subject, the visual pigments of the eye, to ‘a very narrow window through which at a distance
one can see only a crack of light. As one comes closer the view grows wider and wider, until
finally through this same narrow window one is looking at the universe.’ So it is that only when
we bring our focus to bear, first on the individual cells of the body, then on the minute
structures within the cells, and finally on the ultimate reactions of molecules within these
structures—only when we do this can we comprehend the most serious and far-reaching
effects of the haphazard introduction of foreign chemicals into our internal environment.
Medical research has only rather recently turned to the functioning of the individual cell in
producing the energy that is the indispensable quality of life. The extraordinary energy-
producing mechanism of the body is basic not only to health but to life; it transcends in
importance even the most vital organs, for without the smooth and effective functioning of
energy-yielding oxidation none of the body’s functions can be performed. Yet the nature of
many of the chemicals used against insects, rodents, and weeds is such that they may strike
directly at this system, disrupting its beautifully functioning mechanism.
The research that led to our present understanding of cellular oxidation is one of the most
impressive accomplishments in all biology and biochemistry. The roster of contributors to this
work includes many Nobel Prize winners. Step by step it has been going on for a quarter of a
century, drawing on even earlier work for some of its foundation stones. Even yet it is not
complete in all details. And only within the past decade have all the varied pieces of research
come to form a whole so that biological oxidation could become part of the common
knowledge of biologists. Even more important is the fact that medical men who received their
basic training before 1950 have had little opportunity to realize the critical importance of the
process and the hazards of disrupting it.
The ultimate work of energy production is accomplished not in any specialized organ but in
every cell of the body. A living cell, like a flame, burns fuel to produce the energy on which life
depends. The analogy is more poetic than precise, for the cell accomplishes its ‘burning’ with
only the moderate heat of the body’s normal temperature. Yet all these billions of gently
burning little fires spark the energy of life. Should they cease to burn, ‘no heart could beat, no
plant could grow upward defying gravity, no amoeba could swim, no sensation could speed
along a nerve, no thought could flash in the human brain,’ said the chemist Eugene
Rabinowitch.
The transformation of matter into energy in the cell is an ever-flowing process, one of nature’s
cycles of renewal, like a wheel endlessly turning. Grain by grain, molecule by molecule,
carbohydrate fuel in the form of glucose is fed into this wheel; in its cyclic passage the fuel
molecule undergoes fragmentation and a series of minute chemical changes. The changes are
made in orderly fashion, step by step, each step directed and controlled by an enzyme of so
specialized a function that it does this one thing and nothing else. At each step energy is
produced, waste products (carbon dioxide and water) are given off, and the altered molecule of
fuel is passed on to the next stage. When the turning wheel comes full cycle the fuel molecule
has been stripped down to a form in which it is ready to combine with a new molecule coming
in and to start the cycle anew.
This process by which the cell functions as a chemical factory is one of the wonders of the living
world. The fact that all the functioning parts are of infinitesimal size adds to the miracle. With
few exceptions cells themselves are minute, seen only with the aid of a microscope. Yet the
greater part of the work of oxidation is performed in a theater far smaller, in tiny granules
within the cell called mitochondria. Although known for more than 60 years, these were
formerly dismissed as cellular elements of unknown and probably unimportant function. Only
in the 1950s did their study become an exciting and fruitful field of research; suddenly they
began to engage so much attention that 1000 papers on this subject alone appeared within a
five-year period. Again one stands in awe at the marvelous ingenuity and patience by which the
mystery of the mitochondria has been solved. Imagine a particle so small that you can barely
see it even though a microscope has enlarged it for you 300 times. Then imagine the skill
required to isolate this particle, to take it apart and analyze its components and determine their
highly complex functioning. Yet this has been done with the aid of the electron microscope and
the techniques of the biochemist.
It is now known that the mitochondria are tiny packets of enzymes, a varied assortment
including all the enzymes necessary for the oxidative cycle, arranged in precise and orderly
array on walls and partitions. The mitochondria are the ‘powerhouses’ in which most of the
energy-producing reactions occur. After the first, preliminary steps of oxidation have been
performed in the cytoplasm the fuel molecule is taken into the mitochondria. It is here that
oxidation is completed; it is here that enormous amounts of energy are released. The endlessly
turning wheels of oxidation within the mitochondria would turn to little purpose if it were not
for this all-important result. The energy produced at each stage of the oxidative cycle is in a
form familiarly spoken of by the biochemists as ATP (adenosine triphosphate), a molecule
containing three phosphate groups. The role of ATP in furnishing energy comes from the fact
that it can transfer one of its phosphate groups to other substances, along with the energy of
its bonds of electrons shuttling back and forth at high speed. Thus, in a muscle cell, energy to
contract is gained when a terminal phosphate group is transferred to the contracting muscle. So
another cycle takes place—a cycle within a cycle: a molecule of ATP gives up one of its
phosphate groups and retains only two, becoming a diphosphate molecule, ADP. But as the
wheel turns further another phosphate group is coupled on and the potent ATP is restored. The
analogy of the storage battery has been used: ATP represents the charged, ADP the discharged
battery.
