On a Farther Shore (34 page)

In 1943, a sample of just six pounds of DDT arrived in America and was promptly subjected to testing by the U.S. Public Health Service, the U.S. Department of Agriculture, and the Kettering Laboratory at the University of Cincinnati College of Medicine. The results suggested it would be safe and effective in battlefield situations. It was mass-produced during the war to fight typhus, malaria, yellow fever, and encephalitis, and its use against those insect-borne diseases continued after the war.

In 1950, about 12 percent of the DDT made in the United States was shipped overseas for malaria control. Meanwhile, production for agricultural, commercial, and home uses soared.
Domestic DDT use peaked in 1959, when Americans used eighty million pounds of it, and over the course of the nearly three decades during which it was available in the United States, an estimated 1.35 billion pounds were used. A number of companies produced DDT and other synthetic insecticides: DuPont, Dow Chemical Company, Union Carbide Chemicals, Velsicol Chemical Corporation, Monsanto, Thompson Chemicals Corporation, American Cyanamid, and Shell Chemical Company.

DDT is an “organochlorine” compound, that is, a molecule built on a backbone of carbon atoms to which atoms of hydrogen and chlorine are attached. It is sometimes referred to as a “chlorinated hydrocarbon.” The success of DDT—coupled with the fact that researchers almost immediately discovered that insects sometimes
developed a resistance to it—touched off a feverish effort to develop related chlorinated hydrocarbon compounds that also worked as insecticides. DDT was soon joined by a host of toxic cousins.
These included lindane, chlordane, heptachlor, toxaphene, dieldrin, aldrin, and the apocalyptically named endrin, which had a toxicity many times that of DDT. It was a thriving international business, as the United States continued to produce quantities of all these chemicals that far exceeded domestic demand.
In 1952, the combined production of aldrin, dieldrin, endrin, heptachlor, chlordane, and toxaphene was forty-nine million pounds. By the end of the decade it was double that.

Some of these compounds were more dangerous to use than DDT—chlordane and dieldrin, for example, are readily absorbed through the skin—and some cases of severe reactions to DDT were actually reactions to the “carrier” solvent in which it was sprayed. Although the public was warned not to spray DDT on animals, many people did anyway, dousing their cats and dogs with DDT. The sometimes serious skin reactions that occurred in pets were caused not by the DDT, but by the kerosene in which it was dissolved. Organochlorine compounds, whether they are absorbed, inhaled, or ingested, are highly lipophilic, meaning they are readily stored in fatty tissue and can accumulate over time with chronic exposure. They also tend to stick on surfaces and to remain active in soils.

Chemists at the same time discovered that compounds called organophosphates also had insecticidal properties. Organophosphates are not inherently poisonous, and they comprise a diverse group of biologically important molecules—DNA is an organophosphate. But certain manmade organophosphates were developed that are potent disruptors of nerve impulses—the deadly nerve poison sarin is an organophosphate, as is the nerve agent VX. Both are chemical warfare compounds designated as weapons of mass destruction by the United Nations. Insecticides based on organophosphate compounds include parathion and malathion. Organophosphate insecticides are more toxic than those based on organochlorines, though they are less persistent in the environment. Organophosphates are more easily metabolized
and tend not to be stored in fat—but they can do extensive damage to the nervous system during acute exposures, especially in a developing fetus.

The “safety” of a pesticide is a relative question, as the toxicity of any substance depends on the dose and the route of exposure. Calling a compound an “insecticide” identifies its purpose and suggests that its effects are specific to the targeted pests. But, in fact, scientists had determined only that insects could be killed with doses of DDT that didn’t seem harmful to people, and, for all anybody knew, enough DDT would kill a person in the same way it killed a bug. Because all life on earth evolved from common ancestors, all living things share certain biological features. The most obvious is DNA, which is present in all living organisms—other than some viruses—and which performs the same function in all of them. A specific sequence of DNA—a gene—makes RNA, which makes the same protein whether it’s in a mouse or a whale. And the more alike two organisms are, the more their respective genomes resemble each other. A human and a chimpanzee have genomes that are 96 percent identical. Above the molecular level, many biological processes are also “conserved” among different species.

One such feature is the transmission of electrical signals along nerve cells, or neurons. These impulses, powered by the rapid movement of ions across the cell membrane, carry sensory information and control muscle movements. In certain types of neurons these messages must cross gaps—as happens at the juncture between a neuron and a muscle—and this is accomplished by chemical chaperones called neurotransmitters. Once the impulse has been delivered across such a juncture, specialized enzymes neutralize the neurotransmitter and restore the chemical balance in the gap.

During the early development of the organochlorine and organophosphate insecticides, such cellular processes were incompletely understood. But because these poisons caused twitching and rigidity
and convulsions it was thought that they must in some way interfere with nerve impulses, possibly by disrupting the actions of neurotransmitters or by interfering with the flow of ions across the neuron’s cell membrane. Either could lead to the repeated firing and intermittent paralysis of muscle cells. Which is exactly what was observed in the case of insects poisoned by DDT or other insecticides. The ultimate cause of death following such “general uncoordinated activity” was believed to be “metabolic exhaustion.”

After their initial studies, researchers started to wonder whether pesticides, especially the fat-soluble organochlorines, could build up in the body of someone repeatedly exposed to them—and if such a bioaccumulation did occur, what would be the effects of the increasing body burdens of pesticides? But it would be years before scientists would learn that special proteins, embedded in the membranes of cells or deep within their nuclei, act as hormone receptors—and that these receptors can make mistakes, binding to pesticides or their by-products as if they were hormones and thereby initiating willy-nilly, out-of-control cellular responses that can lead to disease and reproductive issues.

