EXCERPTS FROM SAVING THE MOSQUITOES -- The War on DDT
1. Some Background Intelligence: Malaria
The biggest single killer of human beings through history has been malaria. Before the 1940s, 300 million new cases were contracted annually worldwide, and of those stricken, 3 million died. 6 to 7 million cases occurred every year in the United States, primarily in the South and parts of California.
Malaria is caused by a genus of protozoan--the simplest, single-cell animal form--called Plasmodium, which comes in four species. In the human bloodstream they take a form known as merozoites, which burrow into the red blood cells and reproduce asexually, each one producing 6 to 26 new individuals which burst out to infect new blood cells on a cycle that repeats every 48 hours. When the number of merozoites exceeds about 50 per cubic milliliter of blood (a typical drop), the victim suffers a malaria attack every 48 hours. In a heavily infected person, the number of plasmodia present can be as high as 2 million per milliliter.
The severity of the symptoms depends on the species involved, but a typical attack consists of severe frontal headache and pain in the neck, lower back, and limbs, dizziness and general malaise, accompanied by waves of chill and seizures alternating with fever temperatures of up to 104oF and profuse sweating, acute thirst and vomiting being not uncommon. The falciparum variety can kill up to 40 percent of those affected. Deaths occur mainly among children under 5 years old. For those who survive, the pattern continues for several months, and then gives way to symptom-free periods punctuated by relapses that occur over anywhere from a year to ten years. The effects can be sufficiently debilitating to incapacitate 80 percent of a workforce, with such consequences as preventing harvesting of a food crop, thus rendering a population vulnerable to all of the opportunistic threats that come with malnutrition and an impaired immune system, such as hepatitis, tuberculosis, dysentery, and typhoid fever. Transmission from person to person takes place through the ingestion of blood by females of the Anopheles mosquito, and re-injection of Plasmodium into a new victim via the saliva after undergoing another part of its life cycle within the mosquito's stomach.
In 1939, Paul Mueller, a chemist working for J.R. Geigy S.S. in Switzerland, developed a compound, ichloro-diphenyl-trichloroethane--DDT--that was cheap, easy to produce and use, nontoxic to mammals and plants, but extremely toxic on contact to insects and various other arthropods. The Allies quickly recognized its value for wartime use and found it 100 percent effective as a fumigant against the tics and body lice that transmit typhus, which in World War One had killed millions of soldiers and civilians in Europe. In early 1944 an incipient typhus epidemic in Naples was halted with no adverse side effects apart from a few cases of very minor skin irritation, after efforts with more conventional agents achieved only limited results. A plague epidemic in Dakar, West Africa, was stopped by using DDT to eliminate the carrier fleas, and it was mobilized with great success against malaria in the Pacific theater, Southeast Asia, and Africa. After the war, DDT became widely available not only for the reduction of insect-transmitted human diseases but also of a wide range of agricultural, timber, and animal pests. The results from around the world seemed to bear out its promise as the perfect insecticide.
For combating malaria, it was sufficient to spray the walls and ceiling of dwellings once or twice a year. Malaria mosquitoes rested in these places when inactive, and the DDT penetrated via their feet. Incidence in India in the 1940s was over 100 million cases annually, of which 2.5 million died. By 1962 these numbers were down to 5 million and 150,000, while life expectancy had risen from 32 to 47. A 1.5 ounce shot glass of DDT solution covered 12 by 12 feet of wall. The cost per human life saved worked out at about 20 cents per year. In the same period, India's wheat production increased from less than 25 million tons to over 100 million tons per year due to a combination of pest reduction and a healthier workforce. Ceylon--now Sri Lanka--reduced its malaria figures from 3 million cases and 12,000 deaths per year in the early 50s to 31 cases total in 1962, and 17 cases the year after, with zero deaths. Pakistan reported 7 million cases of malaria in 1961, which after the introduction of an aggressive spraying program had fallen to 9,500 by 1967.
