Many types of control projects are routinely utilizing amounts of DDT which are hazardous not only to insect populations generally, but to many species of vertebrate life. In careful appraisals of experimental five pound per acre applications, it has been established that local extermination is a real threat for many invertebrate species. The direct kill of many vertebrates was also found to be appreciable at this dosage level. Single or total seasonal application rates for some types of control may involve 5 to 15 times this amount. Such a pollution of lands and waters, if extended to large continuous blocks, would undoubtedly have most dire effects.
By 1951, the Patuxent pesticides project had determined that the cumulative effect of spraying DDT at a supposedly “safe” concentration over the same area year after year ultimately led to sharp declines in bird populations. Over the course of four years following the first field testing there, bird numbers in the treated areas had fallen by 26 percent, and for a handful of species the decline approached half of the original population.
Meanwhile, an ever-widening uncontrolled experiment was taking place across the country. In 1947, the city of Princeton, New Jersey, launched an effort to eradicate Dutch elm disease by spraying elm trees with DDT. Dutch elm disease is a devastating fungal infection that is transmitted from tree to tree by bark beetles specific to elms and which is almost always lethal. Arriving in North America in 1928, the disease had swept through cities and villages in the eastern United States, where elms were a principal shade tree, and continued its march westward across the continent. Local officials everywhere were desperate for a way to preserve their stately elms. In the first year of the Princeton spraying program, nearly every elm tree in the city was treated with a 1 percent DDT emulsion. For each tree, this worked out to about one and a half pounds of DDT—three-fourths of what the Patuxent group believed was safe for an entire acre of forest. The city doubled the DDT concentration the following year, so that every tree in the city got about three pounds of DDT.
The 1948 spraying produced immediate complaints from residents about dead birds or the sudden disappearance of birds, and a number of landowners declined further treatment for their elms. A group of researchers, including scientists from U.S. Fish and Wildlife and the Bureau of Entomology and Plant Quarantine in the U.S. Department of Agriculture, investigated the Princeton situation in 1949, when the city’s trees were again doused with three pounds of DDT each. It was a challenging environment. Because the whole city was involved it was hard to find a nearby tract of unsprayed elm trees that could serve as a control site. Within the town there were so many elms that it was hard to imagine that birds would not be repeatedly exposed to DDT even as they moved around from tree to tree to avoid the spraying teams—making it hard to assess their total level of exposure.
Only a handful of dead or dying birds—twenty-six in all—were found in Princeton after the spraying. All of the birds recovered alive that later died showed the usual symptoms of DDT poisoning: tremors and the loss of the ability to fly, followed by the inability to stand. Subsequent necropsies showed DDT residues in all of the dead birds, although this wasn’t proof that they had died of DDT poisoning, as similar residues might well have been present in the birds that lived—none of which were captured and examined. The researchers also monitored nests and found that only 44 percent of the nestling birds in the sprayed area survived, whereas 71 percent of nestlings in the untreated tract lived to fledge by midsummer. More noticeable than the direct mortality from the spraying was a general decline in bird numbers. For species that were found in both the sprayed and unsprayed areas, DDT appeared to cause a 22 percent decline in the overall population. Where they went and what happened to them was unknown. But bird numbers in the unsprayed area increased by 6 percent.
Experiments on birds at the Patuxent Research Refuge produced more definitive results—but only slightly. In one test, hatchlings from nesting birds in areas aerially sprayed with DDT suffered “considerable mortality,” with only 28 percent surviving, versus 86 percent that made it to fledging in the unsprayed area. DDT residues were found in the tissues of the dead birds, but in wildly varying amounts. This experiment also showed that birds from the unsprayed area had DDT residues in their tissues—a finding that was hard to understand and that confounded the effort to draw conclusions from the experiment. Since nobody knew what constituted a lethal dose of DDT for hatchling birds—or how tissue levels of DDT corresponded to the amount of DDT ingested—it was hard to say in even a general way what these results meant. Compounding the uncertainty was the fact that the spraying had killed 94 percent of the insects in the test area, so the hatchlings might simply have died of starvation.
By the mid-1950s, however, researchers had designed more precise testing regimens and there was no longer any doubt that DDT was extremely toxic to birds. Experiments at Patuxent found that when adult quail were fed a diet composed of just .025 parts DDT they all died. For some reason, young quail were less susceptible to such small amounts of DDT, though when they were fed a diet that was .05 percent DDT they all died, too. Pheasants were similarly vulnerable to DDT; starlings less so. The researchers were intrigued to find that while all the birds showed DDT concentrations in their body tissues, the amount was unrelated to the dose or to their total consumption of DDT—but instead appeared to correlate directly with the severity of the symptoms of poisoning. These included weight loss followed by tremors and muscular incapacity a day or two before the birds died.
