John I. Pratt, Jr., Frank H. Babers.
Somebody has said that because insects are small an insecticide kills them all over. Our knowledge of the subject is incomplete, but it is enough to belie the statement.
Poisons affect the normal functions of specific cells and tissues of insects just as they are known to do in humans and other higher animals. Basically some chemical process in the animal is affected so as to bring about changes in its functions. Those changes are secondary to the original process that was affected and are frequently mistaken for the initial action of the poison.
A complete knowledge of the way a chemical poisons an insect would have great value in the formulation of insecticides. While preparing an insecticidal mixture, for example, we could add a substance that would help the poison reach the target the organ or tissue it acts upon. Chemicals could be added to weaken or destroy the mechanisms that protect the insect against the poison in question. If we know how one poison acts, we could select or synthesize other chemicals of similar action. Research is giving us that knowledge so that before too long such ideals should become realities.
Insecticides have been classified according to the way they get into the insect's body cavity: Stomach poisons are eaten, contact poisons enter through the skin, and fumigants enter through the breathing tubes or the skin as gases. Some insecticides may enter by all three routes. But often such a classification is used wrongly to refer to the mode of action of an insecticide an entirely different term, which Means the way in which a chemical acts on an animal's system.
In studying the mode of action of an insecticide, we often rely for clues on what we know of the action of the poison on man or other higher animals. Sometimes the mode of action may be similar in vertebrates and in insects, but without experimental evidence it is unwise to assume that such a similarity exists.
The poisonous properties of the inorganic arsenic compounds (paris green, calcium and lead arsenate, sodium arsenite) are due to the formation of the water-soluble compounds, arsenious or arsenic acid, in the digestive tract.
Arsenic is considered a general protoplasmic poison; that is, it poisons the contents of all types of cells. Most tissues and organs therefore are affected in arsenic poisoning. One well-known effect of arsenic on vertebrate animals is the abrasion and destruction of the lining of the intestine. A similar destruction occurs in the mid-intestine of insects. Often it is said that such destruction is the primary reason that arsenic insecticides kill insects. If that were true, it still would not explain what biochemical process is disturbed in order to bring about destruction of the intestinal cells. Investigations with vertebrate animals have shown that arsenic poisons unidentified enzymes, which function in the metabolism of carbohydrates by cells. Probably arsenic acts on the insect system in the same manner.
Nicotine first stimulates and then depresses the nervous system of animals. Paralysis follows rapidly and results in the failure of organs to function. In insects, as in higher animals, the poisoning action of nicotine occurs in the nerve ganglia, which are clumps of nerve tissue at various places in the nervous system. Nicotine seems to have practically no effect on nerve fibers or on the junctions of nerves with muscles. The chemical process of nicotine poisoning in insects is not known.
Pyrethrum powder, the ground flowers of certain species of the chrysanthemum, contains the chemicals, pyrethrin I and II and cinerin I and II, which are the main toxic principles. The rapid paralyzing action of pyrethrum is evident to anybody who has sprayed a room with a household fly spray and watched the flies drop almost immediately to the floor. The insects recover from the paralysis, however, unless a lethal amount of the poison gets on them. Pyrethrin acts directly on the central nervous system of insects. The paralysis is a result of the blocking of transmission of nerve impulses. We know that* destructive changes occur in the nervous tissue of insects poisoned with pyrethrin, but the reason for the changes is obscure.
Rotenone causes paralysis of the breathing mechanism in mammals, possibly by acting on bronchial tissues. All we know now about the method by which rotenone kills insects is that it slows the rate of heart action and breathing. The symptoms may indicate disturbances in the functions of practically any tissues so they really tell us little of the fundamental basis for rotenone poisoning.
Several theories have been advanced to explain how oils kill insects: Oils penetrate the insect's breathing tubes, thus causing suffocation; or they penetrate the tissues and poison them; or certain poisonous, volatile substances in the oils kill by penetrating the tissues as gases. None of the theories has been proved. Maybe each may have some merit, depending on the oil in question.
Nonvolatile oils (such as mineral oil) that contain no poisonous compounds might kill an insect through suffocation. For oils (such as kerosene) that contain volatile, poisonous constituents, the second and third theories might account for the killing action.
In vertebrates, such volatile petroleums as gasoline act first as stimulants then as depressants of the central nervous system. Death is due to respiratory failure if the animal is exposed to the oil for a long time. Work done by George D. Shafer many years ago at the Michigan Agricultural Experiment Station indicates that a similar action occurs in insects. E. H. Smith and G. W. Pearce of the New York State Agricultural Experiment Station demonstrated that oil does not kill eggs of the oriental fruit moth by depriving them of oxygen (suffocation). They obtained some evidence that the oil prevented unknown poisonous substances formed by the egg from passing outward through the eggshell.
The dinitrophenols are used in several phases of insect control most commonly the sodium, calcium, and dicyclohexylamine salts of 2,4,dinitro-6-cyclohexylphenol and the sodium and calcium salts of 4,6,dinitro-o-cresol.
Dinitrophenol increases the metabolic rate of warm-blooded animals. Perhaps the poison acts directly on cells, causing them to increase the rate at which they use oxygen. Fat metabolism is involved because the excess oxygen is used only for burning this body food. Dinitrophenol and dinitrocresol act in the same manner on insects and raise the oxygen requirements by as much as three times the normal amount. The mechanism by which the dinitrophenols cause cells to use abnormally high amounts of oxygen has not been determined.
The characteristic tremors of DDT poisoning are symptoms of a disturbance of the nervous system.
The sensory nerves which carry impulses to the central nervous system--are the most sensitive to DDT poisoning, the nerve ganglia the least sensitive. When DDT gets on an insect's body, it affects hundreds of sensory nerve endings. The nerves then produce impulses faster and stronger than normal. These cause the nerves responsible for moving muscles to produce the tremors typical of DDT poisoning. The capacity of the central nervous system to coordinate sensory impulses is also disrupted, as seen in the stumbling gait and general instability of the insect.
We do not know why DDT poisons nervous tissue. It has been suspected that DDT poisons the enzymes cholinesterase, which is important in the proper functioning of nerves, but considerable research has failed to show that DDT affects the enzyme. Perhaps another enzyme system in nervous tissue is involved. One theory is that DDT causes a depletion of calcium in nervous tissue, which in turn causes spontaneous activity of the nerve.
Promising leads are emerging from research on house flies that are resistant to DDT. Flies can change DDT in their bodies to a nonpoisonous substance and DDT-resistant flies can do this faster than susceptible flies can. The chemical processes involved in this breakdown of DDT are being elucidated and should tell us much about the mode of action of DDT.
Other effects of DDT on the physiology of insects include an increase in the consumption of oxygen and a decrease in the amount of stored food substances in the body. Those are probably secondary effects of DDT poisoning.
Benzene hexachloride occurs in several forms, or isomers, each of which has a slightly different molecular shape. Of the 16 possible isomers, 5 are known the alpha, beta, gamma, delta, and epsilon. The gamma isomer, commonly called lindane, is several hundred times more toxic to insects than the others are.
In vertebrate animals, gamma benzene hexachloride causes stimulation of the central nervous system, but the beta and delta isomers cause depression. The external symptoms of poisoning in insects resemble those of DDT, except that they usually appear more rapidly. As in DDT poisoning, the tremors suggest an effect upon the nervous system, but whether the mechanism of poisoning is the same as that Of DDT remains for future research to explain.