IN 1978, BRUCE KARRH, DuPont’s corporate medical director, was outspoken about the company’s duty “to discover and reveal the unvarnished facts about health hazards,” as he wrote in the Bulletin of the New York Academy of Medicine at the time. When deposed in 2004, Karrh emphasized that DuPont’s internal health and safety rules often went further than the government’s and that the company’s policy was to comply with either laws or the company’s internal health and safety standards, “whichever was the more strict.” In his 1978 article, Karrh also insisted that a company “should be candid, and lay all the facts on the table. This is the only responsible and ethical way to go.”
Yet DuPont only laid out some of its facts. In 1978, for instance, DuPont alerted workers to the results of a study done by 3M showing that its employees were accumulating C8 in their blood. Later that year, Karrh and his colleagues began reviewing employee medical records and measuring the level of C8 in the blood of the company’s own workers in Parkersburg, as well as at another DuPont plant in Deepwater, New Jersey, where the company had been using C8 and related chemicals since the 1950s. They found that exposed workers at the New Jersey plant had increased rates of endocrine disorders. Another notable pattern was that, like dogs and rats, people employed at the DuPont plants more frequently had abnormal liver function tests after C8 exposure.
DuPont elected not to disclose its findings to regulators. The reasoning, according to Karrh, was that the abnormal test results weren’t proven to be adverse health effects related to C8. When asked about the decision in deposition, Karrh said that “at that point in time, we saw no substantial risk, so therefore we saw no obligation to report.”
Not long after the decision was made not to alert the EPA, in 1981, another study of DuPont workers by a staff epidemiologist declared that liver test data collected in Parkersburg lacked “conclusive evidence of an occupationally related health problem among workers exposed to C-8.” Yet the research might have reasonably led to more testing. An assistant medical director named Vann Brewster suggested that an early draft of the study be edited to state that DuPont should conduct further liver test monitoring. Years later, a proposal for a follow-up study was rejected.
If the health effects on humans could still be debated in 1979, C8’s effects on animals continued to be apparent. A report prepared for plaintiffs stated that by then, DuPont was aware of studies showing that exposed beagles had abnormal enzyme levels “indicative of cellular damage.” Given enough of the stuff, the dogs died.
DuPont employees knew in 1979 about a recent 3M study showing that some rhesus monkeys also died when exposed to C8, according to documents submitted by plaintiffs. Scientists divided the primates into five groups and exposed them to different amounts of C8 over 90 days. Those given the highest dose all died within five weeks. More notable was that three of the monkeys who received less than half that amount also died, their faces and gums growing pale and their eyes swelling before they wasted away. Some of the monkeys given the lower dose began losing weight in the first week it was administered. C8 also appeared to affect some monkeys’ kidneys.
Of course, enough of anything can be deadly. Even a certain amount of table salt would kill a lab animal, a DuPont employee named C. E. Steiner noted in a confidential 1980 communications meeting. For C8, the lethal oral dose was listed as one ounce per 150 pounds, although the document stated that the chemical was most toxic when inhaled. The harder question was to determine a maximum safe dosage. How much could an animal — or a person — be exposed to without having any effects at all? The 1965 DuPont study of rats suggested that even a single dose of a similar surfactant could have a prolonged effect. Nearly two months after being exposed, the rats’ livers were still three times larger than normal.
Steiner declared that there was no “conclusive evidence” that C8 harmed workers, yet he also stated that “continued exposure is not tolerable.” Because C8 accumulated in bodies, the potential for harm was there, and Steiner predicted the company would continue medical and toxicological monitoring and described plans to supply workers who were directly exposed to the chemical with protective clothing.
Two years after DuPont learned of the monkey study, in 1981, 3M shared the results of another study it had done, this one on pregnant rats, whose unborn pups were more likely to have eye defects after they were exposed to C8. The EPA was also informed of the results. After 3M’s rat study came out, DuPont transferred all women out of work assignments with potential for exposure to C8. DuPont doctors then began tracking a small group of women who had been exposed to C8 and had recently been pregnant. If even one in five women gave birth to children who had craniofacial deformities, a DuPont epidemiologist named Fayerweather warned, the results should be considered significant enough to suggest that C8 exposure caused the problems.
Photos of Bucky Bailey as a baby as well as article clippings that his mother Sue saved over the years sit on the table at their home in Bluemont, VA. Sue worked in Teflon while pregnant with Bucky, who was born with facial deformities.
As it turned out, at least one of eight babies born to women who worked in the Teflon division did have birth defects. A little boy named Bucky Bailey, whose mother, Sue, had worked in Teflon early in her pregnancy, was born with tear duct deformities, only one nostril, an eyelid that started down by his nose, and a condition known as “keyhole pupil,” which looked like a tear in his iris. Another child, who was two years old when the rat study was published in 1981, had an “unconfirmed eye and tear duct defect,” according to a DuPont document that was marked confidential.
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