In Africa, in what is considered to be its second most important medical benefit after reducing malaria, DDT proved effective in a program to control the bloodsucking tsetse fly, which transmits the protozoan responsible for deadly sleeping sickness and also fatal cattle diseases. According to the World Health Organization, 40 million square miles of land that had been rendered uninhabitable for humans because of tsetse fly infestation became available.
Another serious menace in parts of Africa and Central American is the blackfly that transmits roundworms causing "river blindness" in humans. Before DDT was introduced, more than 20,000 victims of this affliction in Africa were blind, with incidences as high as 30 percent of the populations of some villages. The larvae of the flies live in fast-flowing streams and had proved impossible to control until the occurrence of a fortunate accident in the 1950s in the Volta River basin, when a mule carrying DDT powder to a spraying project slipped while fording a stream and spilled its load into the water. Blackfly larvae were killed for a mile downstream without ill effects on other forms of aquatic life, and a river treatment program was implemented subsequently, greatly reducing the number of river blindness sufferers. No masks or protective clothing was required for the operatives. In this entire period no instance of DDT-induced illness was reported among the estimated 130,000 spraying personnel employed, or the millions of people whose dwellings were treated.
Such being the perversity of human nature, it could only be a matter of time before people started finding reasons why something as good as that couldn't be allowed to continue.
2. (From THE 1971 EPA HEARINGS)
Well-Designed, Well-Executed Experiments: DDT As a Carcinogen
One of the major causes of public concern was the claim that even small amounts of DDT residues could accumulate in the body tissues over time and cause cancers. Samuel Epstein, a principal witness for the EDF, testified that DDT had been shown to be carcinogenic in well-designed experiments, and that in his opinion there was no safe exposure level. This was immediately picked up and echoed widely by the popular press, and also cited in the "Point of View" column in Science (175: 610). None of the press, however, gave space to the testimonies of several other experts, among them Jesse Steinfield, the U.S. Surgeon General, and John Higginson, Director of the International Agency for Research on Cancer, that DDT is not a human carcinogen. Neither did Science condescend to publish a letter from W.H. Butler of the British Medical Research Council, who also testified at the hearing, opposing the view expressed by Epstein. So, regardless of the hyped phrases and the font sizes in which the headlines were set, what can be made of the facts?
Repeated incessantly by the media, and still heard today, was the mantra that a single molecule of a carcinogen is capable of initiating a tumor, and hence no level of exposure is safe. All one can say here is that this goes against the long-established principle of toxicology that recognizes a threshold of dose below which adverse effects become undetectable--and hence to assert their reality becomes a matter of faith, not science. This was acknowledged as far back as the 16th century by Paracelsus, who noted that"The dose makes the poison." Were it not so, it is doubtful whether any individual could ever survive to maturity and perpetuate the species, for in sufficient doses and under suitable conditions just about anything can be made to induce cancers, examples being honey, egg yolk, plain table salt, and even water. Of course, anyone is free to disagree. But when such a view is presented in such a way that it is likely to be taken as representative of expert opinion, the result is clearly misleading.
Now let's return to the well-designed experiments that showed DDT to be a carcinogen. Extensive human and animal studies to assess the toxicity of DDT had been conducted ever since its introduction. In 1956, a group of human volunteers ingesting DDT for periods of from 12 to 18 months at 1,750 times the average amount for the U.S. population showed no adverse effects either at the conclusion of the trial or in follow-up studies 5 years later. A 1964 study of the incidence of different forms of cancer from all areas of the U.S. from 1927 to the early 1960s showed no correlation with the use patterns of DDT, nor with its presence in food or human body tissues. Similar results were reported from studies of industrial workers exposed for years to 600 to 900 times the intake of the general population, inhabitants of tropical countries who had been liberally dusted with DDT, and the work crews employed in applying it as spray and powder. The FDA had conducted prolonged investigations of 15 groups of heavily exposed persons, each group consisting of 100 individuals matched with controls, that looked especially for gradual or delayed effects but found none.
