3. Elixirs of Death

FOR THE FIRST TIME in the history of the world, every human being is now subjected to
contact with dangerous chemicals, from the moment of conception until death. In the less than
two decades of their use, the synthetic pesticides have been so thoroughly distributed
throughout the animate and inanimate world that they occur virtually everywhere. They have
been recovered from most of the major river systems and even from streams of groundwater
flowing unseen through the earth. Residues of these chemicals linger in soil to which they may
have been applied a dozen years before. They have entered and lodged in the bodies of fish,
birds, reptiles, and domestic and wild animals so universally that scientists carrying on animal
experiments find it almost impossible to locate subjects free from such contamination. They
have been found in fish in remote mountain lakes, in earthworms burrowing in soil, in the eggs
of birds—and in man himself. For these chemicals are now stored in the bodies of the vast
majority of human beings, regardless of age. They occur in the mother’s milk, and probably in
the tissues of the unborn child. All this has come about because of the sudden rise and
prodigious growth of an industry for the production of manmade or synthetic chemicals with
insecticidal properties. This industry is a child of the Second World War. In the course of
developing agents of chemical warfare, some of the chemicals created in the laboratory were
found to be lethal to insects. The discovery did not come by chance: insects were widely used
to test chemicals as agents of death for man. The result has been a seemingly endless stream of
synthetic insecticides. In being man-made—by ingenious laboratory manipulation of the
molecules, substituting atoms, altering their arrangement—they differ sharply from the simpler
insecticides of prewar days. These were derived from naturally occurring minerals and plant
products—compounds of arsenic, copper, , manganese, zinc, and other minerals, pyrethrum
from the dried flowers of chrysanthemums, nicotine sulphate from some of the relatives of
tobacco, and rotenone from leguminous plants of the East Indies.

What sets the new synthetic insecticides apart is their enormous biological potency. They have
immense power not merely to poison but to enter into the most vital processes of the body and
change them in sinister and often deadly ways. Thus, as we shall see, they destroy the very
enzymes whose function is to protect the body from harm, they block the oxidation processes
from which the body receives its energy, they prevent the normal functioning of various organs,
and they may initiate in certain cells the slow and irreversible change that leads to malignancy.
Yet new and more deadly chemicals are added to the list each year and new uses are devised so
that contact with these materials has become practically worldwide. The production of
synthetic pesticides in the United States soared from 124,259,000 pounds in 1947 to
637,666,000 pounds in 1960—more than a fivefold increase. The wholesale value of these
products was well over a quarter of a billion dollars. But in the plans and hopes of the industry
this enormous production is only a beginning.

A Who’s Who of pesticides is therefore of concern to us all. If we are going to live so intimately
with these chemicals—eating and drinking them, taking them into the very marrow of our
bones—we had better know something about their nature and their power. Although the
Second World War marked a turning away from inorganic chemicals as pesticides into the
wonder world of the carbon molecule, a few of the old materials persist. Chief among these is
arsenic, which is still the basic ingredient in a variety of weed and insect killers. Arsenic is a
highly toxic mineral occurring widely in association with the ores of various metals, and in very
small amounts in volcanoes, in the sea, and in spring water. Its relations to man are varied and
historic. Since many of its compounds are tasteless, it has been a favorite agent of homicide
from long before the time of the Borgias to the present. Arsenic is present in English chimney
soot and along with certain aromatic hydrocarbons is considered responsible for the
carcinogenic (or cancer-causing) action of the soot, which was recognized nearly two centuries
ago by an English physician. Epidemics of chronic arsenical poisoning involving whole
populations over long periods are on record. Arsenic-contaminated environments have also
caused sickness and death among horses, cows, goats, pigs, deer, fishes, and bees; despite this
record arsenical sprays and dusts are widely used. In the arsenic-sprayed cotton country of
southern United States beekeeping as an industry has nearly died out. Farmers using arsenic
dusts over long periods have been afflicted with chronic arsenic poisoning, livestock have been
poisoned by crop sprays or weed killers containing arsenic. Drifting arsenic dusts from
blueberry lands have spread over neighboring farms, contaminating streams, fatally poisoning
bees and cows, and causing human illness. ‘It is scarcely possible...to handle arsenicals with
more utter disregard of the general health than that which has been practiced in our country in
recent years,’ said Dr. W. C. Hueper, of the National Cancer Institute, an authority on
environmental cancer. ‘Anyone who has watched the dusters and sprayers of arsenical
insecticides at work must have been impressed by the almost supreme carelessness with which
the poisonous substances are dispensed.’ . . .

