Poison Spring (18 page)

The resemblance of a picker’s day to that of an American slave could hardly have been lost on the African-American Owens. “When I arrived at the crew chief’s home at about four a.m., they were already up and the wife was making chicken sandwiches to sell in the fields,” he wrote. “At four-thirty, we loaded on the bus and headed toward the ‘ramp.’ The ramp is a place about a block square where workers assemble in the morning and growers and crew chiefs come to select work crews for the day’s harvest. We drove on and dust began to rise from the muck soils as we headed down the lane toward the cornfield. I looked out the window of the bus, as the sun was coming up, and could see nothing but sweet corn, miles and miles of it.”

As Owens and his crew unloaded from the bus, they noticed workers mounting “an awkward-looking machine.” This was the mule train, from which “pullers” must harvest a minimum of fifty-six ears of corn per minute—almost an ear per second. The puller walks between two rows, pulling three ears of corn in each hand and simultaneously pitching the six ears into a bin just above his head. For this they were paid about three dollars a day.

The pullers are usually wet within the first thirty minutes in the field, a result of heavy dew on the plants caused by the soil’s high water table. Combined with the almost colloidal dust particles, the dew leaves the worker’s clothing as wet and black as the soil. The wet particles penetrate the worker’s outer clothing and also make it difficult to clean undergarments after a day’s work as a puller.

Owens jumped right in, taking a position first as a lead puller, then—when the pace proved too fast—as a wing puller. The rows were six hundred feet long, but they seemed endless. “I began to understand the reason for beginning work so early in the morning,” Owens wrote. “The workers cannot tolerate the intense heat generated by the sun and the corn later in the day. Fine muck particles rise as the train moves along, covering workers with particles resembling coal dust. As we approached the end of the row some fifteen minutes was required for the train to turn around and get started again.”

Out on the wing, the fumes from the train’s engine added to the misery. It was then that Owens, looking off some 500 yards to the left, noticed the planes, “descending to the tassel level of the corn, spraying pesticides, protecting the corn against the earworm . . . I realized that at the pace we were moving we would be pulling the newly sprayed corn before nightfall,” he wrote.

By the end of the day, Owens crew had hand-packed some four thousand crates of corn. Each puller got 12 cents a crate, the packer 10 cents, the box maker 3 cents; the tractor driver, the rickrack worker, and the loader split up the balance. Pullers earned about $30 a day, the packers $25, and on down the line. “Usually about one-fourth of the daily wages were spent at the store for drinks, food, and other items for relaxation.”
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To Owens, the workers’ hardships seemed appalling. The labor camps were infested with crawling insects, mosquitoes, and flies. There was one toilet for every eight workers, and only two-thirds of them were indoors. More than half the labor camps were located within fifty yards of crops sprayed with parathion, guthion, lanate, and sevin.

Owens also knew that most of the migrant farmworkers were hungry most of the time. He found their diet was “grossly inadequate,” since the food they ate “approached the critical level of 50 percent of the recommended minimum daily caloric intake level.”

A man with the teeth of hunger in his belly at the same time he is harvesting crops sprayed with toxins is playing with fire, perhaps even death. The key human enzyme affected by exposure to nerve poisons is known as acetylcholinesterase. Neurotoxic pesticides inhibit the production of this neurotransmitter—and the levels of acetylcholinesterase in the man were taking dangerous dives, Owens noticed, especially when the worker was not eating well. Some 80 percent of the workers developed severe skin rashes; two dozen required medical attention. A worker caught tuberculosis. A child died. A man died. At the Pennsylvania farm where the man died, a helicopter had applied three gallons of the nerve toxins parathion and guthion per acre, 12 times the recommended rate.

The early warning signs of acute or chronic pesticide poisoning are no more distinctive than a headache or dizziness. Unless farmworkers are “down and out,” they are not likely to pay attention to a headache or a “wheezy stomach.” Poor working people don’t stop working “unless they are taken out of a field desperately ill.”

