Internal documents reveal that DuPont long suspected C8 was harmful, yet continued to put the company’s workers and the public at risk.
KEN WAMSLEY SOMETIMES DREAMS that he’s playing softball again. He’ll be at center field, just like when he played slow pitch back in his teens, or pounding the ball over the fence as the crowd goes wild. Other times, he’s somehow inexplicably back at work in the lab. Wamsley calls them nightmares, these stories that play out in his sleep, but really the only scary part is the end, when “I wake up and I have no rectum anymore.”
Wamsley is 73. After developing rectal cancer and having surgery to treat it in 2002, he walks slowly and gets up gingerly from the bench in his small backyard. His voice, which has a gentle Appalachian lilt, is still animated, though, especially when he talks about his happier days. There were many. While Wamsley knew plenty of people in Parkersburg, West Virginia, who struggled to stay employed, he made an enviable wage for almost four decades at the DuPont plant here. The company was generous, helping him pay for college courses and training him to become a lab analyst in the Teflon division.
He enjoyed the work, particularly the precision and care it required. For years, he measured levels of a chemical called C8 in various products. The chemical “was everywhere,” as Wamsley remembers it, bubbling out of the glass flasks he used to transport it, wafting into a smelly vapor that formed when he heated it. A fine powder, possibly C8, dusted the laboratory drawers and floated in the hazy lab air.
At the time, Wamsley and his coworkers weren’t particularly concerned about the strange stuff. “We never thought about it, never worried about it,” he said recently. He believed it was harmless, “like a soap. Wash your hands [with it], your face, take a bath.”
Today Wamsley suffers from ulcerative colitis, a bowel condition that causes him sudden bouts of diarrhea. The disease also can — and his case, did — lead to rectal cancer. Between the surgery, which left him reliant on plastic pouches that collect his waste outside his body and have to be changed regularly, and his ongoing digestive problems, Wamsley finds it difficult to be away from his home for long.
Sometimes, between napping or watching baseball on TV, Wamsley’s mind drifts back to his DuPont days and he wonders not just about the dust that coated his old workplace but also about his bosses who offered their casual assurances about the chemical years ago.
“Who knew?” he asked. “When did they know? Did they lie?”
UNTIL RECENTLY, FEW PEOPLE had heard much about chemicals like C8. One of tens of thousands of unregulated industrial chemicals, perfluorooctanoic acid, or PFOA — also called C8 because of the eight-carbon chain that makes up its chemical backbone — had gone unnoticed for most of its eight or so decades on earth, even as it helped cement the success of one of the world’s largest corporations.
Several blockbuster discoveries, including nylon, Lycra, and Tyvek, helped transform the E. I. du Pont de Nemours company from a 19th-century gunpowder mill into “one of the most successful and sustained industrial enterprises in the world,” as its corporate website puts it. Indeed, in 2014, the company reaped more than $95 million in sales each day. Perhaps no product is as responsible for its dominance as Teflon, which was introduced in 1946, and for more than 60 years C8 was an essential ingredient of Teflon.
Called a “surfactant” because it reduces the surface tension of water, the slippery, stable compound was eventually used in hundreds of products, including Gore-Tex and other waterproof clothing; coatings for eye glasses and tennis rackets; stain-proof coatings for carpets and furniture; fire-fighting foam; fast food wrappers; microwave popcorn bags; bicycle lubricants; satellite components; ski wax; communications cables; and pizza boxes.
Concerns about the safety of Teflon, C8, and other long-chain perfluorinated chemicals first came to wide public attention more than a decade ago, but the story of DuPont’s long involvement with C8 has never been fully told. Over the past 15 years, as lawyers have been waging an epic legal battle — culminating as the first of approximately 3,500 personal injury claims comes to trial in September — a long trail of documents has emerged that casts new light on C8, DuPont, and the fitful attempts of the Environmental Protection Agency to deal with a threat to public health.
This story is based on many of those documents, which until they were entered into evidence for these trials had been hidden away in DuPont’s files. Among them are write-ups of experiments on rats, dogs, and rabbits showing that C8 was associated with a wide range of health problems that sometimes killed the lab animals. Many thousands of pages of expert testimony and depositions have been prepared by attorneys for the plaintiffs. And through the process of legal discovery they have uncovered hundreds of internal communications revealing that DuPont employees for many years suspected that C8 was harmful and yet continued to use it, putting the company’s workers and the people who lived near its plants at risk.
In 2011 and 2012, after seven years of research, the science panel found that C8 was “more likely than not” linked to ulcerative colitis — Wamsley’s condition — as well as to high cholesterol; pregnancy-induced hypertension; thyroid disease; testicular cancer; and kidney cancer. The scientists’ findings, published in more than three dozen peer-reviewed articles, were striking, because the chemical’s effects were so widespread throughout the body and because even very low exposure levels were associated with health effects.
We know, too, from internal DuPont documents that emerged through the lawsuit, that Wamsley’s fears of being lied to are well-founded. DuPont scientists had closely studied the chemical for decades and through their own research knew about some of the dangers it posed. Yet rather than inform workers, people living near the plant, the general public, or government agencies responsible for regulating chemicals, DuPont repeatedly kept its knowledge secret.
Another revelation about C8 makes all of this more disturbing and gives the upcoming trials, the first of which will be held this fall in Columbus, Ohio, global significance: This deadly chemical that DuPont continued to use well after it knew it was linked to health problems is now practically everywhere.
A man-made compound that didn’t exist a century ago, C8 is in the blood of 99.7 percent of Americans, according to a 2007 analysis of data from the Centers for Disease Control, as well as in newborn human babies, breast milk, and umbilical cord blood. A growing group of scientists have been tracking the chemical’s spread through the environment, documenting its presence in a wide range of wildlife, including Loggerhead sea turtles, bottlenose dolphins, harbor seals, polar bears, caribou, walruses, bald eagles, lions, tigers, and arctic birds. Although DuPont no longer uses C8, fully removing the chemical from all the bodies of water and bloodstreams it pollutes is now impossible. And, because it is so chemically stable — in fact, as far as scientists can determine, it never breaks down — C8 is expected to remain on the planet well after humans are gone from it.
In some ways, C8 already is the tobacco of the chemical industry — a substance whose health effects were the subject of a decades-long corporate cover-up.
Eight companies are responsible for C8 contamination in the U.S. (In addition to DuPont, the leader by far in terms of both use and emissions, seven others had a role, including 3M, which produced C8 and sold it to DuPont for years.) If these polluters were ever forced to clean up the chemical, which has been detected by the EPA 716 times across water systems in 29 states, and in some areas may be present at dangerous levels, the costs could be astronomical — and C8 cases could enter the storied realm of tobacco litigation, forever changing how the public thinks about these products and how a powerful industry does business.
In some ways, C8 already is the tobacco of the chemical industry — a substance whose health effects were the subject of a decades-long corporate cover-up. As with tobacco, public health organizations have taken up the cause — and numerous reporters have dived into the mammoth story. Like the tobacco litigation, the lawsuits around C8 also involve huge amounts of money. And, like tobacco, C8 is a symbol of how difficult it is to hold companies responsible, even when mounting scientific evidence links their products to cancer and other diseases.
There is at least one sense in which the tobacco analogy fails. Exposure to tobacco usually contains an element of volition, and most people who smoked it in the past half century knew about some of the risks involved. But the vast majority of Americans — along with most people on the planet — now have C8 in their bodies. And we’ve had no choice in the matter.