ATP is the universal currency of energy—found in all organisms from microbes to man. It
furnishes mechanical energy to muscle cells; electrical energy to nerve cells. The sperm cell, the
fertilized egg ready for the enormous burst of activity that will transform it into a frog or a bird
or a human infant, the cell that must create a hormone, all are supplied with ATP. Some of the
energy of ATP is used in the mitochondrion but most of it is immediately dispatched into the
cell to provide power for other activities. The location of the mitochondria within certain cells is
eloquent of their function, since they are placed so that energy can be delivered precisely
where it is needed. In muscle cells they cluster around contracting fibers; in nerve cells they are
found at the junction with another cell, supplying energy for the transfer of impulses; in sperm
cells they are concentrated at the point where the propellant tail is joined to the head.
The charging of the battery, in which ADP and a free phosphate group are combined to restore
ATP, is coupled to the oxidative process; the close linking is known as coupled phosphorylation.
If the combination becomes uncoupled, the means is lost for providing usable energy.
Respiration continues but no energy is produced. The cell has become like a racing engine,
generating heat but yielding no power. Then the muscle cannot contract, nor can the impulse
race along the nerve pathways. Then the sperm cannot move to its destination; the fertilized
egg cannot carry to completion its complex divisions and elaborations. The consequences of
uncoupling could indeed be disastrous for any organism from embryo to adult: in time it could
lead to the death of the tissue or even of the organism. How can uncoupling be brought about?
Radiation is an uncoupler, and the death of cells exposed to radiation is thought by some to be
brought about in this way. Unfortunately, a good many chemicals also have the power to
separate oxidation from energy production, and the insecticides and weed killers are well
represented on the list. The phenols, as we have seen, have a strong effect on metabolism,
causing a potentially fatal rise in temperature; this is brought about by the ‘racing engine’ effect
of uncoupling. The dinitrophenols and pentachlorophenols are examples of this group that have
widespread use as herbicides. Another uncoupler among the herbicides is 2,4-D. Of the
chlorinated hydrocarbons, DDT is a proven uncoupler and further study will probably reveal
others among this group. But uncoupling is not the only way to extinguish the little fires in
some or all of the body’s billions of cells. We have seen that each step in oxidation is directed
and expedited by a specific enzyme. When any of these enzymes—even a single one of them—
is destroyed or weakened, the cycle of oxidation within the cell comes to a halt. It makes no
difference which enzyme is affected. Oxidation progresses in a cycle like a turning wheel. If we
thrust a crowbar between the spokes of a wheel it makes no difference where we do it, the
wheel stops turning. In the same way, if we destroy an enzyme that functions at any point in
the cycle, oxidation ceases. There is then no further energy production, so the end effect is very
similar to uncoupling.
The crowbar to wreck the wheels of oxidation can be supplied by any of a number of chemicals
commonly used as pesticides. DDT, methoxychlor, malathion, phenothiazine, and various
dinitro compounds are among the numerous pesticides that have been found to inhibit one or
more of the enzymes concerned in the cycle of oxidation. They thus appear as agents
potentially capable of blocking the whole process of energy production and depriving the cells
of utilizable oxygen. This is an injury with most disastrous consequences, only a few of which
can be mentioned here. Merely by systematically withholding oxygen, experimenters have
caused normal cells to turn into cancer cells, as we shall see in the following chapter. Some hint
of other drastic consequences of depriving a cell of oxygen can be seen in animal experiments
on developing embryos. With insufficient oxygen the orderly processes by which the tissues
unfold and the organs develop are disrupted; malformations and other abnormalities then
occur. Presumably the human embryo deprived of oxygen may also develop congenital
deformities.