Modern insecticides are still more deadly. The vast majority fall into one of two large groups of
chemicals. One, represented by DDT, is known as the ‘chlorinated hydrocarbons. The other
group consists of the organic phosphorus insecticides, and is represented by the reasonably
familiar malathion and parathion. All have one thing in common. As mentioned above, they are
built on a basis of carbon atoms, which are also the indispensable building blocks of the living
world, and thus classed as ‘organic’. To understand them, we must see of what they are made,
and how, although linked with the basic chemistry of all life, they lend themselves to the
modifications which make them agents of death.

The basic element, carbon, is one whose atoms have an almost infinite capacity for uniting with
each other in chains and rings and various other configurations, and for becoming linked with
atoms of other substances. Indeed, the incredible diversity of living creatures from bacteria to
the great blue whale is largely due to this capacity of carbon. The complex protein molecule has
the carbon atom as its basis, as have molecules of fat, carbohydrates, enzymes, and vitamins.
So, too, have enormous numbers of nonliving things, for carbon is not necessarily a symbol of
life. Some organic compounds are simply combinations of carbon and hydrogen. The simplest
of these is methane, or marsh gas, formed in nature by the bacterial decomposition of organic
matter under water. Mixed with air in proper proportions, methane becomes the dreaded ‘fire
damp’ of coal mines. Its structure is beautifully simple, consisting of one carbon atom to which
four hydrogen atoms have become attached:

Chemists have discovered that it is possible to detach one or all of the hydrogen atoms and
substitute other elements. For example, by substituting one atom of chlorine for one of
hydrogen we produce methyl chloride:


Take away three hydrogen atoms and substitute chlorine and we have the anesthetic
chloroform:


Substitute chlorine atoms for all of the hydrogen atoms and the result is carbon tetrachloride,
the familiar cleaning fluid:


In the simplest possible terms, these changes rung upon the basic molecule of methane
illustrate what a chlorinated hydrocarbon is. But this illustration gives little hint of the true
complexity of the chemical world of the hydrocarbons, or of the manipulations by which the
organic chemist creates his infinitely varied materials. For instead of the simple methane
molecule with its single carbon atom, he may work with hydrocarbon molecules consisting of
many carbon atoms, arranged in rings or chains, with side chains or branches, holding to
themselves with chemical bonds not merely simple atoms of hydrogen or chlorine but also a
wide variety of chemical groups. By seemingly slight changes the whole character of the
substance is changed; for example, not only what is attached but the place of attachment to
the carbon atom is highly important. Such ingenious manipulations have produced a battery of
poisons of truly extraordinary power. . . .

DDT (short for dichloro-diphenyl-trichloro-ethane) was first synthesized by a German chemist in
1874, but its properties as an insecticide were not discovered until 1939. Almost immediately
DDT was hailed as a means of stamping out insect-borne disease and winning the farmers’ war
against crop destroyers overnight. The discoverer, Paul Müller of Switzerland, won the Nobel
Prize. DDT is now so universally used that in most minds the product takes on the harmless
aspect of the familiar. Perhaps the myth of the harmlessness of DDT rests on the fact that one
of its first uses was the wartime dusting of many thousands of soldiers, refugees, and prisoners,
to combat lice. It is widely believed that since so many people came into extremely intimate
contact with DDT and suffered no immediate ill effects the chemical must certainly be innocent
of harm. This understandable misconception arises from the fact that—unlike other chlorinated
hydrocarbons—DDT in powder form is not readily absorbed through the skin. Dissolved in oil, as
it usually is, DDT is definitely toxic. If swallowed, it is absorbed slowly through the digestive
tract; it may also be absorbed through the lungs. Once it has entered the body it is stored
largely in organs rich in fatty substances (because DDT itself is fat-soluble) such as the adrenals,
testes, or thyroid. Relatively large amounts are deposited in the liver, kidneys, and the fat of the
large, protective mesenteries that enfold the intestines.

