DDT: A renaissance? Robert M. Devlin University of Massachusetts, East Wareham, Mass. 02538
When William Ruckelshaus, former administrator of the EPA, banned the use of DDT in the U.S. on June 14, 1972, he triggered a lot of controversy. Some felt it encouraged the use of more toxic compounds. Others felt it discouraged the production of DDT, causing hardships to many of the undeveloped nations where malaria is prevalent. Malaria, the communicable protozoan disease transmitted by the anopheline mosquito, has been successfully controlled by DDT. As Dr. Robert White-Stevens of the Bureau of Conservation and Environmental Science at Rutgers University has stated, ”More human beings have perished from malaria than all other infectious diseases com bined .” Before the advent of DDT, for example, the malariainfested island of Sardinia, Italy, was inhabited primarily by poor peasants who herded mountain sheep and goats for a living. With DDT spraying, the disease was completely eradicated, going from 78,000 cases to none in just 10 years. Sardinia became one of the better resort areas of the Mediterranean. Before DDT, India suffered over 75 million cases of the disease which accounted for five million deaths per year. After the World Health Organization (WHO) decided in the mid-1950’s to use DDT in India, the number of malaria cases decreased to five million in 10 years and deaths dropped below one hundred thousand. Even more dramatic, the life expectancy of the average Indian during those 10 years increased from 32 to 47 years. On February 2, 1971, officials of WHO made the following statement, “More than 1,000 million people have been freed from the risk of malaria in the past 25 years, mostly thanks to DDT. This is an achievement unparalleled in the annals of public health.” In the malarious countries, many hundreds of thousands of acres of land are now productive, where before DDT they were deserted mosquito-infested wastelands. For hungry, land-starved, overpopulated countries like India, Ceylon, and some South American countries, DDT has been a blessing. The vigor of malaria-free people, directed to food production in formerly malarious wetlands, produced better harvests and therefore, more food. Former Surgeon General of the U.S. Public Health Service, Dr. Jesse L. Steinfeld, in a prepared testimony before the EPA in September 1971, showed his deep concern over the effect a U.S. ban on DDT would have on the malarious countries of the world. The following is a quote from his testimony. “A decision that would result in stopping the production of DDT in the U.S. could in essence be a denial of the use of DDT to some of the most highly malarious areas of the world. The direct result of such a denial would be to bring down upon the affected countries, most of them presently considered to be friendly nations, the affliction of hundreds of millions of cases of malaria and millions of deaths within the next decade. The consequences of denying the use of DDT to the emerging, 322
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developing nations of the world in their struggle against malaria and other vector-borne diseases would be extremely severe.” In developing nations, DDT is also needed to combat pests that invade crops, livestock, and man. I t has been estimated that 1.5 million acres of fir forests in Oregon and Washington will be defoliated by caterpillars of the Douglas fir tussock moth in 1974. The only effective control of the tussock moth is DDT, and, unless foresters are allowed to use the pesticide, these very valuable forests may be lost forever. Literally, the lives of millions of human beings depend on DDT. Not only does DDT control malaria, it also controls other serious diseases, including encephalitis, bubonic plague, yellow fever, cutaneous leishmaniasis, phlebotomus (sand-fly) fever, dengue fever, and Carrion’s disease.
