In studying the mode of action of an insecticide, we often rely for clues on what we know of the action of the poi- Hoyv Insecticides son on man or other higher animals. Sometimes the mode of action may be Poison Insects similar in vertebrates and in insects, but without experimental evidence it is John J. Pratt, Jr,, Frank H. Bahers unwise to assume that such a similarity exists. The poisonous properties of the in- Somebody has said that because in- organic arsenic compounds (paris sects are small an insecticide kills them green, calcium and lead arsenate, all over. Our knowledge of the subject sodium arsenite ) are due to the forma- is incomplete, but it is enough to belie tion of the w^ater-soluble compounds, the statement. arsenious or arsenic acid, in the diges- Poisons affect the normal functions tive tract. of specific cells and tissues of insects Arsenic is considered a general pro- just as they are known to do in humans toplasmic poison ; that is, it poisons the and other higher animals. Basically contents of all types of cells. Most tis- some chemical process in the animal is sues and organs therefore are affected affected so as to bring about changes in arsenic poisoning. One well-known in its functions. Those changes are sec- effect of arsenic on vertebrate animals ondary to the original process that was is the abrasion and destruction of the affected and arc frequently mistaken lining of the intestine. A similar de- for the initial action of the poison. struction occurs in the mid-intestine of A complete knowledge of the way a insects. Often it is said that such de- chemical poisons an insect would have struction is the primary reason that great value in the formulation of in- arsenic insecticides kill insects. If that secticides. While preparing an insecti- were true, it still would not explain cidal mixture, for example, we could what biochemical process is disturbed add a substance that would help the in order to bring about destruction of poison reach the target—the organ or the intestinal cells. Investigations with tissue it acts upon. Chemicals could be vertebrate animals have shown that added to weaken or destroy the mecha- arsenic poisons unidentified enzymes, nisms that protect the insect against which function in the metabolism of the poison in question. If we know how carbohydrates by cells. Probably arse- one poison acts, we could select or nic acts on the insect system in the same synthesize other chemicals of similar manner. action. Research is giving us that Nicotine first stimulates and then de- knowledge so that before too long such presses the nervous system of animals. ideals should become realities. Paralysis follows rapidly and results in Insecticides have been classified ac- the failure of organs to function. In cording to the way they get into the insects, as in higher animals, the poi- insect's body cavity: Stomach poisons soning action of nicotine occurs in the are eaten, contact poisons enter nerve ganglia, which are clumps of through the skin, and fumigants enter nerve tissue at various places in the through the breathing tubes or the skin nervous system. Nicotine seems to have as gases. Some insecticides may enter practically no effect on nerve fibers or by all three routes. But often such a on the junctions of nerves v^^ith mus- classification is used wrongly to refer cles. The chemical process of nicotine to the mode of actioîi of an insecti- poisoning in insects is not known. cide—an entirely different term, which Pyrethrum powder, the ground flow- means the way in which a chemical ers of certain species of the chrysan- acts on an animal's system. themum, contains the chemicals, py- OTOiríé^-.^í— 15 205 206 Yearbook of Agriculture 1952 rethrin I and II and cinerin I and 11, Station indicates that a similar action which are the main toxic principles. occurs in insects. E. H. Smith and G. The rapid paralyzing action of pyre- W. Pearce of the New York State Agri- thrum is evident to anybody who has cultural Experiment Station demon- sprayed a room with a household fly strated that oil does not kill eggs of spray and watched the flies drop almost the oriental fruit moth by depriving immediately to the floor. The insects them of oxygen (suffocation). They ob- recover from the paralysis, however, tained some evidence that the oil pre- unless a lethal amount of the poison vented unknown poisonous substances gets on them. Pyrethrin acts directly on formed by the egg from passing out- the central nervous system of insects. ward through the eggshell. The paralysis is a result of the block- The dinitrophenols are used in sev- ing of transmission of nerve impulses. eral phases of insect control—most We know that destructive changes oc- commonly the