Poison Spring (15 page)

As early as 1947, scientists were noticing that bees contaminated by pesticides acted as if they had been exposed to severe cold. The poisoned bees land “on leaves, twigs, or lumps of soil, selecting warm spots, and generally sitting motionless unless disturbed,” the researchers wrote. “Sometimes they fell from these perches, then revived and departed slowly, as a cold bee does, or in erratic flight to alight again a few yards away. In crawling they were much slower than arsenic poisoned bees. After becoming unable to crawl they would be helpless, sometimes for hours if protected from direct sun. They often lay on their backs or sides making feeble movement with legs and antennae.”
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In other words, farm sprays caused brain damage in bees. Poisons disoriented them, making it often impossible for them to find their way home. This is the main reason millions of bees disappear, leaving behind hives full of pollen, honey, and larvae. This is no “syndrome” or “colony collapse disorder.” This is the deadly result of decades of agribusiness warfare.

Until the 1960s, bees died primarily because of the incredible variety of poisons farmers sprayed on their land, even when fruits and seeds were about to set. As they searched for nectar and pollen, bees would become saturated by these invisible—and deadly—mists and dusts. Even if they somehow survived the toxic clouds and made it back to their hives, they would behave in strange ways: some would stay near the hive and freeze to death; others would be utterly confused, stupefied, even paralyzed. Still others would enter their hives carrying cargoes of poison-laced pollen and nectar, which would devastate the colony in very short time.

In the 1970s, the USDA apiculturist S. E. McGregor warned farmers that no amount of technology could replace the critical role of bees in pollinating the nation’s crops. There are more than three thousand plants giving food to humans, McGregor wrote, but only three hundred are grown widely. Of these, no more than a dozen (grains such as rice, wheat, corn, sorghum, millet, rye, and barley) are responsible for 90 percent of the world’s food. All of these are pollinated by the wind and by insects. Oilseeds (coconuts, cotton, oil palms, olives, peanuts, rape, soybeans, and sunflowers) give humans more than 50 percent of the fats and oils in their diets. Insects pollinate many of these useful crops. All told, a third of our diet is directly or indirectly dependent upon insect-pollinated plants, McGregor wrote. Farmers, he said, should never forget that “no cultural practice will cause fruit or seed to set if its pollination is neglected.”
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This precarious condition worsened sharply in 1974 when EPA licensed the nerve gas parathion, a dark, garlic-smelling poison in a class of nerve toxins known as organophosphates. Parathion was synthesized at the end of World War II in the same industrial German cauldron that cooked up the chemical weapons tabun, sarin, and soman. Parathion was first licensed as an insecticide in the United States in 1948, and for several decades, millions of pounds of this war gas were sprayed throughout the American countryside.
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Once inside a man or a bee, an organophosphate can destroy an enzyme, cholinesterase, which is responsible for the normal functioning of the central nervous system; the victim develops severe convulsions and can die. This may not happen quickly: parathion poisoning first causes headaches, nausea, muscle spasms, and drooling or frothing at the mouth.
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One undiluted drop is lethal to an adult human being; the compound can cripple and kill farmworkers. Some workers die from acute parathion poisoning; others will suffer for decades with intellectual and behavioral disabilities, retinal degeneration (resulting in blindness), paralysis, and cancer.
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Among animals, it takes extraordinarily minute amounts of parathion—40 parts per trillion to 5 parts per billion—to kill freshwater invertebrates. Something like 1 part per billion of parathion is fatal to oysters, and 17 parts per billion kill striped bass. Parathion also causes cancer and blindness and has been shown to rot the sciatic nerve in experimental animals.