FOR ITS FIRST HUNDRED YEARS, DuPont mostly made explosives, which, while hazardous, were at least well understood. But by the 1930s, the company had expanded into new products that brought new mysterious health problems. Leaded gasoline, which DuPont made in its New Jersey plant, for instance, wound up causing madness and violent deaths and life-long institutionalization of workers. And certain rubber and industrial chemicals inexplicably turned the skin of exposed workers blue.
Perhaps most troubling, at least to a DuPont doctor named George Gehrmann, was a number of bladder cancers that had recently begun to crop up among many dye workers. Worried over “the tendency to believe [chemicals] are harmless until proven otherwise,” Gehrmann pushed DuPont to create Haskell Laboratories in 1935. Haskell was one of the first in-house toxicology facilities and its first project was to address the bladder cancers. But the inherent problems of assigning staff scientists to study a company’s own employees and products became clear from the outset.
One of Haskell’s first employees, a pathologist named Wilhelm Hueper, helped crack the bladder cancer case by developing a model of how the dye chemicals led to disease. But the company forbade him from publishing some of his research and, according to epidemiologist and public health scholar David Michaels, fired him in 1937 before going on to use the chemicals in question for decades.
DuPont elected not to disclose its findings to regulators.
C8 would prove to be arguably even more ethically and scientifically challenging for Haskell. From the beginning, DuPont scientists approached the chemical’s potential dangers with rigor. In 1954, the very year a French engineer first applied the slick coating to a frying pan, a DuPont employee named R. A. Dickison noted that he had received an inquiry regarding C8’s “possible toxicity.” In 1961, just seven years later, in-house researchers already had the short answer to Dickison’s question: C8 was indeed toxic and should be “handled with extreme care,” according to a report filed by plaintiffs. By the next year experiments had honed these broad concerns into clear, bright red flags that pointed to specific organs: C8 exposure was linked to the enlargement of rats’ testes, adrenal glands, and kidneys. In 1965, 14 employees, including Haskell’s then-director, John Zapp, received a memo describing preliminary studies that showed that even low doses of a related surfactant could increase the size of rats’ livers, a classic response to exposure to a poison.
The company even conducted a human C8 experiment, a deposition revealed. In 1962, DuPont scientists asked volunteers to smoke cigarettes laced with the chemical and observed that “Nine out of ten people in the highest-dosed group were noticeably ill for an average of nine hours with flu-like symptoms that included chills, backache, fever, and coughing.”
Because of its toxicity, C8 disposal presented a problem. In the early 1960s, the company buried about 200 drums of the chemical on the banks of the Ohio River near the plant. An internal DuPont document from 1975 about “Teflon Waste Disposal” detailed how the company began packing the waste in drums, shipping the drums on barges out to sea, and dumping them into the ocean, adding stones to make the drums sink. Though the practice resulted in a moment of unfavorable publicity when a fisherman caught one of the drums in his net, no one outside the company realized the danger the chemical presented. At some point before 1965, ocean dumping ceased, and DuPont began disposing of its Teflon waste in landfills instead.
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.
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.
A DuPont lawyer referred to C8 as “the material 3M sells us that we poop to the river and into drinking water along the Ohio River.”
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 plant.
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.
In 1999, when a farmer suspected that DuPont had poisoned his cows (after they drank from the very C8-polluted stream DuPont employees had worried over in their draft press release eight years earlier) and filed a lawsuit seeking damages, the truth finally began to seep out. The next year, an in-house DuPont attorney named Bernard Reilly helped open an internal workshop on C8 by giving “a short summary of the right things to document and not to document.” But Reilly — whose own emails about C8 would later fuel the legal battle that eventually included thousands of people, including Ken Wamsley and Sue Bailey — didn’t heed his own advice.
Reilly clearly made the wrong choice when he used the company’s computers to write about C8, which he revealingly called the “the material 3M sells us that we poop to the river and into drinking water along the Ohio River.” But the DuPont attorney was right about two things: If C8 was proven to be harmful, Reilly predicted in 2000, “we are really in the soup because essentially everyone is exposed one way or another.” Also, as he noted in another prescient email sent 15 years ago: “This will be an interesting saga before it’s thru.”
EDITORS NOTE: DuPont, asked to respond to the allegations contained in this article, declined to comment due to pending litigation.
In previous statements and court filings, however, DuPont has consistently denied that it did anything wrong or broke any laws. In settlements reached with regulatory authorities and in a class-action suit, DuPont has made clear that those agreements were compromise settlements regarding disputed claims and that the settlements did not constitute an admission of guilt or wrongdoing. Likewise, in response to the personal injury claims of Ken Wamsley, Sue Bailey, and others, DuPont has rejected all charges of wrongdoing and maintained that their injuries were “proximately caused by acts of God and/or by intervening and/or superseding actions by others, over which DuPont had no control.” DuPont also claimed that it “neither knew, nor should have known, that any of the substances to which Plaintiff was allegedly exposed were hazardous or constituted a reasonable or foreseeable risk of physical harm by virtue of the prevailing state of the medical, scientific and/or industrial knowledge available to DuPont at all times relevant to the claims or causes of action asserted by Plaintiff.”
This article was reported in partnership with The Investigative Fund at The Nation Institute.
Alleen Brown, Hannah Gold, and Sheelagh McNeill contributed to this story.
In this series, Sharon Lerner exposes DuPont’s multi-decade cover-up of the severe harms to health associated with a chemical known as PFOA, or C8, and associated compounds such as PFOS and GenX.
When attorney Robert Bilott filed suit against DuPont on behalf of a West Virginia cattle farmer, he had no way of knowing the case…
HEN JEROMY DARLING WAS 26, he worked in a warehouse that was so big he rode a bike to get around it. One day, as he was pedaling from one place to another, his foot slipped and he bumped his groin on the crossbar. The initial pain was no surprise. What was odd, though, was that the spot he hit continued to hurt for days. Darling was athletic and hearty and, like many young people, hadn’t seriously entertained the possibility of illness. But when the pain persisted, he went to a doctor, who diagnosed him with testicular cancer.
Darling had two surgeries to treat the disease — one to remove his testicle and another to remove lymph nodes from his abdomen. The second left him with 76 staples and a profound exhaustion. It was several months before he was able to return to work, and many more before he felt like himself again. Back then, in 1998, it didn’t occur to Darling to question why he got sick. He just chalked it up to bad luck and focused on getting better.
Now 43 and living in Parkersburg, West Virginia, just a few miles from where he grew up in Belpre, Ohio, Darling has other theories about his cancer. Both towns are within “the Chemical Valley,” which encompasses the hilly area of western West Virginia and eastern Ohio and is home to many big chemical companies.
DuPont’s Washington Works plant, one of the area’s biggest private employers, sits in a bend of the Ohio River just across the water from Belpre. Lately Darling can’t help but think that the sprawling facility, whose smokestacks still poke into the sky near his home, was responsible for his bad luck.