Does it kill birds? Environmentalists claim that DDT is responsible for the drastic declines in the number of osprey, Peregrine falcons, and eagles. Some aspects of this problem are neglected by the environmentalists. I t has been repeatedly established in the pre-DDT literature that these birds of prey were becoming extinct, or at the very least were experiencing severe population declines. Dr. Donald Spencer, a well-known wildlife biologist, has quoted reports, written by ornithologists in the late 1800’s, describing how the osprey was threatened at that time. In 1943, before the use of DDT, Dr. Joseph Hickey of the Audubon Society wrote that a 70% decline in ospreys had occurred as a result of “pole trapping” around fish hatcheries. Peregrine falcons also were becoming rare before DDT was first used in 1945. I n 1940, there were approximately 170 mating pairs in the U.S. Almost 50 years before DDT was used, the great tree-nesting Peregrine population of eastern U.S. had vanished and the extinction of the rare cliff-nesting Peregrines was imminent. Eagles were declining in numbers as far back as 1921. They have battled the disappearance of their food supplies (fish) with the advent of polluted rivers. They have coped with man and his firearms, in Alaska, Wyoming, Colorado, and other states that encourage the sport of eagle killing. Of the 120,645 eagle deaths reported in literature over the past 57 years, eight resulted from other pesticides and only one from DDT. The environmentalists also charge that DDT causes the laying of thin-shelled eggs which decrease the chance of reproductive success. However, there has been no conclusive evidence to support this allegation. An exhaustive 1969 report on the subject by the Mrak Commission for the Department of Health, Education, and Welfare, stated that “There seems at this time to be
a very reasonable doubt that residues of the chlorinated hydrocarbon pesticides-DDT and others-are found in the natural feed of these birds at levels equivalent to the dosage necessary to.produce these effects." In addition, the Wilson Advisory Committee on Pesticides and Other Toxic Chemicals found, in 1969, evidence less than precise for the postulated relationship. between persistent pesticides and the disappearance of the Peregrine falcon (presumably due to eggshell thinning). The Neuberger Committee in 1969 also viewed this relationship as unproved. Nevertheless, a comparison between museu m specimens and eggs laid by raptors after World War / I show a reduction in eggshell thickness since the introduction of DDT. It should be remembered that numerous other chemicals have been released into the environment in great quantities since World War I I . To implicate DDT as the causal relationship between use of the pesticide and eggshell thinning should be demonstrated, and to date this has not been done.
PCBs from the extracts they were analyzing for DDT, although PCB has been found in the tissues of birds and their eggs, in man, fish, and in insects. PCBs are insoluble in water and consequently are stored in the fat tissues of organisms that ingest them. I t is now wellknown that PCBs produce an almost identical gas chromatograph to DDT and DDE. Before 1967, many of the reports on the quantities of DDT and DDE present in samples were exaggerated due to the presence of PCBs, thus invalidating any correlation between the amount of DDT found and the extent of eggshell thinning. Another factor that should be considered is that, despite our expertise in detecting trace amounts of pesticides in the environment, we cannot absolutely be sure of the accuracy of the methods. Recently at the University of Wisconsin, soil samples that had been sealed since 1910 were analyzed for organochlorine pesticides. In 32 of the 34 samples analyzed, several pesticides were detected, even though they did not even exist until 1940.
Does it cause thin eggshells? It cannot be denied that DDT and its metabolite DDE have been found with some consistency in thin-shelled eggs, and in some studies, a rough correlation has been shown between the concentration of DDE found and the amount of thinning observed. Nor can it be denied that the thinning first observed in the eggs of raptors coincided remarkably well with the introduction of DDT use. It should also be considered that, in the vast majority of cases, DDT and DDE were the only chemicals looked for, even though there were many chemicals that came into general use at about the same time as DDT. In other words, DDT was accused because it was present; not because it was shown actually to upset the metabolism of the bird in such a manner as to cause it to produce eggs with thinner-than-normal shells. A good example of a group of chemicals that should have been under suspicion and looked for from the very first is the polychlorinated biphenyls (PCBs). Before 1967, residue chemists made no attempt to eliminate