There are signs that an increase in such disasters is being noticed, even though few look far
enough to find all of the causes. In one of the more unpleasant portents of the times, the Office
of Vital Statistics in 1961 initiated a national tabulation of malformations at birth, with the
explanatory comment that the resulting statistics would provide needed facts on the incidence
of congenital malformations and the circumstances under which they occur. Such studies will
no doubt be directed largely toward measuring the effects of radiation, but it must not be
overlooked that many chemicals are the partners of radiation, producing precisely the same
effects. Some of the defects and malformations in tomorrow’s children, grimly anticipated by
the Office of Vital Statistics, will almost certainly be caused by these chemicals that permeate
our outer and inner worlds. It may well be that some of the findings about diminished
reproduction are also linked with interference with biological oxidation, and consequent
depletion of the all-important storage batteries of ATP. The egg, even before fertilization, needs
to be generously supplied with ATP, ready and waiting for the enormous effort, the vast
expenditure of energy that will be required once the sperm has entered and fertilization has
occurred. Whether the sperm cell will reach and penetrate the egg depends upon its own
supply of ATP, generated in the mitochondria thickly clustered in the neck of the cell. Once
fertilization is accomplished and cell division has begun, the supply of energy in the form of ATP
will largely determine whether the development of the embryo will proceed to completion.
Embryologists studying some of their most convenient subjects, the eggs of frogs and of sea
urchins, have found that if the ATP content is reduced below a certain critical level the egg
simply stops dividing and soon dies.
It is not an impossible step from the embryology laboratory to the apple tree where a robin’s
nest holds its complement of blue-green eggs; but the eggs lie cold, the fires of life that
flickered for a few days now extinguished. Or to the top of a tall Florida pine where a vast pile
of twigs and sticks in ordered disorder holds three large white eggs, cold and lifeless. Why did
the robins and the eaglets not hatch? Did the eggs of the birds, like those of the laboratory
frogs, stop developing simply because they lacked enough of the common currency of energy—
the ATP molecules—to complete their development? And was the lack of ATP brought about
because in the body of the parent birds and in the eggs there were stored enough insecticides
to stop the little turning wheels of oxidation on which the supply of energy depends? It is no
longer necessary to guess about the storage of insecticides in the eggs of birds, which obviously
lend themselves to this kind of observation more readily than the mammalian ovum. Large
residues of DDT and other hydrocarbons have been found whenever looked for in the eggs of
birds subjected to these chemicals, either experimentally or in the wild. And the concentrations
have been heavy. Pheasant eggs in a California experiment contained up to 349 parts per
million of DDT. In Michigan, eggs taken from the oviducts of robins dead of DDT poisoning
showed concentrations up to 200 parts per million. Other eggs were taken from nests left
unattended as parent robins were stricken with poison; these too contained DDT. Chickens
poisoned by aldrin used on a neighboring farm have passed on the chemical to their eggs; hens
experimentally fed DDT laid eggs containing as much as 65 parts per million.
Knowing that DDT and other (perhaps all) chlorinated hydrocarbons stop the energy-producing
cycle by inactivating a specific enzyme or uncoupling the energy-producing mechanism, it is
hard to see how any egg so loaded with residues could complete the complex process of
development: the infinite number of cell divisions, the elaboration of tissues and organs, the
synthesis of vital substances that in the end produce a living creature. All this requires vast
amounts of energy—the little packets of ATP which the turning of the metabolic wheel alone
can produce. There is no reason to suppose these disastrous events are confined to birds. ATP
is the universal currency of energy, and the metabolic cycles that produce it turn to the same
purpose in birds and bacteria, in men and mice. The fact of insecticide storage in the germ cells
of any species should therefore disturb us, suggesting comparable effects in human beings.
And there are indications that these chemicals lodge in tissues concerned with the manufacture
of germ cells as well as in the cells themselves. Accumulations of insecticides have been
discovered in the sex organs of a variety of birds and mammals—in pheasants, mice, and guinea
pigs under controlled conditions, in robins in an area sprayed for elm disease, and in deer
roaming western forests sprayed for spruce budworm. In one of the robins the concentration of
DDT in the testes was heavier than in any other part of the body. Pheasants also accumulated
extraordinary amounts in the testes, up to 1500 parts per million. Probably as an effect of such
storage in the sex organs, atrophy of the testes has been observed in experimental mammals.
Young rats exposed to methoxychlor had extraordinarily small testes. When young roosters
were fed DDT, the testes made only 18 per cent of their normal growth; combs and wattles,
dependent for their development upon the testicular hormone, were only a third the normal
size. The spermatozoa themselves may well be affected by loss of ATP. Experiments show that
the motility of bull sperm is decreased by dinitrophenol, which interferes with the energy-
coupling mechanism with inevitable loss of energy. The same effect would probably be found
with other chemicals were the matter investigated. Some indication of the possible effect on
human beings is seen in medical reports of oligospermia, or reduced production of
spermatozoa, among aviation crop dusters applying DDT. . . .