Epstein's response was to dismiss all of these studies as "irrelevant" or "a travesty of the scientific data." The irrelevance seemed to follow from his emphatic statement that there were no data to be found anywhere in the literature on chronic inhalation studies, which was a significant mode of human exposure. Claus and Bolander offer a list of references to precisely such studies covering the period 1945 to 1969 that were right there, in the literature. A direct contradiction. What more can be said? The latter comment is apparently to be taken as meaning that it's a travesty of the data to find a substance safe simply because no carcinogenic effects can be found among heavily exposed humans after many years.
This attrition left just 7 papers presumably judged to be relevant, separated into two categories: (1) Three that were considered "highly suggestive" but flawed in method or statistical analysis, and (2) The remaining four, "conclusive." One of the first group dealt with rainbow trout (exceptionally sensitive to DDT) reported as developing liver cancers. However, the doses involved, over a period of 20 months, were up to 27,000 times what other researchers had found to be lethal, which makes it difficult to see how any of the fish could have lived at all, let alone develop tumors of any kind, and so results can only be suspect. The second group included two WHO studies that were in progress at the time, one being conducted in France, the other in Italy. Since they were as yet incomplete, the appellation "conclusive" is hardly justified. What, then, of the four papers that this leaves?
First, the two group (1) cases. In 1969, Tarján and Kemény, in Hungary, feeding low dosages to successive generations of a strain of inbred mice, reported a higher tumor incidence among the experimental animals than the controls, becoming statistically significant in the third and fourth generations. But there were puzzling features. For one thing, tumors were lower in the controls than in the breeding stock, indicating some factor in the experiment that was not accounted for. Further, while the strain used was supposed to be leukemia-free, leukemia in fact occurred in both the experimental and control groups. Finally, nothing comparable--nor any cancer of any type--had been found by other researchers working with similar dose levels. A subsequent WHO investigation showed that all of the oddities could be explained by suspected contamination of the feed with aflatoxins--among the most potent of naturally occurring carcinogens. So one can agree with Epstein's assessment of the study's being defective in method or analysis. But of "highly suggestive"? Hardly.
The remaining paper in this category described an earlier series of several experiments with rats. Evaluation of the results was complicated by the fact that more than two thirds of the test animals were lost for one reason or another over the two-year period. Of the 75 from 228 that survived, 4 developed liver tumors compared to 1 percent of the controls. Whether this is statistically significant is debatable, since the four came from different test groups, and no relationship was indicated between dose and effect. On the contrary, some of the rats that showed no liver cell necrosis had reportedly existed for 12 weeks on doses that other workers had found to be 100 percent lethal. Subsequent attempts to duplicate the reported results failed. The British pathologist, Cameron, who conducted one of these endeavors, a Fellow of the Royal College of Pathologists, later knighted for his contributions to the field, observed that the 1947 study had employed formalin as a fixative agent for the tissues, which is not suitable for cytological studies on account of its tendency to produce artifacts of precisely the kind that had been identified as hyperplasia nodules. The inference could therefore be made that the results were "highly suggestive" of wrongly fixed tissue.
This leaves us with two studies qualifying as well-designed and well-executed. In this connection Epstein sprang something of a surprise on the defense by introducing data from an in-house FDA experiment performed between 1964 and 1969 that nobody else had heard of, describing it as an excellent piece of work and expressing puzzlement that its findings had never been published. The experiment involved two compounds, DDT and methoxychlor, fed to two strains of inbred mice. Epstein disregarded all the results for the strain-A mice, which experienced high mortality from a bacterial infection. This was not mentioned in the actual report but came to light in a memorandum from one of the researchers later, which included a terse comment that its effect on the study as a whole had not been determined. A second possible contributory factor was found in the 67th week with the discovery that the strain-A had been fed three times the intended dose for an undetermined period of time. Whether this had also been the case with the strain-B mice was not known. Well, one can only speculate that a good reason for refraining from publication and saving further expenditure of funds and effort might be found right there.