Parathion is also more dangerous to young and female animals than it is to male animals, and it threatens dozens of endangered species throughout the country, including prairie chickens in Texas, geese in California, and a species of freshwater mussel in the Tennessee River. And it’s not just parathion in its original form that causes problems. Once it is sprayed on a field, strange things rapidly begin to happen. The toxin’s molecules rearrange themselves; in the skin and flesh of crops and vegetables or in the land, the compound transforms into not one but several poisons known as metabolites, which can be ten to sixty times more devastating to life than parathion itself.
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And if these chemicals can contaminate farmers and animals, they also can get into our food. In August 1985, Barbara Britton, an EPA scientist, said she was “astonished” to discover parathion levels in food more than five thousand times the level considered safe for nursing infants. Five months later, Britton pointed out what (to her) had become obvious: parathion was “acutely toxic to humans, domestic animals and wildlife,” and jeopardized the “continued existence of 33 endangered species.”
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Parathion’s widespread use and acute toxicity could only mean tragedy for bees, especially when engineers figured out how to increase its effectiveness by making it “time released.” Pennwalt Corporation’s gas, known as Penncap-M, was designed with parathion wrapped in tiny nylon bubbles just 5 to 50 microns in size—just about the size of pollen grains. Now, with the poison remaining inactivated on the surface of a flower for several days, bees would carry these invisible spheres of asphyxiating gas—again, exactly the shape and size of pollen—straight back to the hive, where it would spread death from one season to the next.
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So-called microencapsulated methyl parathion is “the most destructive bee poisoning insecticide ever developed,” according to Carl Johansen, a professor of entomology at Washington State University.
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Johansen’s home state once had some hundred thousand acres of apple trees that depended on bees for pollination. In late 1970s, the state earned $400 million per year from bee-pollinated crops alone. So Washington absolutely required a healthy population of bees. The slightest misuse of Penncap-M was “extremely hazardous to bees” and was certain to cause disaster to pollinating insects, Johansen wrote. Even hobbyist and small-time beekeepers were in danger of being “wiped out by Penncap-M sprays in eastern Washington.”
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A year before Johansen’s dire assessment, the president of the Washington Beekeepers Association warned that the viability of the honeybee industry hangs by a tenuous thread. “Past experience has shown that honey bees cannot survive within foraging distance of blossoming crops or blossoming cover crops or weeds that are subject to treatment, settling or drift of encapsulated insecticides,” Elwood Sires wrote to the director of the Washington State Department of Agriculture. “All insecticides are harmful to honey bees and costly to honey beekeepers, but micro-encapsulated insecticides are deadly to the bee colonies because they are carried back to and stored in the hives.”
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Even if farmers use Penncap-M according to the label directions, they would still cause “serious adverse effects on honey bee populations,” wrote the EPA biologist Norman Cook in the late 1970s. The toxin starts a deadly chain of events: honeybees forage among treated crops, collecting pollen and capsules of poison, which they take to their hives. The capsules contaminate the pollen and honey. It then takes about eight hours for the poison to severely damage or kill the entire colony.

And it does not end there: beekeepers often reuse the destroyed colonies’ combs in new hives, which, within 24 to 48 hours, causes “severe adult mortality” among honeybees of the new hive. Even contaminated combs stored for a year or more remain capable of bringing swift death to honeybees, Cook wrote.

“The most startling aspect is that honey, pollen, and wax from decimated colonies are not destroyed by the beekeepers,” Cook reported. “The wax is remelted and used in new combs. The honey is sold to the public and depending upon honey-extraction processes, contains capsules of Penncap-M. The pollen stored in combs is used in new hives, but can result in adverse effects to new hives. The pollen collected from ‘pollen trap” (and this pollen also contains capsules) is sold in health food stores.”
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By the early 1980s, Frank Robinson, secretary-treasurer of the American Beekeeping Federation, admitted that the country’s beekeepers were suffering “extensive losses each year from the widespread and sometimes indiscriminate use of toxic chemicals.” Vernon W. Miller, a beekeeper from Cutler, Illinois, lost all of his sixty-nine colonies of bees to “the beekeeper’s famous special, Penncap-M.” Miller had been forced to surrender ten years of beekeeping, “as I have neither political clout nor money enough to fight a big corporation [Pennwalt, the owner of Penncap-M]. As the victim, I have no rights.”
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Beekeepers also feared that parathion in honey and pollen could be causing serious harm to public health. Todd D. Hardie, a pollen broker from Franklin, Vermont, told the EPA he was “deeply concerned about pesticides appearing in bee pollen that is used for human consumption.”