For mankind as a whole, a possession infinitely more valuable than individual life is our genetic
heritage, our link with past and future. Shaped through long eons of evolution, our genes not
only make us what we are, but hold in their minute beings the future—be it one of promise or
threat. Yet genetic deterioration through man-made agents is the menace of our time, ‘the last
and greatest danger to our civilization’. Again the parallel between chemicals and radiation is
exact and inescapable. The living cell assaulted by radiation suffers a variety of injuries: its
ability to divide normally may be destroyed, it may suffer changes in chromosome structure, or
the genes, carriers of hereditary material, may undergo those sudden changes known as
mutations, which cause them to produce new characteristics in succeeding generations. If
especially susceptible the cell may be killed outright, or finally, after the passage of time
measured in years, it may become malignant.
All these consequences of radiation have been duplicated in laboratory studies by a large group
of chemicals known as radiomimetic or radiation-imitating. Many chemicals used as
pesticides—herbicides as well as insecticides—belong to this group of substances that have the
ability to damage the chromosomes, interfere with normal cell division, or cause mutations.
These injuries to the genetic material are of a kind that may lead to disease in the individual
exposed or they may make their effects felt in future generations. Only a few decades ago, no
one knew these effects of either radiation or chemicals. In those days the atom had not been
split and few of the chemicals that were to duplicate radiation had as yet been conceived in the
test tubes of chemists. Then in 1927, a professor of zoology in a Texas university, Dr. H. J.
Muller, found that by exposing an organism to X-radiation, he could produce mutations in
succeeding generations. With Muller’s discovery a vast new field of scientific and medical
knowledge was opened up. Muller later received the Nobel Prize in Medicine for his
achievement, and in a world that soon gained unhappy familiarity with the gray rains of fallout,
even the nonscientist now knows the potential results of radiation.
Although far less noticed, a companion discovery was made by Charlotte Auerbach and William
Robson at the University of Edinburgh in the early 1940s. Working with mustard gas, they found
that this chemical produces permanent chromosome abnormalities that cannot be
distinguished from those induced by radiation. Tested on the fruit fly, the same organism
Muller had used in his original work with X-rays, mustard gas also produced mutations. Thus
the first chemical mutagen was discovered. Mustard gas as a mutagen has now been joined by
a long list of other chemicals known to alter genetic material in plants and animals. To
understand how chemicals can alter the course of heredity, we must first watch the basic
drama of life as it is played on the stage of the living cell. The cells composing the tissues and
organs of the body must have the power to increase in number if the body is to grow and if the
stream of life is to be kept flowing from generation to generation. This is accomplished by the
process of mitosis, or nuclear division. In a cell that is about to divide, changes of the utmost
importance occur, first within the nucleus, but eventually involving the entire cell. Within the
nucleus, the chromosomes mysteriously move and divide, ranging themselves in age-old
patterns that will serve to distribute the determiners of heredity, the genes, to the daughter
cells. First they assume the form of elongated threads, on which the genes are aligned, like
beads on a string. Then each chromosome divides lengthwise (the genes dividing also). When
the cell divides into two, half of each goes to each of the daughter cells. In this way each new
cell will contain a complete set of chromosomes, and all the genetic information encoded
within them. In this way the integrity of the race and of the species is preserved; in this way like
begets like.
A special kind of cell division occurs in the formation of the germ cells. Because the
chromosome number for a given species is constant, the egg and the sperm, which are to unite
to form a new individual, must carry to their union only half the species number. This is
accomplished with extraordinary precision by a change in the behavior of the chromosomes
that occurs at one of the divisions producing those cells. At this time the chromosomes do not
split, but one whole chromosome of each pair goes into each daughter cell.
In this elemental drama all life is revealed as one. The events of the process of cell division are
common to all earthly life; neither man nor amoeba, the giant sequoia nor the simple yeast cell
can long exist without carrying on this process of cell division. Anything that disturbs mitosis is
therefore a grave threat to the welfare of the organism affected and to its descendants.
‘The major features of cellular organization, including, for instance, mitosis, must be much older
than 500 million years—more nearly 1000 million,’ wrote George Gaylord Simpson and his
colleagues Pittendrigh and Tiffany in their broadly encompassing book entitled Life. ‘In this
sense the world of life, while surely fragile and complex, is incredibly durable through time—
more durable than mountains. This durability is wholly dependent on the almost incredible
accuracy with which the inherited information is copied from generation to generation.’