Anyway, delving deeper regardless we find that taking both strains together there were actually more tumors among the controls (males 66, females 82) than among the experimental animals (males 63, females 73). For strain-B alone, a slight increase occurs for DDT-fed (males 42, females 50) versus controls (males 39, females 49). However, this applied to benign tumors only. If it is permissible to select just one sub-group from the entire study to make a point, then we could by the same token select just the strain-B females that developed malignant tumors, where the numbers were controls 10, DDT-fed 3. Hence, by a far larger margin, the same study could be shown as equally "conclusively" demonstrating DDT to be an anticarcinogen!
The final paper, however, was the one presented as the proof, the main source that media articles ever since have cited in branding DDT as a carcinogen: the 1969 Bionetics Report, sometimes referred to as the Innes paper, after the first-named of its thirteen authors. The work was part of an ambitious study performed by Bionetics Laboratories, a subsidiary of Litton Industries, under contract to the National Cancer Institute, on the effects of 123 chemical compounds in bioassays on 20,000 mice covering periods of up to 84 weeks. Epstein's confidence notwithstanding, the methods and findings have been widely criticized in the professional literature.
One objection was that the researchers did not assure random distribution of the litters. Genetic disposition counts heavily in tumor occurrences among mice. Subjecting litter mates to the same compound runs the risk that genetic factors can mask the results, making any ensuing statistics worthless. Others were that the study failed to distinguish between malignant tumors and benign nodules, the significance of what was being measured being further obscured by relying on a single figure of "maximum tolerated dose" in lieu of providing more orthodox dose-effect relationships--at levels 100,000 times higher than those of residues typically encountered in food.
But perhaps the greatest oddity, pointed out by Claus and Bolander (p.351) was that whereas the authors of the paper lumped all five control groups together on the grounds that there was no significant variation between them, the actual data showed there to be large differences. For strain-X, as an example, the percentage of mice developing tumors varied from 0 to 41.2 percent for the males and 0 to 16.3 percent for the females. Applying regular statistical procedures reveals that for the group showing the highest tumor incidence--strain-X males at 41.4 percent--with the above degree of variation present in the controls, the maximum part of this that could be attributed to DDT is 5.5 percent, which no amount of manipulation could make significant. Following the same procedure with the strain-Y mice yields higher tumor percentages among the controls than among the DDT-fed groups.
Their skepticism highly aroused by this time, the authors of Ecological Sanity then turned their attention to the report's listing where the tested substances were classified as "tumorigenic," "doubtfully tumorigenic," or "not tumor-producing," i.e. safe. And again, a raft of inconsistencies was found. Substances widely agreed upon as being carcinogenic received a clean score. Others considered to be innocuous--one, in fact, used for the treatment of alcoholics--did not. Compounds with similar molecular structures and chemical behavior received very different ratings. And piperonyl butoxide, which was tested twice, managed to end up on both the "doubtful" and the "safe" lists.
Claus and Bolander point out that a program of this magnitude would involve the preparation of about 48 million tissue sections placed on 2,400,000 microscope slides, requiring 60,000 boxes. Making what appear to be reasonable estimates of the likely workforce, rate of working through such a phenomenal task, and the time available, they doubt that meaningful results would even be possible. They ask (p.362): "What kind of an expert panel is it that can not only so warmly endorse this ambitious but dismally sloppy study and dignify it with the name of the NCI but also provide rationalizations for its obvious weaknesses?"
A Plague of Birds
One of the most serious ravages that can befall woodlands is infestation by the gypsy moth. The larvae devour all the foliage of trees, especially oaks, and in large numbers can strip bare entire areas, forcing other life left without food or habitat to either perish or migrate. This can be unpleasant and even dangerous, as inhabitants of northern New Jersey discovered in the seventies when large numbers of rattlesnakes and copperheads invaded suburban areas there. In 1961, the year before Silent Spring was published, large areas of Pennsylvania were sprayed with DDT to eradicate this pest. The Scranton Bird Club kept careful records but didn't report a single case of bird poisoning. Officials of the National Audubon Society were satisfied that no harm was done to bird life, including nesting birds.