This storage of DDT begins with the smallest conceivable intake of the chemical (which is
present as residues on most foodstuffs) and continues until quite high levels are reached. The
fatty storage depots act as biological magnifiers, so that an intake of as little as of 1 part per
million in the diet results in storage of about 10 to 15 parts per million, an increase of one
hundredfold or more. These terms of reference, so commonplace to the chemist or the
pharmacologist, are unfamiliar to most of us. One part in a million sounds like a very small
amount—and so it is. But such substances are so potent that a minute quantity can bring about
vast changes in the body. In animal experiments, 3 parts per million has been found to inhibit
an essential enzyme in heart muscle; only 5 parts per million has brought about necrosis or
disintegration of liver cells; only 2.5 parts per million of the closely related chemicals dieldrin
and chlordane did the same. This is really not surprising. In the normal chemistry of the human
body there is just such a disparity between cause and effect. For example, a quantity of iodine
as small as two ten-thousandths of a gram spells the difference between health and disease.
Because these small amounts of pesticides are cumulatively stored and only slowly excreted,
the threat of chronic poisoning and degenerative changes of the liver and other organs is very
real.

Scientists do not agree upon how much DDT can be stored in the human body. Dr. Arnold
Lehman, who is the chief pharmacologist of the Food and Drug Administration, says there is
neither a floor below which DDT is not absorbed nor a ceiling beyond which absorption and
storage ceases. On the other hand, Dr. Wayland Hayes of the United States Public Health
Service contends that in every individual a point of equilibrium is reached, and that DDT in
excess of this amount is excreted. For practical purposes it is not particularly important which
of these men is right. Storage in human beings has been well investigated, and we know that
the average person is storing potentially harmful amounts. According to various studies,
individuals with no known exposure (except the inevitable dietary one) store an average of 5.3
parts per million to 7.4 parts per million; agricultural workers 17.1 parts per million; and
workers in insecticide plants as high as 648 parts per million! So the range of proven storage is
quite wide and, what is even more to the point, the minimum figures are above the level at
which damage to the liver and other organs or tissues may begin. One of the most sinister
features of DDT and related chemicals is the way they are passed on from one organism to
another through all the links of the food chains. For example, fields of alfalfa are dusted with
DDT; meal is later prepared from the alfalfa and fed to hens; the hens lay eggs which contain
DDT. Or the hay, containing residues of 7 to 8 parts per million, may be fed to cows. The DDT
will turn up in the milk in the amount of about 3 parts per million, but in butter made from this
milk the concentration may run to 65 parts per million. Through such a process of transfer,
what started out as a very small amount of DDT may end as a heavy concentration. Farmers
nowadays find it difficult to obtain uncontaminated fodder for their milk cows, though the Food
and Drug Administration forbids the presence of insecticide residues in milk shipped in
interstate commerce.

The poison may also be passed on from mother to offspring. Insecticide residues have been
recovered from human milk in samples tested by Food and Drug Administration scientists. This
means that the breast-fed human infant is receiving small but regular additions to the load of
toxic chemicals building up in his body. It is by no means his first exposure, however: there is
good reason to believe this begins while he is still in the womb. In experimental animals the
chlorinated hydrocarbon insecticides freely cross the barrier of the placenta, the traditional
protective shield between the embryo and harmful substances in the mother’s body. While the
quantities so received by human infants would normally be small, they are not unimportant
because children are more susceptible to poisoning than adults. This situation also means that
today the average individual almost certainly starts life with the first deposit of the growing
load of chemicals his body will be required to carry thenceforth.

All these facts—storage at even low levels, subsequent accumulation, and occurrence of liver
damage at levels that may easily occur in normal diets, caused Food and Drug Administration
scientists to declare as early as 1950 that it is ‘extremely likely the potential hazard of DDT has
been underestimated.’ There has been no such parallel situation in medical history. No one yet
knows what the ultimate consequences may be. . . .