These findings, however, had little effect on the widespread use of synthetic pesticides. Nor was the pesticide business slowed by the growing evidence that DDT posed hazards beyond its acute toxicity. DDT that was captured in fatty tissues accumulated over time and could reexpose a bird or animal to its own body burden of poison when fat reserves were utilized—as during a period of food scarcity, for example—and the biological effects of remobilizing stored DDT were unknown. Another “subtle” effect of DDT that had been observed was intergenerational: Birds that consumed as little as three ten-thousandths of an ounce of DDT on a daily basis for two months would show no symptoms but suffered significant reductions in fertility and in the survival of their young. On went the chemical tide anyway. By 1956 there were two hundred registered chemical pesticides—not only insecticides like DDT, but also fungicides, rodent killers, and herbicides—and there were more than six thousand commercial products based on these active ingredients. Annual pesticide production was by then 700 percent of its pre-World War II level, with annual sales estimated at nearly a quarter of a billion dollars.
By 1959, the Patuxent group had cut its best guess at a “safe” concentration for the aerial spraying of DDT in half—down to one pound per acre. At two pounds per acre the collateral damage commenced, as most vertebrate species—birds, mammals, reptiles, amphibians—were affected at that level. Five pounds an acre resulted in “serious mortality among most species.” Aquatic species of fish and shellfish, which had been known to be the most vulnerable to DDT from the start, were of special concern. The recommendations now called for no more than 0.2 pounds per acre over wetlands—and 0.1 pounds or less if there was more than one application.
The threat to aquatic species was demonstrated in a series of spectacular fish kills. In 1954, a half-pound-per-acre DDT spraying program over the Miramichi River drainage in New Brunswick, Canada, was undertaken against an outbreak of spruce budworm. It killed 91 percent of the river’s young Atlantic salmon—good old Salmo salar—and some of the adults. The area was sprayed again in 1956 and the same thing happened once more. Nobody was sure whether the fish succumbed to DDT or starved to death following the massive die-off of stream insects that were killed along with the budworms. In 1955, another DDT campaign against the spruce budworm produced similar results along a one-hundred-mile stretch of the Yellowstone River in Montana. Three months after the area was sprayed with DDT at a rate of one pound per acre, young trout and several other fish species died off en masse. Official
s in this case were sure the cause was starvation after the stream invertebrates in the river were destroyed in the spraying.
A campaign to eradicate gypsy moths in the forests of the eastern United States was begun in 1957. The gypsy moth was an import from Europe that was injurious to hardwood trees, as gypsy moth larvae have a voracious appetite for foliage and are present when trees are leafing out in the spring. Again, fish and shellfish kills were reported from wetlands within or near the sprayed areas—the most notable being a substantial die-off of crabs in a salt marsh on Long Island, New York. But worries increased when a discovery by the Patuxent group indicated there might be previously unimagined long-term effects from exposure to DDT:
Immediate mortality of individuals is not the only cause for concern. Effects that are long-delayed may be serious. During the past year, an important indirect effect was reported: species feeding upon earthworms died from pesticide poisoning a year after the area was treated. The earthworms, known to be resistant to DDT and capable of storing it in their tissues, continued to live while containing reservoirs of DDT sufficient to cause secondary poisoning of their predators. Studies in progress give indication that other pesticides also can be stored by resistant organisms. Few studies have been made to determine what effect this phenomenon has upon wild populations, but field reports from several localities in the Midwestern United States suggest that this may be the reason why the numbers of certain birds are being reduced in local areas.
While the pesticide studies from Patuxent and elsewhere were sometimes inconclusive, one firm rule held up year after year: The more scientists learned about the effects of DDT and other pesticides on wildlife, the greater the collateral damage they observed. And there was another important consideration: The U.S. Fish and Wildlife Service concerned itself only with fish and wildlife. Human beings were someone else’s problem.
In 1950, the American Medical Association’s Council on Pharmacy and Chemistry set up a Committee on Pesticides. The AMA said the need for more information about problems associated with the use of “economic poisons” had been apparent for some time already. Within months the committee produced its first report. The subject was organophosphate insecticides, parathion in particular. The committee said that organophosphate insecticides were “among the most toxic materials commonly used for pest control and are capable of producing severe systemic effects and death unless directions for handling and use are strictly observed.”
Human exposure to organophosphate insecticides was a constant danger because they could be inhaled, ingested, or directly absorbed through the skin or eyes. Symptoms of organophosphate poisoning included unsteadiness, twitching, nausea, cramps, involuntary urination and defecation, blurred vision, giddiness, anxiety, sensations of floating, mental confusion, drowsiness, loss of coordination, generalized weakness, slurred speech, repetition of the final syllables of words, loss of reflexes, coma, convulsions, and death.
Organophosphate poisoning occurred most often among farmworkers who applied them. Symptoms could appear after a single exposure, and they were more severe after repeated exposures or by exposure to two or more different organophosphate insecticides. The committee cited a number of cases. One was a thirty-eight-year-old farmer who could not read and who sprayed his tobacco crop with parathion evidently unaware that the chemical was dangerous. The victim smoked while he sprayed and stood so near the sprayer that he became soaked from head to toe. He died within fifteen hours. Another was a thirty-one-year-old university entomologist who had worked with parathion and other insecticides for months before deciding one day to forgo a mask and protective clothing. Late in the day he complained of nausea and went home—where he died before medical help could arrive.