Yet Silent Spring was to state (p.118) that the robin was on the verge of extinction, as was the eagle; (p.111) "Swallows have been hard hit. . . . Our sky overhead was full of them only four years ago. Now we seldom see any." Here we have another instance of assertion being flatly contradicted by the facts, for the very next year ornithologist Roger Tory Peterson described the robin as "probably North America's number one bird" in terms of numbers. The Audubon Society's figures for annual bird counts bore him out, reporting 8.41 robins per observer in 1941 (pre-DDT) and 104.01 for 1960, representing a more-than twelve-fold increase during the years when DDT use was at its highest. The corresponding figures for the eagle and swallow were increases by factors of 2.57 (counts per observer 3.18, 8.17) and 1.25 (0.08, 0.10) respectively. This pattern was general for most of the species listed, showing 21 times more cowbirds, 38 times more blackbirds, and no less than 131 times more gackles, the average total count per observer being 1,480 in 1941 and 5,860 in 1960. Gulls became so abundant on the East Coast that the Audubon Society itself obtained permission to poison 30,000 of them on Tern Island, Mass., in 1971. Wild turkeys increased from their rare status of the pre-DDT years to such numbers that hunters were bagging 130,000 annually. Of the few species that did decrease, some, such as swans, geese, and ducks, are hunted, while bluebirds are known to be susceptible to cold winters.
Ironically, some of the areas were birds seemed to thrive best were those of heaviest DDT use, such as in marshes sprayed to control mosquitos. Part of the reason seems to be that DDT is also effective in reducing insects that transmit bird diseases and which compete with birds for seeds and fruit. But perhaps even more important, DDT triggers the induction of liver enzymes that detoxify potent carcinogens such as aflatoxins that abound in the natural diets of birds
None of this prevented any real or imagined decline in bird population from being immediately attributed to pesticides. A severe reduction in eastern ospreys turned out to be due to high levels of mercury in the fish upon which they fed and to pole traps set around fish hatcheries--blamed on DDT even though reported as early as 1942. Alaska ospreys continued to do well despite high DDT residues. California brown pelicans increased almost threefold during the heavy DDT years but experienced a sharp decline at the beginning of the seventies--two months after an oil spill at Santa Barbara surrounded their breeding island of Anacapa (not mentioned in the reports of the state and federal wildlife agencies). In 1969 the colony had been severely afflicted by an epidemic of Newcastle Disease transmitted from pelican grounds along the Mexican coast of the Gulf of California (also not mentioned). It was later established that helicopter-borne government investigators collected 72 percent (!) of the intact eggs on Anacapa for analysis and shotgunned incubating pelicans in their nests. DDT was also implied as being connected with the reduction of the Texas pelican, even though the decline had been noted in 1939 and attributed to fishermen and hunters.
The great eastern decline in the peregrine falcon was to a large degree due to the zealousness of egg collectors who have been known to rob hundreds of nests year after year, and then attribute the ensuing population collapse to the encroachments of civilization. In 1969, "biologists" studying peregrines in Colville, Alaska, collected fully one third of the eggs from the colony and then dutifully reported that only two-thirds of the expected number of falcons subsequently hatched.