T MAY HAVE BEEN LUCK, too — good or bad, depending on what side of the case you’re on — that led the attorney Robert Bilott to sue the DuPont company. In any case, he was an unlikely person to take on one of the world’s largest chemical companies. A partner at a corporate firm in Cincinnati, Bilott had spent his first eight years as an attorney on the other side of the table, defending large companies like DuPont. But in 1999 a cattle farmer named Wilbur Tennant came to see him. Tennant told him that DuPont had bought land from his family that was adjacent to his farm, for what the company had assured him would be a non-hazardous landfill, according to a letter Bilott later filed with the Environmental Protection Agency. Soon, a stream his cows drank from started to run smelly and black, with a layer of foam floating on the surface. Within a few years, hundreds of Tennant’s cattle had died. Bilott had no way of knowing at the time that what seemed like a straightforward case would lead to one of the most significant class-action lawsuits in the history of environmental law.
In 2000, after spending more than a year on the case, Bilott still didn’t have any idea what had killed the cows. None of the chemicals DuPont had informed him about could explain the die-off. DuPont even agreed to do a study with the EPA on what might have caused the deaths. The study concluded that the Tennants must have mismanaged their animals, declaring that “there was no evidence of toxicity associated with chemical contamination of the environment.”
It was only after one of the attorneys working on the case stumbled across a document that mentioned a compound called PFOA that he began to solve the mystery. Known within the chemical industry as a “surfactant,” because it reduces the surface tension of water, PFOA — short for perfluorooctanoic acid — was slippery, chemically stable, and a critical ingredient in the manufacture of hundreds of products, including Teflon. Almost no one had heard of the stuff back then. Also called C8 because of the eight-carbon chain that makes up its chemical backbone, PFOA was just one of tens of thousands of unregulated industrial substances manufactured and used by American companies without any significant oversight by environmental or health authorities.
After more digging, the lawyers learned that the Minnesota-based company 3M had just pulled a similar perfluorinated compound, called PFOS, from the market. That led Bilott to make a request that changed the course of the trial about the cows, his career, and the future of the chemical giant he was facing: He asked for all of DuPont’s documentation pertaining to PFOA, or C8, through the legal discovery process.
What he received made it clear that even as the company had been pleading ignorance over what might possibly have killed Tennant’s cows, some DuPont employees were very well aware that C8 had seeped into local water. In fact, company scientists had been charting its presence in the Ohio River and nearby drinking water for almost two decades, and had been documenting its health effects since 1954, just three years after DuPont first used the chemical in one of its signature brands: Teflon.
The documents Bilott received included studies showing that the company had known C8 could affect the livers of dogs and humans. The studies also indicated that C8 encouraged the growth of testicular tumors in rats, that exposed workers suffered more frequently from endocrine disorders, and that the company had also documented elevated rates of certain cancers, including kidney cancer, in workers. Bilott learned that the company had been quietly monitoring public drinking water outside its plant and, since 1984, had been documenting C8’s presence at potentially dangerous levels. As far back as 1991, DuPont had estimated the C8 in a stream from which cattle drank at 100 parts per billion — which was 100 times greater than an internal safety limit the company had set for drinking water. In 2001, DuPont quickly settled the Tennant case for an undisclosed sum.
8 MIGHT SIMPLY have remained a problem for cows if not for another unlikely environmentalist, a Parkersburg elementary school gym teacher and former field coordinator for the AFL-CIO named Joe Kiger. When he first got a letter in October 2000 from the Lubeck Public Service District, the company that provides his drinking water, Kiger almost tossed it. It’s easy to see why. Though it was in regular-sized type, the letter had the tone of pharmaceutical fine print — purposefully impenetrable while also clearly designed not to alarm. The district routinely monitored water, it explained, and the detection of something called PFOA didn’t necessarily mean that it posed any health risk.
Kiger put the letter aside, but a few weeks later, after a friend was diagnosed with cancer, he went back and reread it. What exactly was this chemical, PFOA? And why was Lubeck telling him about it if it really didn’t pose any health risk? He decided to approach the water district and the West Virginia Department of Environmental Protection with these questions. But when he did, he sensed he was being summarily — and nervously — dismissed, which made the teacher only more determined to get answers.
It took months of calls and visits to government offices before someone at the local branch of the federal EPA, who had heard that the Tennant suit had something to do with PFOA, pointed Kiger toward Bilott. The lawyer realized then that the entire water district, which today serves more than 4,000 customers, had been contaminated. In 2001, Bilott filed a class-action suit on behalf of all the people in the area who were exposed to C8-contaminated water — a group that eventually included Kiger and his wife, Darlene, as well as Jeromy Darling, Ken Wamsley, and Sue Bailey among the roughly 80,000 class members who lived or worked in six public water systems near the DuPont plant in Parkersburg.
Kiger didn’t realize it then, but drafts of the notification letter, despite being on the letterhead of Lubeck Public Service District, had been reviewed by DuPont, as a former public affairs manager for DuPont named Craig Skaggs admitted when he was deposed in 2002. Had much more time elapsed before Kiger went back to the letter or before he found someone in a public office who was helpful to him, the statute of limitations that had been triggered by the letter might have run out. According to West Virginia law, two years after they had been officially notified of the contamination, anyone exposed to C8 by drinking the Lubeck water would have lost their right to sue.
VEN CONSIDERING THE remarkable persistence (and luck) of Joe Kiger, Rob Bilott, and Wilbur Tennant, the person who did the most to turn a relatively small dispute over cattle into a mega class-action suit was actually employed by DuPont. Bernard Reilly had been an in-house counsel at DuPont since 1977, and for most of that time he worked in the environmental group within the company’s legal department. Reilly was assigned to help with the Tennant case, and he was worried about the possibility of somehow letting potentially incriminating information he was working on slip out. “Each time you put pen to paper or fingers to keyboard and create a new document,” he warned his colleagues in an email he sent in September 2000, “assume you will have the plaintiffs’ lawyers as recipients since we must produce each and every such document unless it is attorney/client privilege.”
“The lawyer for the farmer finally realizes the surfactant issue. He is threatening to go to the press to embarrass us to pressure us to settle for big bucks. Fuck him.”
Yet ironically it was Reilly himself who spilled the beans about C8 when he sent personal emails about the chemical through the company’s computer system. Consequently, just as Reilly had warned, when Bilott asked for C8-related materials in discovery, he received Reilly’s emails, which made clear not just that the company was hiding something, but also that he himself had become part of the story. One of Reilly’s emails, for instance, contained the following passage: “The lawyer for the farmer finally realizes the surfactant issue. He is threatening to go to the press to embarrass us to pressure us to settle for big bucks. Fuck him.”
Reilly wrote many of his emails, often to his son, from his vacation property in Vermont between October 1998 and May 2002 and interspersed musings about home repair, Otto the family dog, and his favorite snack food (goldfish cashew and almond nutty deluxe snack mix), with candid updates on his legal efforts concerning C8, which he referred to as “the material 3M sells us that we poop to the river and into drinking water.”
Reilly’s emails made clear that he felt the company had done wrong, first by polluting and then by not addressing the problem once it became known. He even revealed that the company knew the level of contamination had exceeded its own safety limits.
Not only do we have people drinking our famous surfactant, but levels in ambient air above our guidelines, sure we have margins of safety in our number, but we should have checked this out years ago and taken steps to remedy, guess the hills on the other side of the river cause great conditions for ambient levels, the plume hits them before it can disperse more fully. Ugh.
The DuPont lawyer was referring to his employer’s “Community Exposure Guidelines,” which specified safety limits of C8 in both air and water that were meant to protect the people living near the plant. Using what they knew about the chemical’s health effects and how long it remained in human tissue, staff scientists in 1991 had set this drinking water guideline at one part per billion. A level measured above that would present a “risk that needs to be disclosed to the community,” one document explained.
