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.
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.
Like Wamsley, Sue Bailey, one of the plaintiffs whose personal injury suits are scheduled to come to trial in the fall, remembers having plenty of contact with C8. When she started at DuPont in 1978, she worked first in the Nylon division and then in Lucite, she told me in an interview. But in 1980, when she was in the first trimester of her pregnancy with Bucky, she moved to Teflon, where she often sat watch over a large pipe that periodically filled up with liquid, which she had to pump to a pond in back of the plant. Occasionally some of the bubbly stuff would overflow from a nearby holding tank, and her supervisor taught her how to squeegee the excess into a drain.
Soon after Bucky was born, Bailey received a call from a DuPont doctor. “I thought it was just a compassion call, you know: can we do anything or do you need anything?” Bailey recalled. “Shoot. I should have known better.” In fact, the doctor didn’t express his sympathies, Bailey said, and instead asked her whether her child had any birth defects, explaining that it was standard to record such problems in employees’ newborns.
While Bailey was still on maternity leave, she learned that the company was removing its female workers from the Teflon division. She remembers the moment—and that it made her feel deceived. “It sure was a big eye-opener,” said Bailey, who still lives in West Virginia but left DuPont a few years after Bucky’s birth.
The Federal Toxic Substances Control Act requires companies that work with chemicals to report to the Environmental Protection Agency any evidence they find that shows or even suggests that they are harmful. In keeping with this requirement, 3M submitted its rat study to the EPA, and later DuPont scientists wound up discussing the study with the federal agency, saying they believed it was flawed. DuPont scientists neglected to inform the EPA about what they had found in tracking their own workers.
When DuPont began transferring women workers out of Teflon, the company did send out a flier alerting them to the results of the 3M study. When Sue Bailey saw the notice on the bench of the locker room and read about the rat study, she immediately thought of Bucky.
Yet when she went in to request a blood test, the results of which the doctor carefully noted to the thousandth decimal point, and asked if there might be a connection between Bucky’s birth defects and the rat study she had read about, Bailey recalls that Dr. Younger Lovelace Power, the plant doctor, said no. According to Karrh’s deposition, he told Karrh the same. “We went back to him and asked him to follow up on it, and he did, and came back saying that he did not think it was related.”
“I said, ‘I was in Teflon. Is this what happened to my baby?’” Bailey remembered. “And he said, ‘No, no.’” Power also told Bailey that the company had no record of her having worked in Teflon. Shortly afterward, she considered suing DuPont and even contacted a lawyer in Parkersburg, who she says wasn’t interested in taking her case against the town’s biggest employer. When contacted for his response to Bailey’s recollections, Power declined to comment.
By testing the blood of female Teflon workers who had given birth, DuPont researchers, who then reported their findings to Karrh, documented for the first time that C8 had moved across the human placenta.
In 2005, when the EPA fined the company for withholding this information, attorneys for DuPont argued that because the agency already had evidence of the connection between C8 and birth defects in rats, the evidence it had withheld was “merely confirmatory” and not of great significance, according to the agency’s consent agreement on the matter.
Ken Wamsley also remembers when his supervisor told him they had taken female workers out of Teflon. “I said, ‘Why’d you send all the women home?’ He said, ‘Well, we’re afraid, we think maybe it hurts the pregnancies in some of the women,’” recalled Wamsley. “They said, ‘Ken, it won’t hurt the men.’”
While some Dupont scientists were carefully studying the chemical’s effect on the body, others were quietly tracking its steady spread into the water surrounding the Parkersburg
plant. After it ceased dumping C8 in the ocean, DuPont apparently relied on disposal in unlined landfills and ponds, as well as putting C8 into the air through smokestacks and pouring waste water containing it directly into the Ohio River, as detailed in a 2007 study by Dennis Paustenbach published in the Journal of Toxicology and Environmental Health.