Action mechanism Recent studies have attempted to establish a physiological mechanism by which DDT causes the formation of thinner-than-normal shells. To date this mechanism has not been elucidated, but possible modes of action have been suggested. Chlorinated hydrocarbons such as DDT could stimulate hepatic microsomal enzymes that could then: 0 degrade the steroid hormones (such as oestradiol) essential for calcification 0 inhibit medullary bond deposition, the main source of calcium during shell formation 0 inhibit carbonic anyhydrase activity in the avian shell gland that provides the carbonate ions necessary for calcium carbonate deposition. Dr. David Peakall (1969) and his associates at Cornell University have shown in at least two studies that the hepatic microsomes of pigeons fed DDT form greater amounts of polar metabolites from oestradiol than microsomes of untreated birds. As might be expected, the increased metabolism of oestradiol caused a significant reduction of the hormone in the blood of treated pigeons. This would suggest that DDT may very well be involved in the thinning of eggshells. However, it should be noted that, although a correlation between the amounts of oestradiol in the blood and shell formation has been established, a causal link between the two has never been shown. In addition, a study by Stephen et al. (1970) on the domestic chicken showed that DDT did not induce but inhibited chicken microsomal enzymes. And PCBs, which are at least as abundant as the chlorinated hydrocarbon pesticides in the environment, have been found by Risebrough et al. (1968) to be "powerful inducers of hepatic enzymes which degrade oestradiol." Volume 8 , Number 4 , April 1974
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Deposition of calcium in the medullaries-hollow parts of the skeleton-is thought to be primarily under the control of oestradiol In the previously mentioned studies of pigeons by Peakall, a drop in blood oestradiol in birds fed DDT was accompanied by a decrease in medullary bone deposition. Peakall's findings in this regard were verified, also with pigeons, by Oestreicher and his associates at Stony Brook. However, a study by the U S Department of Agriculture (Bitman et al 1969) reported no decrease in the deposition of meddllary bone calcium in quail fed large quantities of DDT. A number of investigators have stressed that carbonic anyhdrase plays an active role in eggshell formation This supposition has been questioned by Mueller (1962) because he did not find any change in carbonic anhydrase activity during the different stages of egg formation. Heald et al. (1968) could not demonstrate any significant correlation between carbonic anhydrase activity and shell strength. Nevertheless, the fact that inhibitors of carbonic anhydrase, such as sulfanilamide, reduce the rate of calcium deposition in the shells of both birds and invertebrates strongly confirms the enzyme's role in eggshell formation. In separate studies, Peakall with pigeons and Bitman with Japanese quail, it was shown that DDT can cause a significant reduction in carbonic anhydrase activity. However, their methods of assessing the activity of carbonic anhydrase in vitro has been criticized by Dr Barry Dvorchik and co-workers at the University of Florida College of Medicine. Dvorchik (1971) stated that "it is an unsatisfactory way to investigate inhibitors, because drug (DDT) and enzyme are analyzed together in vitro. This dilutes and distorts the original relation."
Emotions aroused The news media and the publications of special interest groups suggest that once DDT is applied, it persists in the environment indefinitely. Nothing could be further from the truth. At a 1971 hearing concerning federal pesticide legislation, Dr. J. Gordon Edwards submitted a list of more than one hundred scientific references dealing with the breakdown of DDT and its residues. Edwards stated, " I t is obvious that DDT degrades readily in the presence of living things, in organic soil and water, in alkaline soil and water, in the blood or digestive tract of Robert M. Devlin, associate professor of plant physiology at the University of Massachusetts, is primarily interested in the toxicity of pesticides and the effects of plant growth hormones. He has published many papers on pesticides and books on plant physiology. 324
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most kinds of animals, in cold, in heat, and in sunlight. It is untruthful and misleading for any person or organization to imply that DDT does not break down normally under environmental conditions." Bacteria of the soil and digestive tract, fungi, and animals-invertebrates and vertebrates-are all capable of degrading DDT. Even dying insects can degrade up to 50% of the DDT they have absorbed. The common deer mouse takes only 4'/2 days to rid itself of 50% of the DDT it absorbs and the half-life of DDT in the tissues of the common pigeon is only 28 days. Indeed, wildlife biologist D. A. Spencer has stated that he knows "of no species of fish, bird, or mammal, in which studies have been conducted, that cannot degrade and eliminate DDT from their bodies." In an experiment at the EPA Laboratory in Gulf Breeze, Fla., it was shown that 90% of the DDT placed in a bottle of natural seawater completely degrades and disappears in a period of 38 days. It has also been suggested that DDT is hazardous to human health despite its safety record. The most influential speculations were those made by Rachel Carson in Silent Spring. She suggested that persistent pesticides could cause cancer by upsetting the delicate hormonal balance of an organism including the human organism. In other words, without any evidence at all, DDT was called a carcinogen (that which causes cancer). This disclosure had an explosive and dramatic effect on the public whose natural fear of cancer is understandable. A thorough reading of the literature will show that DDT does not induce cancer. Since Silent Spring, the hypothesis that DDT is a carcinogen has been tested in a great number of experiments with mice, rats, hamsters, and dogs. Although in the vast majority of cases negative results have been obtained, the interest, of course, is in those experiments which suggest that the pesticide might have some carcinogenic properties. A