Yet the company hadn’t disclosed — or remedied — the problem, even when it measured C8 above that amount. Instead, in 1991, just months after realizing that the level of C8 in Lubeck’s water had exceeded DuPont’s guideline, the company decided to use a new lab to analyze C8 levels in water.
The new lab came up with C8 levels that were, on average, much lower than the results of DuPont’s in-house lab.
Y THE TIME THE lawsuits were underway, the company decided to find a lab that would more accurately measure the chemical. In 2001, as Reilly explained to his son, it switched back “to a much better analytical method that may bring in numbers that will alarm citizens.”
We learned recently that our analytical technique has very poor recovery, often 25%, so any results we get should be multiplied by a factor of 4 or even 5. However, that has not been the practice, so we have been telling the agencies results that are certainly low. Not a pretty situation, especially since we have been telling the drinking water folks not to worry, results have been under the level we deem “safe” of 1 ppb. We now fear we will get data from a better technique that will exceed the number we have touted as safe. Ugh.
Reilly had been fretting over the company’s responsibility for the contamination for some time. “We really should not let situations arise like this,” he wrote to his son in 1999. “We should have used a commercial landfill and let them deal with these issues.” And he also offered some hints as to why a corporation would knowingly let a toxic chemical seep into ground and water beyond its facility.
The plant tries to save money and apparently did not consider how it might look that this guy’s cows are drinking the rainwater that has percolated through our waste.
When he was deposed in June 2015, though, Reilly said he didn’t mean to suggest that DuPont should have to pay punitive damages.
Reilly, or “The Bernard,” as he signs off on occasion, apparently wasn’t privy to much of what DuPont knew about C8’s effects on humans — and, at least in 1998, didn’t think it harmed them. But he did know there was plenty of evidence that the chemical made lab animals sick. As he made clear to his son, the company was planning to conduct a primate study in 1999, together with 3M, which supplied DuPont with C8. 3M had conducted a monkey study 20 years before that produced disturbing, though not conclusive, findings.
Even before the new primate study was completed, however, Reilly clearly grasped the severity of DuPont’s legal problems. Apparently, though, he thought some of his higher-ups did not. While DuPont pressed for a trial in the Tennant case, he felt that going to trial was a bad idea and, as he wrote to his son in 1999, he took it upon himself to “describe to the plant folks why the guy who is suing us over his cattle grazing downstream of our landfill would crucify us before a jury. … Most simply do not believe how big and bad we would look.”
Preliminary results from the monkey study, released in 1999, only made DuPont look worse. The results showed that C8 caused monkeys to lose weight and made their livers increase in size. The hope had been to find a level at which there were no observable effects. But because even animals given the lowest doses of the chemical experienced enlargement of their livers, and one was so ill it had to be euthanized, no safe level was set after the study.
But DuPont clearly wasn’t ready to give up on its surfactant. Although 3M had decided to stop making C8 in May 2000, just months after the preliminary results of the monkey study were released, DuPont moved to start producing C8 in a new production facility in Fayetteville, North Carolina. Before the plant opened it issued a reassuring statement to the people in the area surrounding the facility: “DuPont has used [C8] for more than 50 years with no observed health effects in workers.” Charles Holliday, the company’s CEO at the time, testified in a sworn deposition in 2004 that after overseeing “very extensive scientific analysis” he believed the chemical was “safe in the way we use and handle it.”
N SEPTEMBER 2004, DuPont agreed to settle the class-action suit filed by Bilott’s firm and two others, which covered a class that had ballooned to 80,000 people in six water districts. The agreement was approved in early 2005 for an amount that could reach $343 million and was unusual in a number of ways. Generally, a legal settlement marks the end of a case, when attorneys and clients divvy up the cash and move on. Because the burden of proving that exposure to an unregulated chemical causes health problems is so onerous, plaintiffs who get any money in such cases may be especially inclined to let the matter drop. But the 2005 settlement of the C8 class-action lawsuit was also a beginning. Instead of just cutting checks, the agreement created a health project to collect medical information on the exposed population and determine whether exposure to C8 had actually harmed people.
At first, some doubted that the health project could enroll enough people to be useful; huge numbers of participants are usually necessary to show that a chemical causes harm. But the team of local researchers, headed by a retired physician named Paul Brooks and a former hospital administrator named Arthur Maher, threw themselves into the task. In part by offering each participant $400, they managed to interview and collect blood samples from 69,000 people who had lived or worked in the six affected water districts for at least a year.
The settlement also created a separate group called the C8 Science Panel composed of three physicians, Kyle Steenland, Tony Fletcher, and David Savitz, who all had backgrounds in epidemiology and public health and were chosen and approved by both teams of lawyers. The science panel used the blood samples and questionnaires from the health project and also conducted its own studies, which were published in peer-reviewed journals and posted on the science panel’s public website, to determine whether any diseases were linked. If they were, the agreement said, DuPont would filter the local water for as long as concentrations of C8 exceeded regulations and set aside $235 million for ongoing medical monitoring of the community. Plus, any of the class members who developed the linked diseases would be entitled to sue for personal injury. DuPont, moreover, agreed not to contest the fact that exposure to the chemical could cause the diseases.
By the time the C8 Science Panel completed its work in 2013, its members had spent eight years and around $33 million exploring the connections between C8 and human health. The panel even came up with a model that could estimate residents’ exposure levels based on where they lived and historical concentrations of C8 in air, groundwater, and the Ohio River. Linking that information to health data helped the three scientists find likely connections to six diseases: high cholesterol; a form of bowel disease called ulcerative colitis; pregnancy-induced hypertension; thyroid disease; testicular cancer; and kidney cancer.
Their results skewered DuPont’s hopes that its animal data might not apply to humans. They also flew in the face of a long-held belief about how chemicals affect people: that the dose makes the poison. That truism, generally attributed to the work of the 16th-century physician Paracelsus, has served as one of the starting points of modern toxicology. And this logic may have led DuPont scientists to conclude, or at least hope, that the small amounts of C8 people living near the plant ingested wouldn’t hurt them.
But Paracelsus hadn’t heard about endocrine disruptors, a recently discovered class of chemicals, to which C8 belongs, that interfere with the hormonal system. When graphed against the amount of chemical exposure, the health effects of endocrine disruptors often don’t take the expected form — an upward sloping line, with the lowest point on the left, where doses are lowest, and the effects steadily increasing along with the exposure levels. Instead, when plotted, the effects of endocrine disruptors can look like an upside down “V” or an upward slope with a dent in the middle, reflecting the fact that effects can, at certain levels, drop even as exposure increases.
Even though the level of C8 contamination required for a water district to become part of the class-action suit was low — just .05 ppb — the data gathered from class members showed apparent health effects. That limit had been chosen because at the time it was the lowest level that could be reliably measured.