Cracking Open the Eggshell Claims
But by the time of the 1971 hearings, the main allegation, still perpetuating the fiction that a catastrophic fall in bird populations was taking place, had become that DDT was the cause not as a result of immediate toxicity, but indirectly through disruption of the reproductive cycle by the thinning of eggshells. This again goes back to Silent Spring, which states (p.120) "For example, quail into whose diet DDT was introduced throughout the breeding season survived and even produced normal numbers of fertile eggs. But few of the eggs hatched." This was a reference to experiments performed by James DeWitt of the U.S. Fish and Wildlife Service, published in the Journal of Agricultural Food and Chemistry in 1956 (4: 10 pp.853-66). The quail were fed 3,000 times the concentration typically encountered in the wild. 80 percent of the eggs from the treated group hatched, compared to 83.9 percent of the untreated controls, so the claim of a "few" was clearly false, and the difference in results hardly significant. Moreover, 92.8 percent of the eggs from the DDT-fed birds were fertile, compared to 89 percent from the controls, which reverses the impression created by the quoted text. Also omitted was that DeWitt's study was actually conducted on quail and pheasant. Of the pheasants, 80 percent of the eggs from the treated birds hatched compared to 57.4 percent for the controls, and 100 percent of the DDT birds survived against 94.8 percent of the control group.
A number of later studies were cited at the EPA hearings, purporting to account for an effect (major decline in bird populations) that wasn't happening. All of them are examined in Ecological Sanity--with more care and thoroughness, it would appear, than by the witnesses who built their cases on them.
A 1969 experiment (Heath et al) on mallard ducks, performed at the Patuxent Wildlife Center at Laurel, Maryland, reported that birds fed DDT and DDE (the major metabolic residue from DDT breakdown) suffered a mortality among embryos and hatchlings of from 30 to 50 percent. The first thing that struck Claus and Bolander upon reviewing the paper was an enormous range of variation with the control groups that nobody else had apparently objected to. For instance, the number of eggs laid per hen in one control group was 39.2, whereas in another it was 16.8. This difference alone was far greater than any of the differences said to be "significant" among the experimental birds. The difference in live 14-day-old hatchlings in the same groups was 16.1 versus 6.0, which again was greater (69 percent) than the 50 percent deficit in ducklings per hen reported for the birds fed the highest DDT diet. When the variations among the controls are greater than the variations between the control and experimental animals, it should be obvious that some factor other than the test variable is operating (a bacterial infection, for example), which affects both groups. Claus and Bolander conclude (p.406):
"On the basis of these absurd differences . . . the entire study becomes meaningless, and all of the conclusions presented by the authors have to be discarded." And (p.408) "How this paper could have been passed for publication in Nature is unfathomable, for even rapid scanning of the tables presented in the article should have made it immediately evident to the referees that the data for the two series of control birds invalidated the whole experiment."
But published in Nature it was (227: 47-48), and it remains virtually unchallenged as one of the most frequently cited references in support of the contention that sublethal concentrations of DDT can be held responsible for declines in wildlife populations.
The same issue of Nature (was there some editorial decision to convey a message here?) carried another paper cited at the hearings, this time by Bitman and coworkers, describing experiments on Japanese quail. It concluded from direct measurements that DDT and related compounds induce a decrease in eggshell calcium and produce thinner eggshells. How were these conclusions arrived at?
The quantities of test compound fed to the experimental birds were of the order of 100 times that found in the natural environment. As if this were not enough, the experimenters also introduced "calcium stress" in the form of a diet (given both to the control and two experimental groups) reduced from the normal level of around 3 percent calcium content to 0.56 percent. The question that the results needed to answer was, "Did the feeding of DDT add to any calcium depletion caused by the calcium stress conditions? The authors of the experiment claimed that it did.
Their results, however, showed no significant differences in the calcium content of the blood or the bones that were analyzed from the three groups. It seems odd that if the calcium reserves of the parent birds showed no reduction, there should be a significant difference in the eggshells they produce. The significance reported was 0.07 percent, arising from 2.03 percent calcium content measured in the shells from the controls, versus 1.95 and 1.96 for the test groups. While mathematically the claim of significance is correct, it turns out that the method followed was to analyze the shell for the weight of calcium, which was then expressed as a percentage of the fresh weight of the entire egg. The weights of the shells themselves were not given, leaving wide open the possibility that eggs smaller and presumably lighter in total weight could nevertheless have possessed shells that were heavier. Hence it's not possible to tell from the presented data whether the percentage of eggshell calcium was reduced or not, which was the whole point of the exercise.