Chlordane, another chlorinated hydrocarbon, has all these unpleasant attributes of DDT plus a
few that are peculiarly its own. Its residues are long persistent in soil, on foodstuffs, or on
surfaces to which it may be applied. Chlordane makes use of all available portals to enter the
body. It may be absorbed through the skin, may be breathed in as a spray or dust, and of course
is absorbed from the digestive tract if residues are swallowed. Like all other chlorinated
hydrocarbons, its deposits build up in the body in cumulative fashion. A diet containing such a
small amount of chlordane as 2.5 parts per million may eventually lead to storage of 75 parts
per million in the fat of experimental animals. So experienced a pharmacologist as Dr. Lehman
has described chlordane in 1950 as ‘one of the most toxic of insecticides—anyone handling it
could be poisoned.’ Judging by the carefree liberality with which dusts for lawn treatments by
suburbanites are laced with chlordane, this warning has not been taken to heart. The fact that
the suburbanite is not instantly stricken has little meaning, for the toxins may sleep long in his
body, to become manifest months or years later in an obscure disorder almost impossible to
trace to its origins. On the other hand, death may strike quickly. One victim who accidentally
spilled a 25 per cent industrial solution on the skin developed symptoms of poisoning within 40
minutes and died before medical help could be obtained. No reliance can be placed on
receiving advance warning which might allow treatment to be had in time.

Heptachlor, one of the constituents of chlordane, is marketed as a separate formulation. It has
a particularly high capacity for storage in fat. If the diet contains as little as of 1 part per million
there will be measurable amounts of heptachlor in the body. It also has the curious ability to
undergo change into a chemically distinct substance known as heptachlor epoxide. It does this
in soil and in the tissues of both plants and animals. Tests on birds indicate that the epoxide
that results from this change is more toxic than the original chemical, which in turn is four times
as toxic as chlordane. As long ago as the mid-1930s a special group of hydrocarbons, the
chlorinated naphthalenes, was found to cause hepatitis, and also a rare and almost invariably
fatal liver disease in persons subjected to occupational exposure. They have led to illness and
death of workers in electrical industries; and more recently, in agriculture, they have been
considered a cause of a mysterious and usually fatal disease of cattle. In view of these
antecedents, it is not surprising that three of the insecticides that are related to this group are
among the most violently poisonous of all the hydrocarbons. These are dieldrin, aldrin, and
endrin. Dieldrin, named for a German chemist, Diels, is about 5 times as toxic as DDT when
swallowed but 40 times as toxic when absorbed through the skin in solution. It is notorious for
striking quickly and with terrible effect at the nervous system, sending the victims into
convulsions. Persons thus poisoned recover so slowly as to indicate chronic effects. As with
other chlorinated hydrocarbons, these long-term effects include severe damage to the liver.
The long duration of its residues and the effective insecticidal action make dieldrin one of the
most used insecticides today, despite the appalling destruction of wildlife that has followed its
use. As tested on quail and pheasants, it has proved to be about 40 to 50 times as toxic as DDT.
There are vast gaps in our knowledge of how dieldrin is stored or distributed in the body, or
excreted, for the chemists’ ingenuity in devising insecticides has long ago outrun biological
knowledge of the way these poisons affect the living organism. However, there is every
indication of long storage in the human body, where deposits may lie dormant like a slumbering
volcano, only to flare up in periods of physiological stress when the body draws upon its fat
reserves. Much of what we do know has been learned through hard experience in the
antimalarial campaigns carried out by the World Health Organization. As soon as dieldrin was
substituted for DDT in malaria-control work (because the malaria mosquitoes had become
resistant to DDT), cases of poisoning among the spraymen began to occur. The seizures were
severe—from half to all (varying in the different programs) of the men affected went into
convulsions and several died. Some had convulsions as long as four months after the last
exposure.

Aldrin is a somewhat mysterious substance, for although it exists as a separate entity it bears
the relation of alter ego to dieldrin. When carrots are taken from a bed treated with aldrin they
are found to contain residues of dieldrin. This change occurs in living tissues and also in soil.
Such alchemistic transformations have led to many erroneous reports, for if a chemist, knowing
aldrin has been applied, tests for it he will be deceived into thinking all residues have been
dissipated. The residues are there, but they are dieldrin and this requires a different test. Like
dieldrin, aldrin is extremely toxic. It produces degenerative changes in the liver and kidneys. A
quantity the size of an aspirin tablet is enough to kill more than 400 quail. Many cases of human
poisonings are on record, most of them in connection with industrial handling. Aldrin, like most
of this group of insecticides, projects a menacing shadow into the future, the shadow of
sterility. Pheasants fed quantities too small to kill them nevertheless laid few eggs, and the
chicks that hatched soon died. The effect is not confined to birds. Rats exposed to aldrin had
fewer pregnancies and their young were sickly and short-lived. Puppies born of treated mothers
died within three days. By one means or another, the new generations suffer for the poisoning
of their parents. No one knows whether the same effect will be seen in human beings, yet this
chemical has been sprayed from airplanes over suburban areas and farmlands.