The implication of this finding alone is frightening. Pesticides cripple and kill. They are also responsible for subtle and not so subtle changes in human behavior. A migrant farmworker at the end of a harvest season is not the same person he was when he started his migration. He has been subjected to a variety of “body insults” such as spray poisoning, a bad diet, and very bad living conditions.

Fifty-six percent of the farmworkers had “abnormal kidney and liver functions: 78 percent had severe chronic skin rash; and 54 percent abnormalities in chest cavities,” Owens reported. “Migrant workers are young workers, i.e., mean age of 25 years, but their health statistics resemble those of middle-aged Americans.”
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Owens’s research has broad implications. Hundreds of thousands of American- and foreign-born laborers suffer the rigors of working on pesticide-laden farms. The Owens brothers must have known their findings would be considered adversarial by the very government that was funding them. Indeed, they spent considerable time between 1974 and 1982 begging the EPA and the National Science Foundation for further research support. But the National Science Foundation dropped the Owenses in 1977, and the next year, the EPA granted them less than $10,000. That would be their last check from the EPA.
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The EPA was apparently uninterested in the Owenses’ concern that farm sprays caused debilitating sickness to the migrants laboring in the midst of poison-drenched vegetables and other crops. A senior EPA scientist and manager told the Owens brothers that more EPA money might become available as long as they offered “no attempt to draw ‘cause-effect’ correlations” between pesticides and health effects.

“I then told the ‘Bros.’ that once EPA had this report, we would seriously review . . . any proposal they put together for the support of further analytical work (not that we would fund it, but that we would consider it),” the EPA official wrote.
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Yet the Owenses’ study, “The Extent of Exposure of Migrant Workers to Pesticides and Pesticide Residues,” submitted both under the Carter administration in May 1978 and under the Reagan administration in May 1982, clearly showed the connection between toxic sprays and sickness among farmhands.

There were other reasons why the EPA dismissed the work of the Owens brothers. In the late 1970s, the agency was agonizing over another study done at Colorado State University, in which scientists studied the long-term effects of acute poisoning by the same nerve poisons that had so damaged the migrants in the Owens study. In this case, researchers examined not just farmers and nursery workers but people who worked in pesticide-formulating plants, aircraft spray pilots, even an agricultural chemicals salesman.

In their May 1980 report to the EPA, the scientists concluded that people exposed to acute poisoning with organophosphate pesticides—even just once in their entire lives—had experienced neurological problems, damage to fine motor and language functioning, and reduced memory and cognitive, intellectual, and perceptual function. Fully a quarter of the one hundred subjects suffered brain damage.
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The chemicals responsible for these life-threatening effects were primarily parathion, methyl parathion, and malathion—all nerve poisons. Methyl parathion caused 54 of the acute poisonings in Texas, while ethyl parathion was responsible for 42 acute poisonings, 24 of which took place in Colorado and 18 in Texas. In Colorado, malathion had poisoned six of the study subjects.

Hale Vandermer, an EPA scientist, warned his bosses about the implication of the Colorado study. What if additional studies confirmed these findings? Could people exposed to nerve pesticides end up with shattered nervous systems or brain damage? If these results held up, Vandermer reasoned, the country would face “a health problem of epidemic proportions.” After all, he noted, beyond America’s farmers, more than 56 percent of American families use organophosphate pesticides to kill insects
inside their homes.
Vandermer prepared a memo for EPA’s top policy official, assistant administrator Steve Jellinek, but his warning never reached him.
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The Owens brothers’ work and the Colorado study had clearly unsettled senior EPA officials. Credible science was telling them the agrochemical nerve gases used by millions of farmers and urban residents were making people sick, even killing them outright. Their moral and legal obligation to protect public health ought to have convinced them to ban all those dangerous organophosphate toxins. But instead, they elected to look the other way, prolonging the profitable lives of these neurotoxins.