study by Fitzhugh and Nelson (1947) of the FDA on rats fed DDT for two years gave the first hint of possible carcinogenic properties. The authors described the treated rats as having a tendency toward hepatocarcinogenesis (formation of liver tumors). They felt that the liver tumors found could be regarded as low-grade hepatic cell carcinomas. Their observations, however, have been criticized because it was shown in their paper that the DDT effects on the liver were reversible. It is now known that the changes produced by DDT in rat liver are not characteristic of DDT alone, but similar if not identical to those produced by phenobarbital, the botanical insecticide pyrethrum, and others. The changes in the liver produced by these compounds primarily involve the endoplasmic reticulum for formation of microsomal enzymes. I t is now well-known that the effects of carcinogens on
target tissues leading to tumor formation are irreversible. The study that has created by far the greatest furor is that performed by the Bionetics Research Laboratories (BRL) for the National Cancer Institute in 1969. This was a broad study of the carcinogenic potential of a number of synthetic compounds including several pesticides. The dose rate was 116,000 times greater than that obtained in the average U.S. daily diet. No attempt was made to distinguish benign from malignant tumors. The Technical Panel on Carcinogenesis set up by the Mrak Commission concluded that the BRL report demonstrated that DDT increased the incidence of cancer in mice under the experimental conditions employed. However, this does not prove carcinogenicity for human beings at the very much lower level to which they are actually exposed. The panel was not unanimous in its evaluation of the biological significance of the BRL study. It was agreed that the study was designed, with the use of strains of mice in which spontaneous cancer is common, to achieve the greatest possible sensitivity to potential carcinogens. The use of very high doses of chemicals and the feeding of these chemicals via stomach tubes in the preweaning period was to some members of the panel unrealistic and of questionable value. Some members also felt that the BRL study may have been unfairly biased because of a lack of randomization. The finding by the BRL study of hepatomas in certain strains of mice fed DDT has recently been confirmed by studies at the International Agency for Research on Cancer (IARC) at Lyons and Milan. More realistic doses were used and DDT was administered only through the diet. However, hepatomas are apparently benign liver tumors and should not be confused with malignant tumors which are true cancerous growths. Professional opinion is divided as to whether hepatomas constitute the early stages in malignant tumor formation. Dr. John Higginson, director of IARC and well-known pathologist and epidemiologist, testified that the significance to man of hepatomas in mice fed DDT is unknown. The fact that some of the strains of mice used for
testing carcinogenicity of DDT have a tendency to form hepatomas, and the fact that the hepatomas formed cannot be compared to anything found in man, makes the use of mice in this type of study of questionable value. For example, two substances, which have produced tumors in mice, isoniazide and penicillin-(;, are completely safe for man based on human experience. Results from epidemiological tests are also completely negative so far. Extensive epidemiological studies, conducted by the WHO, are now in progress in many countries including the U.S., Brazil, Israel, and India. To date, no correlation has been shown between the levels of DDT found and the prevalence of cancer. With the present knowledge in mind, Higginson has concluded that there is no evidence that DDT is in any way a carcinogen to man. His belief was supported by the American Medical Association (May 1970), and the Surgeon General of the U.S. Public Health Servce.
Still a dilemma It cannot be proved that DDT is completely harmless when used in the proper manner, because it is logically impossible to prove a negative. There is a lack of evidence of harm after 25 years of heavy use and exposure: The distribution of DDT throughout the world for public health and agricultural purposes has been massive and virtually free of acute or chronic adverse effects on man. Dr. W. J. Hayes, renowned toxicologist, sums it up well: "We live in a chemical age. In the long run we have no choice but to adapt to it. There just are not enough people who will part willingly with the comforts such as increased food, shelter, and health, which modern chemistry has brought. By proper toxicologlcal study, it is possible to determine that some compounds are too dangerous for almost any use, while others are suitable for one use, but not for another. Unless these distinctions can be made at a professional level and enforced by the appropriate federal, state, and local agencies, without emotional appeals in the mass media, the people of this country may suffer a loss of confidence not only in their government but in the organization of society. Through a nameless fear we may not only lose our position of leadership, but suffer needless privation. The problem is much broader than the fate of any particular pesticide, drug, or food additive that has been in the news recently." Additional reading Adler, C. A,, "Ecological Fantasies," Green Eagle Press, New York, N.Y., 1973. Beatty, R. G., "The DDT Myth," John Day, New York, N.Y., 1973. Maddox, J., "The Doomsday Syndrome," McGraw-Hill, New York, N.Y., 1972. Volume 8 , Number 4, April 1974 325