Endrin is the most toxic of all the chlorinated hydrocarbons. Although chemically rather closely
related to dieldrin, a little twist in its molecular structure makes it 5 times as poisonous. It
makes the progenitor of all this group of insecticides, DDT, seem by comparison almost
harmless. It is 15 times as poisonous as DDT to mammals, 30 times as poisonous to fish, and
about 300 times as poisonous to some birds. In the decade of its use, endrin has killed
enormous numbers of fish, has fatally poisoned cattle that have wandered into sprayed
orchards, has poisoned wells, and has drawn a sharp warning from at least one state health
department that its careless use is endangering human lives. In one of the most tragic cases of
endrin poisoning there was no apparent carelessness; efforts had been made to take
precautions apparently considered adequate. A year-old child had been taken by his American
parents to live in Venezuela. There were cockroaches in the house to which they moved, and
after a few days a spray containing endrin was used. The baby and the small family dog were
taken out of the house before the spraying was done about nine o’clock one morning. After the
spraying the floors were washed. The baby and dog were returned to the house in
midafternoon. An hour or so later the dog vomited, went into convulsions, and died. At 10 p.m.
on the evening of the same day the baby also vomited, went into convulsions, and lost
consciousness. After that fateful contact with endrin this normal, healthy child became little
more than a vegetable—unable to see or hear, subject to frequent muscular spasms,
apparently completely cut off from contact with his surroundings. Several months of treatment
in a New York hospital failed to change his condition or bring hope of change. ‘It is extremely
doubtful,’ reported the attending physicians, ‘that any useful degree of recovery will occur.’ . . .

The second major group of insecticides, the alkyl or organic phosphates, are among the most
poisonous chemicals in the world. The chief and most obvious hazard attending their use is that
of acute poisoning of people applying the sprays or accidentally coming in contact with drifting
spray, with vegetation coated by it, or with a discarded container. In Florida, two children found
an empty bag and used it to repair a swing. Shortly thereafter both of them died and three of
their playmates became ill. The bag had once contained an insecticide called parathion, one of
the organic phosphates; tests established death by parathion poisoning. On another occasion
two small boys in Wisconsin, cousins, died on the same night. One had been playing in his yard
when spray drifted in from an adjoining field where his father was spraying potatoes with
parathion; the other had run playfully into the barn after his father and had put his hand on the
nozzle of the spray equipment.

The origin of these insecticides has a certain ironic significance. Although some of the chemicals
themselves—organic esters of phosphoric acid—had been known for many years, their
insecticidal properties remained to be discovered by a German chemist, Gerhard Schrader, in
the late 1930s. Almost immediately the German government recognized the value of these
same chemicals as new and devastating weapons in man’s war against his own kind, and the
work on them was declared secret. Some became the deadly nerve gases. Others, of closely
allied structure, became insecticides. The organic phosphorus insecticides act on the living
organism in a peculiar way. They have the ability to destroy enzymes—enzymes that perform
necessary functions in the body. Their target is the nervous system, whether the victim is an
insect or a warm-blooded animal. Under normal conditions, an impulse passes from nerve to
nerve with the aid of a ‘chemical transmitter’ called acetylcholine, a substance that performs an
essential function and then disappears. Indeed, its existence is so ephemeral that medical
researchers are unable, without special procedures, to sample it before the body has destroyed
it. This transient nature of the transmitting chemical is necessary to the normal functioning of
the body. If the acetylcholine is not destroyed as soon as a nerve impulse has passed, impulses
continue to flash across the bridge from nerve to nerve, as the chemical exerts its effects in an
ever more intensified manner. The movements of the whole body become uncoordinated:
tremors, muscular spasms, convulsions, and death quickly result. This contingency has been
provided for by the body. A protective enzyme called cholinesterase is at hand to destroy the
transmitting chemical once it is no longer needed. By this means a precise balance is struck and
the body never builds up a dangerous amount of acetylcholine. But on contact with the organic
phosphorus insecticides, the protective enzyme is destroyed, and as the quantity of the enzyme
is reduced that of the transmitting chemical builds up. In this effect, the organic phosphorus
compounds resemble the alkaloid poison muscarine, found in a poisonous mushroom, the fly
amanita.