Immediately after learning of the preliminary results of the Colorado study, EPA managers did two things. First, they put together a kind of Potemkin “farmworker program” right in the office of the top pesticides boss, Edwin Johnson.

As I’ve already described, the late 1970s and early 1980s were an especially trying time for the EPA. The Agent Orange crisis, especially when 2,4,5-T and dioxin were found to have caused injury to women in Oregon, had forced the EPA to restrict (and finally ban) 2,4,5-T in 1983. Now organophosphates, which are central nervous system poisons, were being shown to cause brain damage in humans. The EPA’s political bosses decided that something had to be done: not to ban more chemicals, but to deflect public opinion from these findings. The “farmworker program” filled the bill.

I spent a year working for this program, writing a series of memos about the harsh working conditions of farmworkers. But as admirable as the project may have seemed from the outside, in reality it was a pure public relations ploy: we put out press releases touting how much the government was doing to protect farmworkers who suffered the worst effects from organophosphates exposure. By the end of 1980, the EPA scientist James Boland had two thousand copies of the Colorado study. Yet few (if any) of those copies ever saw the light of day. Boland told me that the copies were warehoused in a government facility until the order came to trash them.
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Next, EPA senior managers canceled a special study of malathion, a parathion-like nerve toxin, being conducted by the Medical University of South Carolina. In Charleston, both people and mosquitoes were being fogged with malathion nine months out of every year, so it was almost inevitable that people would react to the toxin, suffering from symptoms including nasal and lung congestion, skin diseases, migraine headaches, gastroenteritis and gastrointestinal bleeding, and cardiovascular disorders.
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Malathion was hardly a new worry. In 1976, the U.S. Army Environmental Hygiene Agency had reported that one could disrupt a rat’s behavior with low dosages of malathion while leaving its blood and brain cholinesterase pretty much intact. This meant, the army agency said, “that it may be misleading to assume that behavior is normal following malathion exposure simply because blood ChE activity is within normal ranges.”
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In Saku, a Japanese community of about thirty thousand people raising apples, peaches, grapes, and rice, farmers used helicopters to spray parathion, malathion, EPN, and sumithion (all nerve toxins) on their crops. The result? People got sick. In 1971, Satoshi Ishikawa and three other professors from the School of Medicine of the University of Tokyo published a study of the effects of these poisons on children from four to sixteen years old. They found that after lengthy exposure to the nerve poisons, 98 percent of the children suffered a reduction in their vision and 95 percent had a narrowing of peripheral visual fields. Three-quarters had neurological and brain abnormalities; many had atrophied optic nerve and liver dysfunction.
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A pair of pathologists named Harvey L. Bank and Diane Melendez had been testing the effects of malathion on Charleston’s people, and despite the EPA’s decision to cancel their study, they sent their results to the agency anyway. Their conclusions were clear: malathion hypersensitivity was a widespread disease among the people of Charleston, and people’s immunological and allergic reactions took place at minute amounts of exposure to pesticides—far lower than the amounts EPA managers and risk assessors had certified as “safe.”
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I don’t know whether the EPA managers were looking only at the alarming implications of the South Carolina study when they cut it short by pulling their support and funding, or if they had done their homework and knew that malathion was not the harmless stuff they claimed it to be. But I guess that by the time they decided to do away with the South Carolina study, they knew the USDA was going to spray malathion in the orange groves of Northern California to “eradicate” the Mediterranean fruit fly. Suppressing unpleasant facts about malathion cleared the way for the USDA to indiscriminately endanger hundreds of thousands of people in the San Francisco Bay Area.
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In 1976, the EPA was under pressure from Congress to plug the regulatory holes it had inherited from the USDA. This translated into fifty thousand pesticide products with dubious safety records. The EPA also had to deal with more than four thousand compound “tolerances”; that is, it had to evaluate the maximum amount of pesticides to be allowed in food. This also happened to be the time when news of the massive IBT fraud (which I will discuss in the next chapter) had begun to challenge all past assumptions of scientific integrity in the regulation of pesticides.