It gets even more interesting when we look at the measuring of eggshell thickness. This was done with a mechanical screw-type micrometer after the shell membranes were removed. An average reduction is reported of 69.5 x 10-4 inches for the controls to 66.7 x 10-4 in. and 65.6 x 10-4 in. for the eggs of two groups of test birds, and is described as "highly significant." Well, let's look at it.
Converting these figures to metric at the same accuracy as that given--namely of three significant figures--yields figures for reduction in thickness of 0.00711 and 0.00991 millimeters. The last two digits of each are below the resolving power of a light microscope, and eliminating them leaves reported thinnings of 7 and 10 microns. (1 micron = 0.001 mm--about half the size of a well-developed bacterium.) Screw micrometers available at the time were not considered to resolve differences below 50 microns reliably. More recent devices graduated to 10 microns are useful for gauging thicknesses of materials like metal foil, but for compressible samples such as paper--or eggshells--the determination of "end point" is a subjective quantity based on feel, typically resulting in variations of 10 to 30 microns. To borrow the phrase so beloved of textbook writers, it is left as an exercise for the reader to judge if such methods could have given results acclaimed as being highly significant.
3. (From THE 1971 EPA HEARINGS)
The Scientists' Findings and the Administrator's Ruling
The hearings went on for seven months, during which 125 witnesses were heard and 9,362 pages of testimony recorded. The EPA's hearing examiner, Judge Edmund Sweeney, was even-handed in his dealings, which seemed to infuriate environmentalists and drew criticism from The New York Times and Science, neither of which sent reporters to cover the proceedings. The scientific advisors had also followed the testimony and were unanimous in their 80-page recommendation that the claims were unsubstantiated and there was no reason for DDT to be banned. Sweeney issued his conclusions on April 25. 1972. They included the following:
DDT is not a carcinogenic hazard to man . . .
DDT is not a mutagenic or teratogenic hazard to man . . .
The uses of DDT under the registrations involved here do not have a deleterious effect on freshwater fish, estuarine organisms, wild birds, or other wildlife . . .
The adverse effect on beneficial animals from the use of DDT under the registration involved here is not unreasonable on balance with its benefit . . . There is a present need for the continued use of DDT for the essential uses defined in this case.
This was in line with the professional scientific and medical scientific pleas that had been made worldwide. During the EPA hearings the World Health Organization issued a statement that included:
"Improvement in health occasioned by antimalarial campaigns has broken the vicious cycle of poverty and disease in many areas by preventing incapacity and death. . . . [N]o economic alternative to DDT is available and the . . . consequences of the withdrawal of DDT would be very grave. . . . [T]he safety record of DDT for man is truly remarkable."
Six weeks after Sweeney's findings, on June 2, 1972, the EPA Administrator, William Ruckleshaus, reversed the decision, rejected the scientific evidence, and ordered a ban on the sale and production of DDT. Ruckleshaus had not attended any of the sessions during the seven-month hearing and admitted that he had not read the transcript. The decision, he stated, was taken for political reasons. Environmentalist groups have campaigned vigorously ever since for a full ban on all use, by all nations.
Today, more than 2 billion people--40 percent of the world's population--live in malarious countries. Around 300 million are infected, and something like 100 million cases are estimated to occur each year along with millions of deaths, most of them children. Africa is one of the worst sufferers, with nearly 85 percent of the world's cases. More than 30 percent of childhood deaths there are caused by malaria. Perhaps the most charitable interpretation of the 1972 decision would be that it was intended as a demonstration by a fledgling federal agency, in its first major test, that it was genuinely a disinterested arm of the national executive and not a lackey to financial or private corporate interests. One can only say here that if public perceptions are to take precedence over fact in the formulation of policy, it's a sad day for science. Critics have seen the ruling as part of a deliberate policy of population control, in a period when global overpopulation has been widely promoted as one of the greatest problems that the world faces.