Repeated exposures may lower the cholinesterase level until an individual reaches the brink of
acute poisoning, a brink over which he may be pushed by a very small additional exposure. For
this reason it is considered important to make periodic examinations of the blood of spray
operators and others regularly exposed. Parathion is one of the most widely used of the organic
phosphates. It is also one of the most powerful and dangerous. Honeybees become ‘wildly
agitated and bellicose’ on contact with it, perform frantic cleaning movements, and are near
death within half an hour. A chemist, thinking to learn by the most direct possible means the
dose acutely toxic to human beings, swallowed a minute amount, equivalent to about .00424
ounce. Paralysis followed so instantaneously that he could not reach the antidotes he had
prepared at hand, and so he died. Parathion is now said to be a favorite instrument of suicide in
Finland. In recent years the State of California has reported an average of more than 200 cases
of accidental parathion poisoning annually. In many parts of the world the fatality rate from
parathion is startling: 100 fatal cases in India and 67 in Syria in 1958, and an average of 336
deaths per year in Japan. Yet some 7,000,000 pounds of parathion are now applied to fields and
orchards of the United States—by hand sprayers, motorized blowers and dusters, and by
airplane. The amount used on California farms alone could, according to one medical authority,
‘provide a lethal dose for 5 to 10 times the whole world’s population.’

One of the few circumstances that save us from extinction by this means is the fact that
parathion and other chemicals of this group are decomposed rather rapidly. Their residues on
the crops to which they are applied are therefore relatively short-lived compared with the
chlorinated hydrocarbons. However, they last long enough to create hazards and produce
consequences that range from the merely serious to the fatal. In Riverside, California, eleven
out of thirty men picking oranges became violently ill and all but one had to be hospitalized.
Their symptoms were typical of parathion poisoning.

The grove had been sprayed with parathion some two and a half weeks earlier; the residues
that reduced them to retching, half-blind, semiconscious misery were sixteen to nineteen days
old. And this is not by any means a record for persistence. Similar mishaps have occurred in
groves sprayed a month earlier, and residues have been found in the peel of oranges six
months after treatment with standard dosages. The danger to all workers applying the organic
phosphorus insecticides in fields, orchards, and vineyards, is so extreme that some states using
these chemicals have established laboratories where physicians may obtain aid in diagnosis and
treatment. Even the physicians themselves may be in some danger, unless they wear rubber
gloves in handling the victims of poisoning. So may a laundress washing the clothing of such
victims, which may have absorbed enough parathion to affect her.

Malathion, another of the organic phosphates, is almost as familiar to the public as DDT, being
widely used by gardeners, in household insecticides, in mosquito spraying, and in such blanket
attacks on insects as the spraying of nearly a million acres of Florida communities for the
Mediterranean fruit fly. It is considered the least toxic of this group of chemicals and many
people assume they may use it freely and without fear of harm. Commercial advertising
encourages this comfortable attitude. The alleged ‘safety’ of malathion rests on rather
precarious ground, although—as often happens—this was not discovered until the chemical
had been in use for several years. Malathion is ‘safe’ only because the mammalian liver, an
organ with extraordinary protective powers, renders it relatively harmless. The detoxification is
accomplished by one of the enzymes of the liver. If, however, something destroys this enzyme
or interferes with its action, the person exposed to malathion receives the full force of the
poison.