“As a broker of North American pollen, primarily from California and Colorado, I feel a great responsibility to consumers who eat the tons of pollen that we sell,” Hardie wrote. “Some of our pollen comes from high mountains, where there is supposedly no possible link with pesticides, but most of the pollen is coming from agricultural areas where pesticides are used. Would it be possible to get bee pollen tested in [an] EPA laboratory?”
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An EPA official wrote back that the FDA, not EPA, would take care of his problem. Not a word about Hardie’s legitimate fears.

Why the silence? The late 1970s were a time when honey was still a favored food for infants. But then scientists discovered that some babies dying of the so-called sudden infant death syndrome or crib death had eaten honey contaminated with lethal botulinum toxin. In 1978, the Sioux Honey Association, the world’s largest honey producer, urged parents not to give honey to children less than a year old.

Could there be a connection between crib death and pesticides? Botulinum toxin occurs in nature, but like the man-made parathion, it is an asphyxiating nerve poison that can choke a human being just as it can choke an insect. Organophosphate sprays, like parathion, combine with other toxic chemicals to form synergistic super-poisons. Even minute amounts of parathion could become monstrously toxic in the presence of minute amounts of botulinum toxin. There may be something in some infants’ intestines that triggers the lethal reaction. Tiny capsules of parathion in the honey and other foods infants eat could be that trigger. Parathion alone could also do the job.

Botulinum spores are everywhere in the environment, and in most cases they are harmless. But they have also been connected to sudden infant death syndrome (SIDS), which kills as many as ten thousand American infants every year. Botulinum spores create toxin-producing bacteria in the intestines of infants, and these bacteria give off the deadly clostridium that kills the infant by respiratory arrest. In other words, botulism acts like parathion or other nerve poisons.
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Thus an infant with any nerve pesticide in his stomach might face death not merely because of the toxic power of parathion alone but from the botulinum spores lying dormant in the stomach as well. The two poisons interact with deadly effects. It may be that the parathion molecules activate the botulinum spores.
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The widespread use of deadly Penncap-M slow-release bubbles worried and angered three ecologists at the EPA, particularly Norman Cook. They knew that in addition to killing bees and other beneficial insects, the encapsulated parathion causes various degrees of neurological damage and, quite possibly, death for small and large mammals, terrestrial and water invertebrates, and birds—even at rates of just a pound of poison per acre. The gizzards of most birds would grind down and rupture the nerve poison microcapsules, causing crippling disease or death.

The EPA ecologists also knew that bees would continue to die from the encapsulated parathion because Pennwalt Corporation had persuaded the EPA to approve the spraying of the company’s product during the spring bloom, when all pollinating insects would be out foraging for nectar and pollen. They told their bosses that Pennwalt’s parathion was showing up in both honey and pollen. The least Pennwalt ought to do—according to the law—was to notify EPA about such serious public health hazards. (The Federal Insecticide, Fungicide and Rodenticide Act [FIFRA] allows the EPA to punish companies not reporting the hazardous effects of its products.) But Pennwalt did nothing, and the EPA—as it had done so many times before—simply turned away.

In February 1980, Pennwalt tried to convince the EPA that its nerve capsules were safe. But the ecologists who reviewed Pennwalt’s data concluded that such information was “a parody of scientific research.” They also said they had yet to come across any other spray that was “as uniquely hazardous to bees as Penncap-M.”
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Clayton Bushong, the senior EPA manager heading the group of ecologists concerned about the farmers’ toxins killing bees, was caught in a political vortex, with worried scientists on one side and a powerful corporation on the other. Bushong did what responsible bureaucrats do: he sent memos up the food chain. Having digested Johansen’s warnings and the findings of scientific research about the dangers of Penncap-M, Bushong advised his superiors that pesticides in “time release” capsules cause “extreme hazards to nontarget pollinating insect populations,” the consequences of which “would not only be environmentally disastrous but also would be disastrous to the production of food crops which require pollination by insects.”
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