The science panel data has since been used to link C8 with other effects beyond those six diseases, but according to the terms of the suit, the list of diseases cannot be amended. The attorneys’ clear-cut solution fell short of capturing the messy science of epidemiology. According to panel member David Savitz, a professor of epidemiology at Brown University, scientists still haven’t untangled all of the ties between C8 and disease. “It is quite possible, even likely, that some of the diseases we found no probable link for will, in time, turn out to be related to C8,” he said. Of course, as a careful scientist, Savitz knows that the contrary is true as well, because everything in science is potentially falsifiable. “But it’s also quite likely that some of the diseases for which we did declare a probable link will turn out, with improved research, to have been incorrectly judged when they are not associated with risk of those diseases. There was very little research done before the C8 Science Panel’s work, and while we extended the research considerably, it was and remains quite limited for drawing firm judgments.” It’s that permanent and irresolvable uncertainty that companies like DuPont are so adept at exploiting.
However, recent studies published in peer-reviewed journals such as Human Reproduction, Occupational and Environmental Medicine, and The Journal of Pediatrics have tied C8 to an incredible range of health effects, including ovarian cancer; prostate cancer; lymphoma; reduced fertility; arthritis; hyperactivity and altered immune responses in children; and hypotonia, or “floppiness,” in infants.
AD THE C8 HEALTH project not reached the number of people it did, or had the science panel not been as diligent about crunching all the data, epidemiologists might not have been able to recognize the elevated disease rates for what they were. In the water district with the highest level of exposure — Little Hocking, Ohio — there were eight cases of testicular cancer, a seemingly small number that is five times what would be expected in an unexposed population of that size. For kidney cancer, the rate of disease was up to two times higher than usual.
The link to high cholesterol, while clear enough to have been recognized and agreed upon by all three physicians on the science panel, also might have been missed because the study results were so nuanced. Yet in part because the study was so large, the researchers were able to show that the greater a person’s exposure to C8, the greater his or her chance of having elevated cholesterol.
Together, these diseases became part of a pattern. Considered in isolation, however, each illness is typically seen as a chance occurrence, which is what Jodie Boylen thought when she was diagnosed with kidney cancer. A lawyer who works on child neglect cases in the prosecutor’s office in Parkersburg, Boylen had been feeling exhausted before her doctor found her tumor in 2013. At that point, the link between C8 and kidney cancer had already been made by the science panel data, though she hadn’t heard about it. When she did, from a colleague who was working on the class-action case, she joined the class. Boylen also began thinking about the house she had lived in with her three children between 1989 and 1998. Not only was it in one of the affected water districts, their house was right on the shore of Lake Washington, a small body of water that was just a mile from the DuPont plant. “We drank it. We swam in that lake every day we could,” Boylen, now 53, remembered recently. “We lived in that lake in the summer.”
Boylen had surgery to remove her kidney tumor in 2013 and is hopeful that the cancer won’t return. But she still worries about her children. “They were in the water more than I was, they went to school in that district,” she said in a recent interview in her Parkersburg home. “What’s going to happen to them in a couple of years?”
Jeromy Darling, too, is now cancer-free. But 17 years after his diagnosis, the financial legacy of his ordeal is still with him. Because he was uninsured at the time of his illness, he wound up declaring bankruptcy after being hit with more than $75,000 in bills for his surgeries. “I had all the good cards, all the good interest rates. All that went away,” he said in a recent interview. “It’s embarrassing. I work forty-plus hours a week and I can’t get a credit card now.”
Darling was unable to buy a house because he couldn’t get a mortgage, so his girlfriend of 20 years bought their current home by herself. And he hasn’t married her because he didn’t want his bad credit history to rub off on her good one. The couple even changed their plans about having children together after Darling’s doctors told him his sperm count was greatly reduced due to his cancer diagnosis. “We didn’t try because you don’t want to have that disappointment,” he said. “It’s almost better to put it out of your mind.”
When they got together, each of them had already had one child. Like Boylen, Darling is focused on the children’s health and the fact that they grew up in the chemical valley, drinking the same C8-contaminated water he did.
O DATE, SOME 3,500 personal injury claims have been filed as part of the 2005 class-action settlement. The first trial, scheduled for September in Columbus, Ohio, takes up the case of Carla Bartlett, who maintains that her kidney cancer was caused by exposure to C8. Attorneys for DuPont, because of the terms of the class-action settlement, will be unable to contest the general causal connection between kidney cancer and C8 exposure, but they will almost certainly argue that other factors are more likely to be responsible. The deposition of a DuPont expert named Douglas Weed suggests a possible line of attack: that Bartlett, who lives just a few miles downriver from the DuPont plant, developed the cancer because she’s overweight. Or, perhaps, just by chance.
The role of luck — that two things often correlate just by chance — was a major point of Weed’s testimony, for which DuPont paid the former employee of the National Cancer Institute more than $100,000. During his deposition in March 2015, the doctor estimated that since leaving the government agency eight years ago he has made between $5 million and $6 million providing expert testimony to companies in such corporate defense cases.
Surely, after all that they’ve endured, Bartlett, Darling, Boylen, and the other plaintiffs would agree that sometimes bad things just happen. But their list of unfortunate — and unlikely — occurrences would no doubt include the leakage of a toxic and biologically potent chemical into their water and the subsequent contamination of their bodies, where it may have caused diseases that have forever changed their lives.
Perhaps the most remarkable and unlikely occurrence of all is not the fact that the contamination happened, or even that it turned out to be harmful, but that it was discovered. It’s easy to imagine how — without Tennant, Bilott, or Kiger; without Reilly’s revealing emails; and without the exuberance of the health project and the diligence of the science panel — DuPont’s secrets might never have emerged. Had the stars aligned that way, C8 would still be largely unknown, just one of the tens of thousands of unregulated chemicals we don’t notice as they silently pollute our world.
EDITOR’S NOTE: DuPont, asked to respond to the allegations contained in this article, declined to comment due to pending litigation.
In previous statements and court filings, however, DuPont has consistently denied that it did anything wrong or broke any laws. In settlements reached with regulatory authorities and in the class-action suit, DuPont has made clear that those agreements were compromise settlements regarding disputed claims and that the settlements did not constitute an admission of guilt or wrongdoing. Likewise, in response to the personal injury claims of Jodie Boylen, Jeromy Darling, and others, DuPont has rejected all charges of wrongdoing and maintained that their injuries were “proximately caused by acts of God and/or by intervening and/or superseding actions by others, over which DuPont had no control.” DuPont also claimed that it “neither knew, nor should have known, that any of the substances to which Plaintiff was allegedly exposed were hazardous or constituted a reasonable or foreseeable risk of physical harm by virtue of the prevailing state of the medical, scientific and/or industrial knowledge available to DuPont at all times relevant to the claims or causes of action asserted by Plaintiff.”
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.”
This article was reported in partnership with The Investigative Fund at The Nation Institute.
Alleen Brown, Hannah Gold, and Sheelagh McNeill contributed to this story.
In this series, Sharon Lerner exposes DuPont’s multi-decade cover-up of the severe harms to health associated with a chemical known as PFOA, or C8, and associated compounds such as PFOS and GenX.
The Environmental Protection Agency has long known that C8 is harmful to human health. But the chemical, which is in the bloodstream of 99.7…
MIKE ROMINE GREW UP in Blennerhasset, West Virginia, not far from DuPont’s Parkersburg plant. Throughout his childhood and young adulthood, Romine was probably exposed through his drinking water to C8, a slippery, soap-like chemical used to make Teflon pans and Stainmaster carpet and hundreds of other products. His home was served by the Lubeck water district, one of six districts near the plant later found to be severely contaminated with the chemical, but his greatest exposure to C8 almost certainly came from working at the DuPont plant, where he was a welding inspector.
