counteracting this new advantage of pale skins. It would be the dark-skinned people who would tend to die out. In the end, you would have dark skins in Africa and pale skins in Scandinavia, and both would be “fit”.

In the same way, any child born into a primitive hunting society who found himself with a mutated gene that brought about nearsightedness would be at a distinct disadvantage. In a modern technological society, however, nearsighted individuals, doing more poorly at outdoor games, are often driven into quieter activities that involve reading, thinking, and studying. This may lead to a career as a scientist, scholar, or professional man, categories that are valuable in such a society and are encouraged. Nearsightedness would therefore spread more generally through civilized societies than through primitive ones.

Then, too, a gene may be advantageous when it occurs in low numbers and disadvantageous when it occurs in high numbers. Suppose there were a gene among humans that so affected the personality as to make it difficult for a human being to endure crowded conditions. Such individuals would make good explorers, farmers, and herdsmen, but poor city dwellers. Even in our modern urbanized society, such a gene in moderate concentration would be good, since we still need our outdoorsmen. In high concentration, it would be bad, for then the existence of areas of high population density (on which our society now seems to depend) might become impossible.

In any species, then, each gene exists in a number of varieties upon which an absolute “good” or “bad” cannot be unequivocally stamped. These varieties make up the gene pool, and it is this gene pool that makes evolution possible.

A species with an invariable set of genes could not change to suit altered conditions. Even a slight shift in the nature of the environment might suffice to wipe it out.

The possession of a gene pool lends flexibility, however. As conditions change, one combination of varieties might gain over another and this, in turn, might produce changes in body characteristics that would then further alter the relative “goodness” or “badness” of certain gene patterns.

Thus, over the past million years, for example, the human brain has, through mutations and appropriate shifts in emphasis within the gene pool, increased notably in size.

Genetic Load

Some gene mutations produce characteristics so undesirable that it is difficult to imagine any reasonable change in environmental conditions that would make them beneficial. There are mutations that lead to the nondevelopment of hands and feet, to the production of blood that will not clot, to serious malformations of essential organs, and so on. Such mutations are unqualifiedly bad.

The badness may be so severe that a fertilized ovum may be incapable of development; or, if it develops, the fetus miscarries or the child is stillborn; or, if the child is born alive, it dies before it matures so that it can never have children of its own. Any mutation that brings about death before the gene producing it can be passed on to another generation is a lethal mutation.

A gene governing a lethal characteristic may be dominant. It will then kill even though the corresponding gene on the other chromosome of the pair is normal. Under such conditions, the lethal gene is removed in the same generation in which it is formed.

The lethal gene may, on the other hand, be recessive. Its effect is then not evident if the gene it is paired with is normal. The normal gene carries on for both.

When this is the case, the lethal gene will remain in existence and will, every once in a while, make itself evident. If two people, each serving as a carrier for such a gene, have children, a sperm cell carrying a lethal may fertilize an egg cell carrying the same type of lethal, with sad results.

Every species, including man, includes individuals who carry undesirable genes. These undesirable genes may be passed along for generations, even if dominant, before natural selection culls them out. The more seriously undesirable they are, the more quickly they are removed, but even outright lethal genes will be included among the chromosomes from generation to generation provided they are recessive. These deleterious genes make up the genetic load.

The only way to avoid a genetic load is to have no mutations and therefore no gene pool. The gene pool is necessary for the flexibility that will allow a species to survive and evolve over the eons and the genetic load is the price that must be paid for that. Generally, the capacity for a species to reproduce itself is sufficiently high to make up, quite easily, the numbers lost through the combination of deleterious genes.

The size of a genetic load depends on two factors: The rate at which a deleterious gene is produced through mutation, and the rate at which it is removed by natural selection. When the rate of removal equals the rate of production, a condition of genetic equilibrium is reached and the level of occurrence of that gene then remains stable over the generations.

Even though deleterious genes are removed relatively rapidly, if dominant, and lethal genes are removed in the same generation in which they are formed, a new crop of deleterious genes will appear by mutation with every succeeding generation. The equilibrium level for such dominant deleterious genes is relatively low, however.

Deleterious genes that are recessive are removed much more slowly. Those persons with two such genes, who alone show the bad effects, are like the visible portion of an iceberg and represent only a small part of the whole. The heterozygotes, or carriers, who possess a single gene of this sort, and who live out normal lives, keep that gene in being. If people in a particular population marry randomly and if one out of a million is born homozygous for a certain deleterious recessive gene (and dies of it), one out of five hundred is heterozygous for that same gene, shows no ill effects, and is capable of passing it on.

It may be that the heterozygote is not quite normal but does show some ill effects—not enough to incommode him seriously, perhaps, but enough to lower his chances slightly for mating and bearing children. In that case, the equilibrium level for that gene will be lower than it would otherwise be.

It may also be that the heterozygote experiences an actual advantage over the normal individual under some conditions. There is a recessive gene, for instance, that produces a serious disease called sickle-cell anemia. People possessing two such genes usually die young. A heterozygote possessing only one of these genes is not seriously affected and has red blood cells that are, apparently, less appetizing to malaria parasites. The heterozygote therefore experiences a positive advantage if he lives in a region where the incidence of certain kinds of malaria is high. The equilibrium level of the sickle-cell anemia gene can, in other words, be higher in malarial regions than elsewhere.