By 1982, Karrh had become worried about the possibility of “current or future exposure of members of the local community from emissions leaving the plant’s perimeter,” as he explained in a letter to a colleague in the plastics department. After noting that C8 stays in the blood for a long time—and might be passed to others through blood donations—and that the company had only limited knowledge of its long-term effects, Karrh recommended that “available practical steps be taken to reduce that exposure.”
To get a sense of exactly how extensive that exposure was, in March 1984 an employee was sent out to collect samples, according to a memo by a DuPont staffer named Doughty. The employee went into general stores, markets, and gas stations, in local communities as far as 79 miles downriver from the Parkersburg plant, asking to fill plastic jugs with water, which he then took back for testing. The results of those tests confirmed C8’s presence at elevated levels.
Faced with the evidence that C8 had now spread far beyond the Parkersburg plant, internal documents show, DuPont was at a crossroads. Could the company find a way to reduce emissions? Should it switch to a new surfactant? Or stop using the chemical altogether? In May 1984, DuPont convened a meeting of 10 of its corporate business managers at the company’s headquarters in Wilmington, Delaware, to tackle some of these questions. Results from an engineering study the group reviewed that day described two methods for reducing C8 emissions, including thermal destruction and a scrubbing system.
“None of the options developed are . . . economically attractive and would essentially put the long term viability of this business segment on the line,” someone named J. A. Schmid summarized in notes from the meeting, which are marked “personal and confidential.”
The executives considered C8 from the perspective of various divisions of the company, including the medical and legal departments, which, they predicted, “will likely take a position of total elimination,” according to Schmid’s summary. Yet the group nevertheless decided that “corporate image and corporate liability”—rather than health concerns or fears about suits—would drive their decisions about the chemical. Also, as Schmid noted, “There was a consensus that C-8, based on all the information available from within the company and 3M, does not pose a health hazard at low level chronic exposure.”
Though they already knew that it had been detected in two local drinking water systems and that moving ahead would only increase emissions, DuPont decided to keep using C8.
In fact, from that point on, DuPont increased its use and emissions of the chemical, according to Paustenbach’s 2007 study, which was based on the company’s purchasing records, interviews with employees, and historical emissions from the Parkersburg plant. According to the study, the plant put an estimated 19,000 pounds of C8 into the air in 1984, the year of the meeting. By 1999, the peak of its air emissions, the West Virginia plant put some 87,000 pounds of C8 into local air and water. That same year, the company emitted more than 25,000 pounds of the chemical into the air and water around its New Jersey plant, as noted in a confidential presentation DuPont made to the New Jersey Department of Environmental Protection in 2006. All told, according to Paustenbach’s estimate, between 1951 and 2003 the West Virginia plant eventually spread nearly 2.5 million pounds of the chemical into the area around Parkersburg.
Essentially, DuPont decided to double-down on C8, betting that somewhere down the line the company would somehow be able to “eliminate all C8 emissions in a way yet to be developed that would not economically penalize the bussiness [sic],” as Schmid wrote in his 1984 meeting notes. The executives, while conscious of probable future liability, did not act with great urgency about the potential legal predicament they faced. If they did decide to reduce emissions or stop using the chemical altogether, they still couldn’t undo the years of damage already done. As the meeting summary noted, “We are already liable for the past 32 years of operation.”
When contacted by The Intercept for comment, 3M provided the following statement. “In more than 30 years of medical surveillance we have observed no adverse health effects in our employees resulting from their exposure to PFOS or PFOA. This is very important since the level of exposure in the general population is much lower than that of production employees who worked directly with these materials,” said Dr. Carol Ley, 3M vice president and corporate medical director. “3M believes the chemical compounds in question present no harm to human health at levels they are typically found in the environment or in human blood.” In May 2000, 3M announced that it would phase out its use of C8.