Romine spent some of his time in the company’s Teflon division, and he particularly remembers taking part in the “Teflon shut down,” a spring-time ritual. For a few days each year, the company would shut down operations in the plant to prepare for the coming year. Romine helped install new piping. He didn’t know what C8 was at the time, but there was a white powdery substance dusting many of the surfaces in the plant. “It’s on the pipe, on the inside of it,” said Romine. “You don’t all the time have on gloves. It’s on your coveralls.”
Twelve years ago, when Romine was 58, he was diagnosed with kidney cancer. No one in his family had ever suffered from this rare disease. Surgeons removed the cancerous organ, leaving Romine with reduced kidney function. Now he has to urinate frequently and his doctors have suggested that he change his diet and refrain from running, an activity that had been a regular part of his life before the surgery. Every six months he must return to the doctor to have his remaining kidney checked.
Today, Romine has mixed feelings about DuPont. He worked for the company full-time as a contractor for eight years, and his best friend was employed in one of DuPont’s labs. “In my heart, I felt I was DuPont,” said Romine, who has enduring respect for the company. “DuPont has really good safety rules, good people, good personnel,” he said. “I enjoyed working down there.”
Still, for all the good DuPont has done his community as an employer and as a supporter of local organizations and sports teams, Romine is concerned that the company has not been fully honest — especially after a panel of scientists, funded by a class-action settlement, found that kidney cancer and five other diseases had been strongly linked to C8 exposure. “DuPont made me money,” he said, “but I certainly think now they needed to come clean with whatever happened.”
IN MARCH 2001, an attorney named Robert Bilott embarked on an ambitious plan to force DuPont to come clean — to tell what it knew about C8 and, he hoped, eliminate the chemical from the water consumed by Romine and others throughout the country. Bilott sent packages of evidence to the federal Environmental Protection Agency, the West Virginia Department of Environmental Protection, and the Attorney General of the United States, among other regulators. Inside were more than 100 documents he had received through discovery in a lawsuit he had filed in 1999 on behalf of a West Virginia farmer named Wilbur Tennant, whose cows died after being exposed to PFOA, also called C8 because of the eight-carbon chain that makes up its chemical backbone. The documents showed that DuPont, which since the early 1950s had used C8 to manufacture Teflon and other products in its Parkersburg plant, had known for years that C8 posed health dangers and had spread beyond the company’s West Virginia plant into local sources of drinking water.
Bilott even arranged to go to Washington, D.C., to personally present his findings to the EPA. When DuPont attorneys learned about Bilott’s plan, they tried to stop him with a last-minute gag order. They were unsuccessful, however, as Bernard Reilly, one of the company’s in-house lawyers, noted in an email to his son on March 27, 2001:
Court yesterday did not agree to shut up plaintiff lawyer in our Parkersburg situation and today he testifies an EPA hearing and will try to slam us one more time.
Bilott did make his case to the federal regulators and reiterated the request he made in the letter that accompanied his evidence, that the agency regulate C8 under the Toxic Substances Control Act “on the grounds that it ‘may be hazardous to human health and the environment.’”
By some measures, Bilott has in fact been successful in slamming DuPont, but 14 years after he sent his evidence to the EPA, the company has managed to avoid a full reckoning for its actions. And C8, which is in the bloodstream of 99.7 percent of Americans, remains unregulated at the national level.
During the five decades in which DuPont used and profited from C8, the company had only infrequently discussed the chemical with environmental authorities, and it kept most of its extensive internal research on the chemical confidential. After Bilott sent out his packages of evidence, however, DuPont’s relationships to government agencies shifted dramatically. Bilott’s revelations had the power to tarnish the company’s reputation and lead to huge legal and cleanup costs, so DuPont focused on weathering the scrutiny of regulators and keeping its name — and profits — unscathed.
Although Bilott and his clients eventually prevailed in a ground-breaking class-action lawsuit filed the same year he approached the EPA, that settlement had limited applicability. Action by the EPA could hold DuPont accountable nationally.
Locally, the matter was well in hand. Several regulators at the West Virginia Department of Environmental Protection had already shown their allegiance to the company, one of the state’s biggest employers. In October 1996, after the regional office of the EPA began investigating a complaint about one of the company’s landfills, Eli McCoy, the director of the West Virginia DEP, allegedly sent the company a document “to aid DuPont in diffusing any potential enforcement action,” as Bilott put it in a letter to the EPA. After a few weeks of negotiation, the West Virginia DEP signed off on a consent decree, in exchange for a mere $200,000 penalty and minor upgrades from DuPont. McCoy then went to work for a consulting firm DuPont hired to help it comply with that agreement.
He wasn’t the only regulator who followed the money. As Callie Lyons reported in her 2007 book, Stain-Resistant, Nonstick, Waterproof, and Lethal, three attorneys handling C8 at the West Virginia DEP emerged on the other side of the revolving door as employees of the same local law firm that defended the chemical on behalf of DuPont. Reached for comment, McCoy said that he did not recall details of the matter, noting that he had not worked for the West Virginia DEP for 18 years.
The EPA presented a potentially more challenging situation. The federal agency has the authority to regulate C8 under several laws, including the Toxic Substances Control Act and the Clean Water Act. Through either route, regulation could trigger hefty cleanup costs. In 2002, the EPA initiated what is called a “priority review,” a critical first step toward regulation, which entails assessing a chemical’s risk to determine whether it should restrict or ban it. The EPA puts a special priority on chemicals that are toxic, persist in the environment, and accumulate in people’s bodies. C8 fit the bill on all three counts.
In response, DuPont assembled a high-powered team that included former EPA officials to oversee its C8 communications with the federal agency. Michael McCabe, a consultant who managed the company’s communications and C8 strategy with the EPA starting in 2003, had served as deputy administrator of the agency until 2001. Linda Fisher, a lawyer who succeeded him in the No. 2 position at the EPA, was also central to DuPont’s C8 campaign. In fact, just over a year after leaving the agency in June 2003, Fisher was already deeply involved in the defense of C8. It surely didn’t hurt that William Reilly, who led the EPA from 1989 to 1993, sat on DuPont’s board of directors.
DuPont’s C8 team benefited from inside information about what regulators were thinking about the chemical, according to testimony McCabe gave when he was deposed in 2007. They knew what was in some of the agency’s documents before they became public and saw at least one presentation before it was given. The DuPont team even drafted quotes to be attributed to EPA officials, which DuPont later embedded in press releases. In his deposition, McCabe said the practice of asking the EPA for a quote was “customary.”
Several other firms also served as consultants, including a company called the Weinberg Group. In an April 2003 memo, P. Terrence Gaffney, the group’s vice president for product defense, proposed “a fresh new approach” to help DuPont with its defense of C8:
The constant theme which permeates our recommendations on the issues faced by DuPont is that DUPONT MUST SHAPE THE DEBATE AT ALL LEVELS. We must implement a strategy at the outset which discourages governmental agencies, the plaintiff’s bar, and misguided environmental groups from pursuing this matter any further than the current risk assessment contemplated by the Environmental Protection Agency (EPA) and the matter pending in West Virginia. We strive to end this now.