Here is one subject area in which additional research is urgently needed. It may be that the usefulness of a single deleterious gene is greater than we may suspect in many cases, and that there are greater advantages to heterozygousness than we know. This may be the basis of what is sometimes called “hybrid vigor”. In a world in which human beings are more mobile than they have ever been in history and in which intercultural marriages are increasingly common, information on this point is particularly important.

Mutation Rates

It is easier to observe the removal of genes through death or through failure to reproduce than to observe their production through mutation. It is particularly difficult to study their production in human beings, since men have comparatively long lifetimes and few children, and since their mating habits cannot well be controlled.

For this reason, geneticists have experimented with species much simpler than man—smaller organisms that are short-lived, produce many offspring, and that can be penned up and allowed to mate only under fixed conditions. Such creatures may have fewer chromosomes than man does and the sites of mutation are more easily pinned down.

An important assumption made in such experiments is that the machinery of inheritance and mutation is essentially the same in all creatures and that therefore knowledge gained from very simple species (even from bacteria) is applicable to man. There is overwhelming evidence to indicate that this is true in general, although there are specific instances where it is not completely true and scientists must tread softly while drawing conclusions.

The animals most commonly used in studies of genetics and mutations are certain species of fruit flies, called Drosophila. The American geneticist, Hermann J. Muller, devised techniques whereby he could study the occurrence of lethal mutations anywhere along one of the four pairs of chromosomes possessed by Drosophilia.

A lethal gene, he found, might well be produced somewhere along the length of a particular chromosome once out of every two hundred times that chromosome underwent replication. This means that out of every 200 sex cells produced by Drosophilia, one would contain a lethal gene somewhere along the length of that chromosome.

That particular chromosome, however, contained at least 500 genes capable of undergoing a lethal mutation. If each of those genes is equally likely to undergo such a mutation, then the chance that any one particular gene is lethal is one out of 200 × 500, or 1 out of 100,000.

This is a typical mutation rate for a gene in higher organisms generally, as far as geneticists can tell (though the rates are lower among bacteria and viruses). Naturally, a chance for mutation takes place every time a new individual is born. Fruit flies have many more offspring per year than human beings, since their generations are shorter and they produce more young at a time. For that reason, though the mutation rate may be the same in fruit flies as in man, many more actual mutations are produced per unit time in fruit flies than in men.

This does not mean that the situation may be ignored in the case of man. Suppose the rate for production of a particular deleterious gene in man is 1 out of 100,000. It is estimated that a human being has at least 10,000 different genes, and therefore the chance that at least one of the genes in a sex cell is deleterious is 10,000 out of 100,000 or 1 out of 10.

Furthermore, it is estimated that the number of gene mutations that are weakly deleterious are four times as numerous as those that are strongly deleterious or lethal. The chances that at least one gene in a sex cell is at least weakly deleterious then would be 4 + 1 out of 10, or 1 out of 2.

Naturally, these deleterious genes are not necessarily spread out evenly among human beings with one to a sex cell. Some sex cells will be carrying more than one, thus increasing the number that may be expected to carry none at all. Even so, it is supposed that very nearly half the sex cells produced by humanity carry at least one deleterious gene.

Even though only half the sex cells are free of deleterious genes, it is still possible to produce a satisfactory new generation of men. Yet one can see that the genetic load is quite heavy and that anything that would tend to increase it would certainly be undesirable, and perhaps even dangerous.

We tend to increase the genetic load by reducing the rate at which deleterious genes are removed, that is, by taking care of the sick and retarded, and by trying to prevent discomfort and death at all levels.

There is, however, no humane alternative to this. What’s more, it is, by and large, only those with slightly deleterious genes who are preserved genetically. It is those persons with nearsightedness, with diabetes, and so on, who, with the aid of glasses, insulin, or other props, can go on to live normal lives and have children in the usual numbers. Those with strongly deleterious genes either die despite all that can be done for them even today or, at the least, do not have a chance to have many children.

The danger of an increase in the genetic load rests more heavily, then, at the other end—at measures that (usually inadvertently or unintentionally) increase the rate of production of mutant genes. It is to this matter we will now turn.

RADIATION

Ionizing Radiation

Our modern technological civilization exposes mankind to two general types of genetic dangers unknown earlier: Synthetic chemicals (or unprecedentedly high concentrations of natural ones) absent in earlier eras, and intensities of energetic radiation equally unknown or unprecedented.

Chemicals can interfere with the process of replication by offering alternate pathways with which the cellular machinery is not prepared to cope. In general, however, it is only those cells in direct contact with the chemicals that are so affected, such as the skin, the intestinal linings, the lungs, and the liver (which is active in altering and getting rid of foreign chemicals). These may undergo somatic mutations, and an increased incidence of cancer in those tissues is among the drastic results of exposure to certain chemicals.

Such chemicals are not, however, likely to come in contact with the gonads where the sex cells are produced. While individual persons may be threatened by the manner in which the environment is being permeated with novel chemicals, the next generation is not affected in advance.

Radiation is another matter. In its broadest sense, radiation is any phenomenon spreading out from some source in all directions. Physically, such radiation may consist of waves or of particles.[3] Of the wave forms the two best-known are sound and electromagnetic radiations.

Sound carries very low concentrations of energy. This energy is absorbed by living tissue and converted into heat. Heat in itself can increase the mutation rate but the effect is a small one. The body has effective machinery for keeping its temperature constant and the gonads are not likely to suffer unduly from exposure to heat.