Dupont confronted its potential liability in part by rehearsing the media strategy it would take if word of the contamination somehow got out. In the weeks after the 1984 meeting, an internal public relations team drafted the first of several “standby press releases.” The guide for dealing with the imagined press offered assurances that only “small quantities of [C8] are discharged to the Ohio River” and that “these extremely low levels would have no adverse affects.” When a hypothetical reporter, who presumably learned that DuPont was choosing not to invest in a system to reduce emissions, asks whether the company’s decision was based on money, the document advises answering “No.”
The company went on to draft these just-in-case press releases at several difficult junctures, and even the hypothetical scenarios they play out can be uncomfortable. In one, drafted in 1989, after DuPont had bought local fields that contained wells it knew to be contaminated, the company spokesperson in the script winds up in an outright lie. Although internal documents list “the interests of protecting our plant site from public liability“’ as one of the reasons for the purchase, when the hypothetical reporter asks whether DuPont purchased the land because of the water contamination, the suggested answer listed in the 1989 standby release was to deny this and to state instead that “it made good business sense to do so.”
DuPont drafted another contingency press release in 1991, after it discovered that C8 was present in a landfill near the plant, which it estimated could produce an exit stream containing 100 times its internal maximum safety level. Fears about the possible health consequences were enough to spur the company to once again rehearse its media strategy. (“What would be the effect of cows drinking water from the . . . stream?” the agenda from a C8 review meeting that year asked.) Yet other recent and disturbing discoveries had also provoked corporate anxieties.
In 1989, DuPont employees found an elevated number of leukemia deaths at the West Virginia plant. Several months later, they measured an unexpectedly high number of kidney cancers among male workers. Both elevations were plant-wide and not specific to workers who handled C8. But, the following year, the scientists clarified how C8 might cause at least one form of cancer in humans. In 1991, it became clear not just that C8-exposed rats had elevated chances of developing testicular tumors—something 3M had also recently observed—but, worse still, that the mechanism by which they developed the tumors could apply to humans.
Nevertheless, the 1991 draft press release said that “DuPont and 3M studies show that C-8 has no known toxic or ill health effects in humans at the concentrations detected” and included this reassuring note: “As for most chemicals, exposure limits for C-8 have been established with sufficient safety factors to ensure there is no health concern.”
Yet even this prettified version of reality in Parkersburg never saw the light of day. The standby releases were only to be used to guide the company’s media response if its bad news somehow leaked to the public. It would be almost 20 years after the first standby release was drafted before anyone outside the company understood the dangers of the chemical and how far it had spread beyond the plan
t.
In the meantime, fears about liability mounted along with the bad news. In 1991, DuPont researchers recommended another study of workers’ liver enzymes to follow up on the one that showed elevated levels more than a decade before. But Karrh and others decided against the project, which was predicted to cost $45,000. When asked about it in a deposition, Karrh characterized the decision as the choice to focus resources on other worthy scientific projects. But notes taken on a discussion of whether or not to carry out the proposed study included the bullet point “liability" and the hand-written suggestion: “Do the study after we are sued.”
In a 2004 deposition, Karrh denied that the notes were his and said that the company would never have endorsed such a comment. Although notes from the 1991 meeting describe the presence of someone named “Kahrr,” Karrh said that he had no idea who that person was and didn’t recall being present for the meeting. When contacted by The Intercept, Karrh declined to comment.
As the secrets mounted so too did anxiety about C8, which DuPont was by now using and emitting not just in West Virginia and New Jersey, but also in its facilities in Japan and the Netherlands. By the time a small committee drafted a “white paper” about C8 strategies and plans in 1994, the subject was considered so sensitive that each copy was numbered and tracked. The top-secret document, which was distributed to high-level DuPont employees around the world, discussed the need to “evaluate replacement of C-8 with other more environmentally safe materials” and presented evidence of toxicity, including a paper published in the Journal of Occupational Medicine that found elevated levels of prostate cancer death rates for employees who worked in jobs where they were exposed to C8. After they reviewed drafts, recipients were asked to return them for destruction.
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