The memo bragged that the company had long experience in managing chemical PR crises. “Beginning with Agent Orange in 1983,” Gaffney wrote, “we have successfully guided clients through myriad regulatory, litigation, and public relations challenges.” Weinberg’s proposal included using “focus groups of mock jurors to determine the best ‘themes’ for defense verdicts,” retaining “leading scientists to consult on the range of issues involving PFOA so as to develop a premium expert panel,” and efforts to “reshape the debate by identifying likely known health benefits of PFOA exposure by … constructing a study to establish not only that PFOA is safe … but that it offers real health benefits.”
The “Weinberg memo” gained a level of infamy when a copy was made public in 2006. Two years later, Rep. John Dingell of Michigan brought it up in a Congressional investigation, noting, “The tactics apparently employed by the Weinberg Group raise serious questions about whether science is for sale at these consulting groups.” DuPont, which has asked the judge in the upcoming trials to exclude any mention of the Weinberg Group, denied that it hired the consulting company to work on C8. But court documents, including invoices (one of which mentions PFOA specifically), suggest otherwise. Two years later, the Weinberg Group again offered its services to DuPont and in an email made reference to “the C8/fluorocarbon chemicals controversy” and noted that “the Weinberg Group which offers services in evidence-based advocacy was given some discrete assignments in developing strategies for helping DuPont in its advocacy.” Reached by telephone, Matthew Weinberg, the CEO of the Weinberg Group, declined to comment, but then added: “The Weinberg Group is no longer engaged in any of this work. We’re an FDA consulting firm.”
ALTHOUGH THE EPA is specifically charged with the task of protecting the public by reducing the risk of exposure to commercial chemicals, the agency is also limited in what it can require of industry. Unlike the Food and Drug Administration, which reviews prescription medications before they can be brought to market, the EPA has little power to prevent a company from using a chemical before it is proven to be safe. Although in Europe chemicals must be proven safe before they are put on the market, in the United States — despite repeated revelations that widely used industrial chemicals (including PCBs, fire retardants, and many others) have severe public health and environmental effects — chemical manufacturers have few legal obligations to ensure that their products are safe. In America, killer chemicals are essentially innocent until proven guilty.
Another conundrum of our chemical regulatory system is that regulators must depend on the manufacturers for data on the chemicals they wish to regulate. Yet this information can be difficult to obtain, precisely because the chemicals are unregulated. To move forward with the priority review of the chemical it had begun in 2002, the EPA needed to know how polluted with C8 were the water, air, soil, plants, animals, humans, and food sources near the DuPont plant in West Virginia.
DuPont and other companies that used C8, including Daikin, 3M, and Dyneon, quickly volunteered to provide the information. The companies came up with several research proposals and then together, represented by an entity called the Fluoropolymers Manufacturers Group, lobbied the EPA to make the agreement regarding the chemical completely voluntary. Among the alleged benefits of the voluntary option were “quicker implementation” and that “monitoring data can be obtained sooner,” members of the manufacturers group argued at a January 2004 meeting with the EPA. Of course, the problem with a voluntary agreement is that it would be unenforceable.
Without a legally binding agreement, the EPA was unable to enforce the terms of its interactions with DuPont. Mostly, the agency relied on negotiated consent agreements. If DuPont didn’t like the terms, it could simply walk away from the deal. In one of these agreements, a regional consent order dated March 2002, DuPont agreed to provide clean water to residents near its plant whose drinking water was contaminated above a certain level. Despite the fact that the company had set its own internal safety limit for the maximum amount of C8 in drinking water at 1 part per billion (ppb), in the consent order the company agreed only to a limit of 14 ppb. Two months later, that “trigger level” was raised to 150 ppb, where it stayed until 2006.
While it was pressing for an unenforceable national agreement, DuPont was also negotiating the future of C8. When its legal troubles concerning C8 had first begun, the company had clearly banked on continuing to use C8, as evidenced by its 2002 decision to invest $23 million in a facility to produce it. But by 2005, after DuPont settled the class-action suit over water contamination around its West Virginia plant, according to the sworn testimony of McCabe, the company told regulators it was open to the possibility of phasing out C8.
On this front, too, the company set the terms. In an October 2005 meeting with the EPA, McCabe presented a slide about the company’s “critical needs,” among them that “EPA restate safety of products and no health effects.” McCabe also asked the EPA to make a public statement acknowledging DuPont’s leadership in withdrawing C8, and to ensure that all the other companies using the product also be required to retire it.
Around this time, DuPont reached out to the Bush White House, as emails that emerged in discovery showed. McCabe admitted in a deposition that DuPont wanted to let the EPA know that the Bush administration was supportive of its proposal. McCabe, in his deposition, said that such contacts were “not unusual.”
PERHAPS IT IS ALSO not unusual that all of the company’s pending questions around C8 — whether the company would be fined for withholding information about the chemical from the government; whether it would retire its chemical; and whether it would be subject to binding regulation by the EPA — were resolved in a matter of months, shortly after the contacts between DuPont and the White House.
A month after the company finalized its voluntary commitment to research the extent of contamination around its West Virginia plant, the EPA resolved the matter of the fine. The settlement reached that month stemmed from DuPont’s unlawful failure to alert the EPA about information regarding its risk to human health. Specifically, the company withheld what it knew about the toxicity of C8, the presence of C8 in drinking water, the presence of C8 in the blood of people living near its West Virginia plant, and in the babies of some of its female workers, two of whom were born with birth defects.
At the time, the EPA trumpeted the fact that its $10.5 million fine of DuPont was “the largest civil administrative penalty EPA has ever obtained under any federal environmental statute.” The settlement also required the company to spend $6 million on “supplemental environmental projects.” Less remarked upon was the fact that the fine was a small fraction of the maximum $300 million the agency technically could have collected.
The total $16.5 million penalty was an even smaller fraction of the $1.6 billion in quarterly sales that DuPont’s performance materials division was enjoying at that time — less, in fact, than the division’s sales in a single day.
The following month, DuPont finalized the specifics of its one significant concession: to participate in what the EPA called a “global stewardship program,” which in practice meant a 95 percent reduction in C8 emissions by 2010 and eliminating use of the chemical by 2015. In January 2006, Susan Stalnecker, a DuPont vice president, sent a letter to Stephen Johnson, then head of the EPA, confirming the agreement and alluding to DuPont’s plan to replace C8 with another chemical, noting that “success in this effort will depend on timely review and approvals for these new products.”
As McCabe’s deposition shows, the plan was carried out according to the company’s specific terms. As DuPont had requested, the EPA invited the seven other companies that used C8, including 3M, to also participate in the stewardship program, and all agreed to reduce their emissions and phase it out. And, as DuPont had requested, the EPA issued reassuring statements about C8 and the products that contained it. On January 25, 2006, in the announcement of the global stewardship program, the agency said that “to date EPA is not aware of any studies specifically relating current levels of PFOA exposure to human health effects.” On the same day, DuPont issued a press release containing the agency’s statement.
Five days later, a draft report by an EPA Science Advisory Board that was reviewing C8 found the chemical to be a “likely human carcinogen.” DuPont vice president Susan Stalnecker sent an email to her team:
Publicity around SAB report has linked the Teflon brand to cancer. Coverage has been broad in print and network media. Significant disruptions in our markets and are [sic] consumers are very, very concerned.
What’s telling about the email is the company’s attitude toward the EPA and its assumption that of course the agency would cooperate in the damage-control campaign.
In our opinion, the only voice that can cut through the negative stories, is the voice of EPA. We need EPA … to quickly (like first thing tomorrow) say the following: Consumer products sold under the Teflon brand are safe.