Unfortunately for all of us, opportunities for this sort of thing to happen are legion. A few years
ago a team of Food and Drug Administration scientists discovered that when malathion and
certain other organic phosphates are administered simultaneously a massive poisoning
results—up to 50 times as severe as would be predicted on the basis of adding together the
toxicities of the two. In other words, of the lethal dose of each compound may be fatal when
the two are combined. This discovery led to the testing of other combinations. It is now known
that many pairs of organic phosphate insecticides are highly dangerous, the toxicity being
stepped up or ‘potentiated’ through the combined action. Potentiation seems to take place
when one compound destroys the liver enzyme responsible for detoxifying the other. The two
need not be given simultaneously. The hazard exists not only for the man who may spray this
week with one insecticide and next week with another; it exists also for the consumer of
sprayed products. The common salad bowl may easily present a combination of organic
phosphate insecticides. Residues well within the legally permissible limits may interact. The full
scope of the dangerous interaction of chemicals is as yet little known, but disturbing findings
now come regularly from scientific laboratories. Among these is the discovery that the toxicity
of an organic phosphate can be increased by a second agent that is not necessarily an
insecticide. For example, one of the plasticizing agents may act even more strongly than
another insecticide to make malathion more dangerous. Again, this is because it inhibits the
liver enzyme that normally would ‘draw the teeth’ of the poisonous insecticide.

What of other chemicals in the normal human environment? What, in particular, of drugs? A
bare beginning has been made on this subject, but already it is known that some organic
phosphates (parathion and malathion) increase the toxicity of some drugs used as muscle
relaxants, and that several others (again including malathion) markedly increase the sleeping
time of barbiturates. . . .

In Greek mythology the sorceress Medea, enraged at being supplanted by a rival for the
affections of her husband Jason, presented the new bride with a robe possessing magic
properties. The wearer of the robe immediately suffered a violent death. This death-by-
indirection now finds its counterpart in what are known as ‘systemic insecticides’. These are
chemicals with extraordinary properties which are used to convert plants or animals into a sort
of Medea’s robe by making them actually poisonous. This is done with the purpose of killing
insects that may come in contact with them, especially by sucking their juices or blood.

The world of systemic insecticides is a weird world, surpassing the imaginings of the brothers
Grimm—perhaps most closely akin to the cartoon world of Charles Addams. It is a world where
the enchanted forest of the fairy tales has become the poisonous forest in which an insect that
chews a leaf or sucks the sap of a plant is doomed. It is a world where a flea bites a dog, and
dies because the dog’s blood has been made poisonous, where an insect may die from vapors
emanating from a plant it has never touched, where a bee may carry poisonous nectar back to
its hive and presently produce poisonous honey.

The entomologists’ dream of the built-in insecticide was born when workers in the field of
applied entomology realized they could take a hint from nature: they found that wheat growing
in soil containing sodium selenate was immune to attack by aphids or spider mites. Selenium, a
naturally occurring element found sparingly in rocks and soils of many parts of the world, thus
became the first systemic insecticide. What makes an insecticide a systemic is the ability to
permeate all the tissues of a plant or animal and make them toxic. This quality is possessed by
some chemicals of the chlorinated hydrocarbon group and by others of the organophosphorus
group, all synthetically produced, as well as by certain naturally occurring substances. In
practice, however, most systemics are drawn from the organophosphorus group because the
problem of residues is somewhat less acute. Systemics act in other devious ways. Applied to
seeds, either by soaking or in a coating combined with carbon, they extend their effects into the
following plant generation and produce seedlings poisonous to aphids and other sucking
insects. Vegetables such as peas, beans, and sugar beets are sometimes thus protected. Cotton
seeds coated with a systemic insecticide have been in use for some time in California, where 25
farm labourers planting cotton in the San Joaquin Valley in 1959 were seized with sudden
illness, caused by handling the bags of treated seeds. In England someone wondered what
happened when bees made use of nectar from plants treated with systemics. This was
investigated in areas treated with a chemical called schradan. Although the plants had been
sprayed before the flowers were formed, the nectar later produced contained the poison. The
result, as might have been predicted, was that the honey made by the bees also was
contaminated with schradan.

Use of animal systemics has concentrated chiefly on control of the cattle grub, a damaging
parasite of livestock. Extreme care must be used in order to create an insecticidal effect in the
blood and tissues of the host without setting up a fatal poisoning. The balance is delicate and
government veterinarians have found that repeated small doses can gradually deplete an
animal’s supply of the protective enzyme cholinesterase, so that without warning a minute
additional dose will cause poisoning.

There are strong indications that fields closer to our daily lives are being opened up. You may
now give your dog a pill which, it is claimed, will rid him of fleas by making his blood poisonous
to them. The hazards discovered in treating cattle would presumably apply to the dog. As yet
no one seems to have proposed a human systemic that would make us lethal to a mosquito.
Perhaps this is the next step. . . .