Putting aside the long-term health hazards arising from pesticide exposure—cancer and birth defects, for example—fatal or serious human “intoxications” by organochlorine insecticides were thought to be rare, usually the result of careless application by agricultural workers, suicide attempts, or accidental ingestion by children. Whether pesticides were environmentally safe—that is, whether their continued use over long periods posed a risk to ecosystems generally—was a different question, one the FWS had continued to ask, ever since its preliminary investigations on DDT in 1945.

The first tests were inconclusive. DDT from aerial spraying across forestlands killed insects and was powerfully lethal to fish and shellfish in waters that received overspray. The absence of obvious harm to birds, mammals, and amphibians in the field trials was contradicted by lab experiments showing that DDT was toxic to every kind of
animal tested. Outside the lab, repeated field testing over the same areas showed that as DDT concentrations increased, more species were harmed. The same was true in laboratory experiments, where every species tested—mice, rabbits, bobwhite quail, frogs—got sick or died from DDT exposure. One intriguing finding was that birds seemed to tolerate being sprayed with DDT, but fell ill or died when they were fed DDT.

As expected, these interweaving lines of inquiry, in the field and in the lab, consistently showed that the higher the dose, the more lethal the effect. This preliminary research led to guidelines intended to limit the concentrations of DDT used in spraying projects. As the scientists at Patuxent saw it, using DDT to treat buildings for mosquitoes or even soldiers in delousing programs presented a limited threat to the environment. Using it on croplands, forests, and residential neighborhoods upped the ante. “
As soon as DDT was taken outdoors,” they reported in 1947, “the dangers were instantly multiplied.”

These early investigations did not keep pace with the rapidly expanding use of DDT almost everywhere and all at once—especially in the growing use of airplanes in aerial spraying operations. In a summary report at the close of 1947, the Patuxent group said unknowns about DDT still outweighed the evidence of its safety in general use, particularly with respect to collateral damage that might befall “beneficial” species in ways that could profoundly alter ecosystems:

The investigators struggled to reconcile effects seen in the lab—which could be controlled but might not predict what would happen in the environment—with findings from the field, where the supposedly controlled “dosing” of an area with DDT was an imprecise endeavor, complicated by weather and forest cover and local topography. Birds and animals sometimes simply fled areas being sprayed with DDT, leaving researchers to wonder whether they had safely moved out or became sick somewhere else. The investigators presumed that killing much of the insect population in a spraying operation would starve certain other species that eat insects. How could anyone determine, in such an open and complex environment, whether birds and animals that disappeared were poisoned or simply departed for some other reason?

Some effects of DDT spraying were surprising. Trout in northern Idaho whose diets usually consisted of ants, worms, and water-hatching insects suddenly turned up with bellies full of crayfish that had been paralyzed by DDT, whereas trout in nearby streams that hadn’t been sprayed seemed not to eat crayfish at all. But like all of the results from this study—which involved aerial spraying over an area of four hundred thousand acres—this finding was of limited value because of the problems inherent in conducting well-controlled experiments in such a vast environment. The sprayers were careless about where they dropped DDT, and they didn’t stick to a reliable schedule. In the end, the investigators were never sure whether they were checking a treated area or an untreated one or, for that matter, whether any given finding was a “before” or “after” observation.

It was also apparent, as the Patuxent group investigated private spraying operations, that DDT was commonly being applied in concentrations far above FWS recommendations, which were two pounds per acre—and only one-fifth pound per acre in areas with aquatic
habitats.
In one orchard in Allegany County, Maryland, a grower trying to control codling moths treated his trees multiple times over the course of the summer with DDT at concentrations of between fifteen and twenty-two and a half pounds per acre—for an estimated season’s total approaching
seventy
pounds an acre. The researchers said a “cursory” survey found only about a third as many birds on the property as there were in surrounding areas that hadn’t been sprayed.

In response to the burgeoning market for synthetic pesticides, Congress in 1947 passed the Federal Insecticide, Fungicide, and Rodenticide Act—which, though often modified, would live on in perpetuity as the primary legal authority for the regulation of these and related products. In its initial incarnation, FIFRA stipulated how pesticides in interstate commerce were to be formally registered and labeled, but the law in no way limited the sale or use of pesticides. It was this anything-goes environment—which was sure to play out over the course of many seasons in many years—that most worried the Patuxent group. Based on their own studies, it appeared by 1949 that DDT could be applied at a rate of two pounds per acre as many as four times a year without causing harm to nesting birds. Mammals appeared to be even less susceptible to DDT than birds were, but care and lower concentrations had to be used near water. Nobody knew what a higher dose—between two and four pounds an acre—would do. At five pounds per acre there were grave consequences.

In one study of a spraying program for gypsy moths, 83 percent of the bird population was wiped out within two weeks. A year later bird numbers in the area were still around 15 percent below normal. In other areas, where similar spray concentrations appeared to be less lethal to birds, the explanation was often that the birds had completed their nesting periods and simply flew away when the spraying began. None of these findings addressed the question of what happened when spray concentrations were ten or fifteen or even thirty times the recommended levels. Most important, they shed no light on how spraying the same places over a long period might multiply, over and over, year after year, the amount of DDT in the environment.

In their 1949 assessment, the Patuxent researchers said this was their biggest concern: “
Although the immediate advantages of DDT as a control agent have been demonstrated on a wide scale, the possible hazards, particularly those resulting from repeated and long-time use of the insecticide, are not so well known.”

A year later, the Patuxent researchers began backing away from the proposition that applications of DDT at low concentrations could be considered “safe.” Even at low rates of application—like the ounce or two per acre needed to control mosquitoes—DDT disturbed food chains and caused a variety of species to desert treated areas. And there were some invertebrate species, including mites and aphids, that were resistant to DDT and whose populations exploded when competing species were exterminated with insecticides—an effect by which one group of pests was simply exchanged for another.