sodium, calcium, and cur in the nervous tissue of insects poi- dicyclohexylamine salts of 2,4,dinitro- soned with pyrethrin, but the reason 6-cyclohexylphenol and the sodium and for the changes is obscure. calcium salts of 4,6,dinitro-o-crcsol. Rotenone causes paralysis of the Dinitrophenol increases the meta- breathing mechanism in mammals, bolic rate of warm-blooded animals. possibly by acting on bronchial tissues. Perhaps the poison acts directly on All we know now about the method by cells, causing them to increase the rate which rotenone kills insects is that it at which they use oxygen. Fat metab- slows the rate of heart action and olism is involved because the excess breathing. The symptoms may indicate oxygen is used only for burning this disturbances in the functions of prac- body food. Dinitrophenol and dinitro- tically any tissues so they really tell us cresol act in the same manner on in- little of the fundamental basis for sects and raise the oxygen require- rotenone poisoning. ments by as much as three times the Several theories have been advanced normal amount. The mechanism by to explain how oils kill insects: Oils which the dinitrophenols cause cells to penetrate the insect's breathing tubes, use abnormally high amounts of oxy- thus causing suffocation; or they pene- gen has not been determined. trate the tissues and poison them; or The characteristic tremors of DDT certain poisonous, volatile substances poisoning are symptoms of a disturb- in the oils kill by penetrating the tissues ance of the nervous system. as gases. None of the theories has been The sensory nerves—which carry proved. Maybe each may have some impulses to the central nervous sys- merit, depending on the oil in ques- tem—are the most sensitive to DDT tion. poisoning, the nerve ganglia the least Nonvolatile oils (such as mineral sensitive. When DDT gets on an in- oil) that contain no poisonous com- sect's body, it affects hundreds of sen- pounds might kill an insect through sory nerve endings. The nerves then suffocation. For oils (such as kerosene) produce impulses faster and stronger that contain volatile, poisonous con- than normal. These cause the nerves stituents, the second and third theories responsible for moving muscles to pro- might account for the killing action. duce the tremors typical of DDT poi- In vertebrates, such volatile petro- soning. The capacity of the central leums as gasoline act first as stimulants nervous system to coordinate sensory then as depressants of the central nerv- impulses is also disrupted—as seen in ous system. Death is due to respiratory the stumbling gait and general in- failure if the animal is exposed to the stability of the insect. oil for a long time. Work done by We do not know why DDT poisons George D. Shafer many years ago at nervous tissue. It has been suspected the Michigan Agricultural Experiment that DDT poisons the enzymes cholin- How Insecticides Poison Insects 207 esterase, which is important in the B vitamins—that is, it might compete proper functioning of nerves, but con- with and replace m^i"o-inositol in some siderable research has failed to show vital physiological process. Meso-moú- that DDT affects the enzyme. Perhaps tol will alleviate somewhat the poison- another enzyme system in nervous ing of certain yeasts by gamma benzene tissue is involved. One theory is that hexachloride, but several attempts to DDT causes a depletion of calcium in demonstrate a similar process in ins(xts nervous tissue, w'hich in turn causes have failed. Chemical investigations, spontaneous activity of the nerve. which now indicate that mi?5o-inositol Promising leads are emerging from and gamma benzene hexachloride do research on house flies that are resistant not have similar molecular shapes, may to DDT. Flies can change DDT in explain the failure- to prove the hy- their bodies to a nonpoisonous sub- pothesis. stance and DDT-resistant flies can do The organic phosphates—hexaethyl this faster than susceptible flies can. tetraphosphate (HETP), tetraethyl llie chemical processes involved in pyrophosphate (TEPP), and diethyl this breakdown of DDT are being elu- p-nitrophenyl thiophosphate (para- cidated and should tell us much about thion) —are highly toxic to animals. In the mode of action of DDT. insects and in warm-blooded animals, Other efl'ects of DDT on the physi- they poison the cholinesterase. ology of insects include an increase in A chemical called acetylcholine is the consumption of oxygen and a de- formed in certain nerves and aids in crease in the amount of stored food the transmission of nerve impulses. substances in the body. Those are If it is not destroyed immediately probably secondary efl'ects of DDT after it has served its purpose, it will poisoning.