So far in this chapter we have been discussing the deadly chemicals that are being used in our
war against the insects. What of our simultaneous war against the weeds? The desire for a
quick and easy method of killing unwanted plants has given rise to a large and growing array of
chemicals that are known as herbicides, or, less formally, as weed killers. The story of how
these chemicals are used and misused will be told in Chapter 6; the question that here concerns
us is whether the weed killers are poisons and whether their rise is contributing to the
poisoning of the environment.

The legend that the herbicides are toxic only to plants and so pose no threat to animal life has
been widely disseminated, but unfortunately it is not true. The plant killers include a large
variety of chemicals that act on animal tissue as well as on vegetation. They vary greatly in their
action on the organism. Some are general poisons, some are powerful stimulants of
metabolism, causing a fatal rise in body temperature, some induce malignant tumors either
alone or in partnership with other chemicals, some strike at the genetic material of the race by
causing gene mutations. The herbicides, then, like the insecticides, include some very
dangerous chemicals, and their careless use in the belief that they are ‘safe’ can have disastrous
results. Despite the competition of a constant stream of new chemicals issuing from the
laboratories, arsenic compounds are still liberally used, both as insecticides (as mentioned
above) and as weed killers, where they usually take the chemical form of sodium arsenite. The
history of their use is not reassuring. As roadside sprays, they have cost many a farmer his cow
and killed uncounted numbers of wild creatures. As aquatic weed killers in lakes and reservoirs
they have made public waters unsuitable for drinking or even for swimming. As a spray applied
to potato fields to destroy the vines they have taken a toll of human and nonhuman life.

In England this latter practice developed about 1951 as a result of a shortage of sulfuric acid,
formerly used to burn off the potato vines. The Ministry of Agriculture considered it necessary
to give warning of the hazard of going into the arsenic-sprayed fields, but the warning was not
understood by the cattle (nor, we must presume, by the wild animals and birds) and reports of
cattle poisoned by the arsenic sprays came with monotonous regularity. When death came also
to a farmer’s wife through arsenic-contaminated water, one of the major English chemical
companies (in 1959) stopped production of arsenical sprays and called in supplies already in the
hands of dealers, and shortly thereafter the Ministry of Agriculture announced that because of
high risks to people and cattle restrictions on the use of arsenites would be imposed. In 1961,
the Australian government announced a similar ban. No such restrictions impede the use of
these poisons in the United States, however.

Some of the ‘dinitro’ compounds are also used as herbicides. They are rated as among the most
dangerous materials of this type in use in the United States. Dinitrophenol is a strong metabolic
stimulant. For this reason it was at one time used as a reducing drug, but the margin between
the slimming dose and that required to poison or kill was slight—so slight that several patients
died and many suffered permanent injury before use of the drug was finally halted. A related
chemical, pentachlorophenol, sometimes known as ‘penta’, is used as a weed killer as well as
an insecticide, often being sprayed along railroad tracks and in waste areas. Penta is extremely
toxic to a wide variety of organisms from bacteria to man. Like the dinitros, it interferes, often
fatally, with the body’s source of energy, so that the affected organism almost literally burns
itself up. Its fearful power is illustrated in a fatal accident recently reported by the California
Department of Health. A tank truck driver was preparing a cotton defoliant by mixing diesel oil
with pentachlorophenol. As he was drawing the concentrated chemical out of a drum, the
spigot accidentally toppled back. He reached in with his bare hand to regain the spigot.
Although he washed immediately, he became acutely ill and died the next day.

While the results of weed killers such as sodium arsenite or the phenols are grossly obvious,
some other herbicides are more insidious in their effects. For example, the now famous
cranberry-weed killer aminotriazole, or amitrol, is rated as having relatively low toxicity. But in
the long run its tendency to cause malignant tumors of the thyroid may be far more significant
for wildlife and perhaps also for man. Among the herbicides are some that are classified as
‘mutagens’, or agents capable of modifying the genes, the materials of heredity. We are rightly
appalled by the genetic effects of radiation; how then, can we be indifferent to the same effect
in chemicals that we disseminate widely in our environment?

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