But in all the thousand million years envisioned by these authors no threat has struck so
directly and so forcefully at that ‘incredible accuracy’ as the mid-20th century threat of man-
made radiation and man-made and man-disseminated chemicals. Sir Macfarlane Burnet, a
distinguished Australian physician and a Nobel Prize winner, considers it ‘one of the most
significant medical features’ of our time that, ‘as a by-product of more and more powerful
therapeutic procedures and the production of chemical substances outside of biological
experiences, the normal protective barriers that kept mutagenic agents from the internal
organs have been more and more frequently penetrated.’
The study of human chromosomes is in its infancy, and so it has only recently become possible
to study the effect of environmental factors upon them. It was not until 1956 that new
techniques made it possible to determine accurately the number of chromosomes in the
human cell—46—and to observe them in such detail that the presence or absence of whole
chromosomes or even parts of chromosomes could be detected. The whole concept of genetic
damage by something in the environment is also relatively new, and is little understood except
by the geneticists, whose advice is too seldom sought. The hazard from radiation in its various
forms is now reasonably well understood—although still denied in surprising places. Dr. Muller
has frequently had occasion to deplore the ‘resistance to the acceptance of genetic principles
on the part of so many, not only of governmental appointees in the policy-making positions,
but also of so many of the medical profession.’ The fact that chemicals may play a role similar
to radiation has scarcely dawned on the public mind, nor on the minds of most medical or
scientific workers. For this reason the role of chemicals in general use (rather than in laboratory
experiments) has not yet been assessed. It is extremely important that this be done.
Sir Macfarlane is not alone in his estimate of the potential danger. Dr. Peter Alexander, an
outstanding British authority, has said that the radiomimetic chemicals ‘may well represent a
greater danger’ than radiation. Dr. Muller, with the perspective gained by decades of
distinguished work in genetics, warns that various chemicals (including groups represented by
pesticides) ‘can raise the mutation frequency as much as radiation...As yet far too little is
known of the extent to which our genes, under modern conditions of exposure to unusual
chemicals, are being subjected to such mutagenic influences.’
The widespread neglect of the problem of chemical mutagens is perhaps due to the fact that
those first discovered were of scientific interest only. Nitrogen mustard, after all, is not sprayed
upon whole populations from the air; its use is in the hands of experimental biologists or of
physicians who use it in cancer therapy. (A case of chromosome damage in a patient receiving
such therapy has recently been reported.) But insecticides and weed killers are brought into
intimate contact with large numbers of people. Despite the scant attention that has been given
to the matter, it is possible to assemble specific information on a number of these pesticides,
showing that they disturb the cell’s vital processes in ways ranging from slight chromosome
damage to gene mutation, and with consequences extending to the ultimate disaster of
malignancy. Mosquitoes exposed to DDT for several generations turned into strange creatures
called gynandromorphs—part male and part female.
Plants treated with various phenols suffered profound destruction of chromosomes, changes in
genes, a striking number of mutations, ‘irreversible hereditary changes’. Mutations also
occurred in fruit flies, the classic subject of genetics experiments, when subjected to phenol;
these flies developed mutations so damaging as to be fatal on exposure to one of the common
herbicides or to urethane. Urethane belongs to the group of chemicals called carbamates, from
which an increasing number of insecticides and other agricultural chemicals are drawn. Two of
the carbamates are actually used to prevent sprouting of potatoes in storage—precisely
because of their proven effect in stopping cell division. Another antisprouting agent, maleic
hydrazide, is rated a powerful mutagen. Plants treated with benzene hexachloride (BHC) or
lindane became monstrously deformed with tumorlike swellings on their roots. Their cells grew
in size, being swollen with chromosomes which doubled in number. The doubling continued
in future divisions until further cell division became mechanically impossible. The herbicide 2,4-
D has also produced tumorlike swellings in treated plants. Chromosomes become short, thick,
clumped together. Cell division is seriously retarded. The general effect is said to parallel closely
that produced by Xrays.