Yet another was a twenty-six-year-old member of a spraying crew using parathion in a citrus grove, whose job was to keep the tanks filled. After two weeks on the job he got sick and was hospitalized. Following a recuperation that lasted a month he returned to work. On his first day back he reached into the solution in one tank up to his elbows. He also neglected to wear a protective mask, as he complained that they made him uncomfortable and prevented him from smoking while he worked. The next morning he felt ill and was rushed to the hospital, where he died six hours later. There were also cases involving workers in pesticide production plants, including one foreman who, along with a coworker, was splashed with highly purified parathion. He sent the coworker to the showers, but declined to clean himself up and died twenty-one hours later. Then there was a ten-year-old child who found a whiskey bottle in the crook of a tree and decided to drink some of its contents, which were later determined to be tetraethyl pyrophosphate, or TEPP, an insecticide closely related to parathion. The child foamed at the mouth and died within fifteen minutes.
The AMA was worried not only about such acute poisonings, but also about the long-term effects of pesticide accumulations in body fat. Scientists at the time had only a limited understanding of the hormonal and enzyme activities in fat tissue, but they knew that the deposition or mobilization of fat also involved the liver. It thus seemed a “reasonable assumption” that a buildup of chlorinated hydrocarbon poisons could disrupt important metabolic processes.
Studies already completed on DDT showed that fat tissue was a “biologic magnifier” of the insecticide. Rats that were fed tiny amounts of DDT over periods of time gradually built up body burdens of the poison, resulting in slowing heart rates and liver damage. And while researchers still lacked assays to detect the storage of other chlorinated hydrocarbon insecticides in fat tissue, everything pointed in that direction. Chlordane was known to have a “high order of chronic toxicity,” and dieldrin and aldrin appeared to be as bad or worse. Researchers had to assume that chlorinated hydrocarbons would not be stored only in fatty tissues, but in any tissue or organ where fats were present. These included the membranes of every cell in the body—which are composed of a double layer of lipid molecules—as well as embryonic fat cells that help regulate fetal development.
By the spring of 1951, the AMA was advising physicians on how to treat patients poisoned by dieldrin and aldrin, particularly in the southern United States, where these new insecticides were coming into wide use on cotton and tobacco crops. Both appeared to be as toxic as parathion if absorbed through the skin and were believed to be somewhere between three and six times as toxic as DDT.
Like the Patuxent researchers—who complained of being unable to thoroughly test insecticides as fast as they were being developed—the AMA struggled to assess the effects of increasing insecticide use in residential and commercial settings. In 1952, the Committee on Pesticides began looking at electric and thermal vaporizing devices that had been newly invented to fumigate houses, schools, restaurants, industrial plants, and hospitals. Some vaporizers worked continuously, sending out a steady invisible fog of insecticide. Nobody knew whether such “atmospheric dispersal” was safe, or even how effective it was. The committee found that “technologic improvements in chemicals and in methods of dispersal” came faster than did knowledge of “the physiologic actions of the insecticidal ingredients, particularly with respect to their chronic toxicity and inhalation hazards.” These devices discharged insecticides—usually DDT or lindane—as vapors or fumes that were airborne for a time before recrystallizing on floors, walls, and ceilings, where they remained a potent contact poison for long periods. At least that was the idea.
Testing showed that insecticides dispersed unevenly from vaporizers and tended to concentrate at potentially unsafe levels in the air and on the surfaces closest to the machines. DDT sometimes accumulated so heavily on the walls and ceilings near the vaporizers that crystals of the insecticide flaked off and fell to the floor, coating it with toxic dust. Lindane, the committee said, looked to be safer than DDT in vaporizers—although this wasn’t certain, and the main factor driving an increasing use of lindane wasn’t safety but rather the growing resistance some insects had to DDT.
Although cases of alle
rgy-like reactions were being reported among people in homes or businesses where insecticide vaporizers had been installed, the AMA found that the government had limited authority under FIFRA to regulate either the devices or the insecticides they dispersed. This was especially problematic because the AMA also found that few people used the devices properly. The supposed safety and miraculous effectiveness of synthetic pesticides were so widely believed that people often tampered with vaporizers to increase their output. The AMA put part of the blame on the manufacturers of vaporizers, whom they accused of promoting the devices for use in homes, hospitals, nurseries, or anywhere food was handled—even though the evidence suggested such uses were risky.
By 1954, the AMA categorically opposed the use of insecticide vaporizers in homes. Lindane had largely replaced DDT as the poison of choice in such machines. Two years earlier the AMA had reported that the toxicity of lindane was comparable to DDT in some situations, different in others, and in general difficult to assess. It was known that lindane didn’t accumulate in fat tissues as readily as DDT did, which led to the promotion of lindane as an insecticide that was safer than DDT for use in devices that dispersed insecticides continuously. But more research now indicated that lindane was “stored in significant amounts” in the brain and liver. Researchers also suspected that acute toxicity results obtained in testing on lab animals did not translate to humans.
On a Farther Shore Page 27
