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Authors: Rachel Carson

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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, 1/100 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 laborers 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 use 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 assume, 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.

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