These are but a few illustrations; many more could be cited. As yet there has been no
comprehensive study aimed at testing the mutagenic effects of pesticides as such. The facts
cited above are by-products of research in cell physiology or genetics. What is urgently needed
is a direct attack on the problem. Some scientists who are willing to concede the potent effect
of environmental radiation on man nevertheless question whether mutagenic chemicals can, as
a practical proposition, have the same effect. They cite the great penetrating power of
radiation, but doubt that chemicals could reach the germ cells. Once again we are hampered by
the fact that there has been little direct investigation of the problem in man. However, the
finding of large residues of DDT in the gonads and germ cells of birds and mammals is strong
evidence that the chlorinated hydrocarbons, at least, not only become widely distributed
throughout the body but come into contact with genetic materials. Professor David E. Davis at
Pennsylvania State University has recently discovered that a potent chemical which prevents
cells from dividing and has had limited use in cancer therapy can also be used to cause sterility
in birds. Sublethal levels of the chemical halt cell division in the gonads. Professor Davis has had
some success in field trials. Obviously, then, there is little basis for the hope or belief that the
gonads of any organism are shielded from chemicals in the environment.
Recent medical findings in the field of chromosome abnormalities are of extreme interest and
significance. In 1959 several British and French research teams found their independent studies
pointing to a common conclusion—that some of humanity’s ills are caused by a disturbance of
the normal chromosome number. In certain diseases and abnormalities studied by these
investigators the number differed from the normal. To illustrate: it is now known that all typical
mongoloids have one extra chromosome. Occasionally this is attached to another so that the
chromosome number remains the normal 46. As a rule, however, the extra is a separate
chromosome, making the number 47. In such individuals, the original cause of the defect must
have occurred in the generation preceding its appearance. A different mechanism seems to
operate in a number of patients, both in America and Great Britain, who are suffering from a
chronic form of leukemia. These have been found to have a consistent chromosome
abnormality in some of the blood cells. The abnormality consists of the loss of part of a
chromosome. In these patients the skin cells have a normal complement of chromosomes. This
indicates that the chromosome defect did not occur in the germ cells that gave rise to these
individuals, but represents damage to particular cells (in this case, the precursors of blood cells)
that occurred during the life of the individual. The loss of part of a chromosome has perhaps
deprived these cells of their ‘instructions’ for normal behavior.
The list of defects linked to chromosome disturbances has grown with surprising speed since
the opening of this territory, hitherto beyond the boundaries of medical research. One, known
only as Klinefelter’s syndrome, involves a duplication of one of the sex chromosomes. The
resulting individual is a male, but because he carries two of the X chromosomes (becoming XXY
instead of XY, the normal male complement) he is somewhat abnormal. Excessive height and
mental defects often accompany the sterility caused by this condition. In contrast, an individual
who receives only one sex chromosome (becoming XO instead of either XX or XY) is actually
female but lacks many of the secondary sexual characteristics. The condition is accompanied by
various physical (and sometimes mental) defects, for of course the X chromosome carries genes
for a variety of characteristics. This is known as Turner’s syndrome. Both conditions had been
described in medical literature long before the cause was known.
An immense amount of work on the subject of chromosome abnormalities is being done by
workers in many countries. A group at the University of Wisconsin, headed by Dr. Klaus Patau,
has been concentrating on a variety of congenital abnormalities, usually including mental
retardation, that seem to result from the duplication of only part of a chromosome, as if
somewhere in the formation of one of the germ cells a chromosome had broken and the pieces
had not been properly redistributed. Such a mishap is likely to interfere with the normal
development of the embryo. According to present knowledge, the occurrence of an entire extra
body chromosome is usually lethal, preventing survival of the embryo. Only three such
conditions are known to be viable; one of them, of course, is mongolism. The presence of an
extra attached fragment, on the other hand, although seriously damaging is not necessarily
fatal, and according to the Wisconsin investigators this situation may well account for a
substantial part of the so far unexplained cases in which a child is born with multiple defects,
usually including mental retardation. This is so new a field of study that as yet scientists have
been more concerned with identifying the chromosome abnormalities associated with disease
and defective development than with speculating about the causes. It would be foolish to
assume that any single agent is responsible for damaging the chromosomes or causing their
erratic behavior during cell division. But can we afford to ignore the fact that we are now filling
the environment with chemicals that have the power to strike directly at the chromosomes,
affecting them in the precise ways that could cause such conditions? Is this not too high a price
to pay for a sproutless potato or a mosquitoless patio? We can, if we wish, reduce this threat to
our genetic heritage, a possession that has come down to us through some two billion years of
evolution and selection of living protoplasm, a possession that is ours for the moment only,
until we must pass it on to generations to come. We are doing little now to preserve its
integrity. Although chemical manufacturers are required by law to test their materials for
toxicity, they are not required to make the tests that would reliably demonstrate genetic effect,
and they do not do so.
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