According to a February 17, 2006, email from Susan Stalnecker to DuPont CEO Charles Holliday, Linda Fisher then contacted Marcus Peacock at the EPA and expressed DuPont’s concerns about the need for the EPA to make a statement. That February, a group of high-profile health ethicists and epidemiologists hired by DuPont to consult on C8 advised the company against making any further public statements denying that C8 poses a risk to human health.
On March 2, 2006, the EPA obligingly issued another statement saying, “The agency does not believe that consumers need to stop using their cookware, clothing, or other stick-resistant, stain-resistant products.” The agency’s own research has since shown that consumer products are in fact a source of C8 exposure. While Teflon-coated pans appear to account for only a small amount of Americans’ C8 exposure, other consumer products, such as coatings for stain-resistant carpets, floor wax, and upholstery, are greater sources of contamination, according to a 2009 EPA analysis of 116 consumer products.
McCabe, in his December 2007 deposition, insisted that the highly favorable public statements by the EPA were “not a quid pro quo” for the company’s agreeing to phase out C8.
The Intercept requested comment from McCabe and Fisher but received no reply. Stalnecker did not respond to emails requesting comment. The EPA declined to comment on the suggestion that it had engaged in a quid pro quo with DuPont. In a statement (see below), DuPont asserted that Fisher “has never represented DuPont on PFOA matters with the EPA.”
DuPont has phased out the use of C8, but in other respects the company simply failed to live up to its end of the bargain. DuPont did file three reports about C8 contamination in air, water, soil, and biota around its Parkersburg plant in 2008. But a team of independent peer reviewers found that these reports suffered from “significant limitations and omissions” and asked the company to fill in several gaps. Among dozens of additional requests, the reviewers asked DuPont to perform more frequent and extensive sampling of the Ohio River; to expand the 2-mile area where it was measuring the impact of C8 exposure; and to provide more data on the presence of C8 in local water, soil, air, fish, game, and meat, and in the blood and breast milk of residents in the area of the plant. DuPont then revised its report, but the EPA again requested that extensive additional research be done in 2010.
In 2011, the EPA reiterated the need for more data, noting in particular that the company did not test milk from cows in contaminated areas. The next year, without fulfilling many of the reviewers’ outstanding requests, DuPont submitted what it said would be the final version of the report it had promised under the voluntary agreement it had reached with the EPA in 2005. At the time the agreement was hammered out, proponents had noted that it would be public — and, as such, that people would know if the company failed to keep its promises. But little public mention was made when DuPont submitted in November 2012 its final report that was supposed to help with monitoring C8. Without any legal recourse, the EPA quietly filed it away, and a national standard for C8 contamination in drinking water was never set.
MEANWHILE, REGULATORS in New Jersey were waging their own battle against C8. Back in 2006, the state began to consider setting a drinking water standard for the chemical. The New Jersey Department of Environmental Protection knew there was some contamination around a DuPont plant in Deepwater, a community about 20 miles down the Delaware River from Philadelphia. In September 2003, groundwater tests under the plant had revealed C8 levels as high as 46.6 ppb. In some workers at the New Jersey plant, in 2007, blood levels were very high; one was measured at 4,400 ppb. According to data from the CDC, blood levels of the chemical in the general U.S. population in 2007 averaged around 4 ppb.
A group of 15 scientists and water experts known as the New Jersey Drinking Water Quality Institute was responsible for proposing drinking water standards in the state. Their task was clearly laid out by New Jersey law: to determine maximum contaminant levels, including the exact amount of a chemical that, when drunk by a million people over their lifetimes, causes no more than one case of cancer. For more than 20 years, the institute had been crunching numbers to arrive at the maximum allowable level of a given contaminant and then submitting the figure to the state’s Department of Environmental Protection. During most of that time, the group had carried out its charge with little intervention and even less fanfare.
Eileen Murphy, head of the Division of Science, Research and Technology at the New Jersey DEP, was closely studying C8 at the time and was invited, along with members of her staff, to meet with DuPont executives.
Murphy was investigating whether C8 was dangerous. The EPA had already classified the chemical as a likely human carcinogen — a term applied to chemicals that cause tumors in more than one species — and she knew about numerous studies that indicated it to be toxic. She said as much at the meeting. Murphy and the DuPont representatives then “disagreed widely over the interpretation of the toxicology studies,” Murphy remembered recently. “They said our interpretation was overly conservative.” Afterward, “we never heard from them again,” Murphy said. “They just went higher than us. And liked that path better.”
In 2007 the Drinking Water Quality Institute came up with the figure for C8 and sent it to the New Jersey DEP. The proposed standard was .04 ppb.
When DuPont learned about the proposal, a tiny fraction of the level the company had helped West Virginia set a few years before, McCabe and his communications team went to work. If the proposed safety level were enacted, the company could face enormous cleanup and liability costs. McCabe drafted letters arguing that New Jersey’s numbers were far too low and sent them to the commissioner of New Jersey DEP, the governor’s office, and the state’s Economic Development Office.
DuPont representatives later came to subsequent meetings at the New Jersey DEP, to which Murphy was no longer invited. Not long after, in October 2008, Murphy was preparing to submit for peer review an article about C8 in New Jersey water systems that one of her colleagues had written, when Lisa Jackson, who was then New Jersey’s DEP commissioner, asked her to stop its progress toward publication. The article explained the agency’s logic for setting .04 as a safety standard and noted that it had already detected C8 above that level in five drinking water systems.
“I did it anyway,” Murphy recalled in an interview this past spring. “I was reassigned after that.” Indeed, shortly after Murphy submitted the article for peer review, she was relieved of her position as division head, in which she had managed a team of PhD scientists like herself. Instead, Murphy was given a post with few responsibilities and in the months before she left the agency filled her time by working on low-level projects and helping the secretaries with their typing. Lisa Jackson went on to serve as administrator of the federal EPA under Barack Obama. She is currently vice president of environment, policy, and social initiatives for Apple. The Intercept left repeated messages for Lisa Jackson requesting comment and attempted to contact her via email, but received no reply.
In September 2010, the Drinking Water Quality Institute began to move forward with the .04 water standard, nine months after Chris Christie became of governor of New Jersey. Christie had made it clear, with his “red tape commission” and pro-business executive orders, that he was unlikely to pass new regulations. But the Christie administration went even further; not only did it apparently block the proposed standard, it also effectively disbanded the water quality group. Although the institute and its committees had met nearly 50 times in the five years prior, after the September 2010 meeting the group did not convene again for almost four years.
Meanwhile, the New Jersey DEP had created a new body called the Science Advisory Board, to advise on a number of environmental issues, including water quality. In 2011, three DuPont scientists, each of whom have worked on C8, were appointed to the board.
This past spring, the Drinking Water Quality Institute met for only the second time since it attempted to set a C8 standard in 2010 (the first was in 2014). The chair of the recently resurrected group, a toxicology professor named Keith Cooper, told me that he’s committed to setting a new drinking water standard for C8. “These recommendations are for the health and safety of the people of New Jersey,” said Cooper, who added that he would do everything he could to push back if the standards fail to move forward this time around, including bring the matter to the current DEP commissioner, Bob Martin. “First I will meet with Martin and then I will request to meet with Christie.”
But because the last set of proposed regulations never made it into law and have officially sunset, the whole process must begin again, which means at least another year of legal, scientific, and administrative preparations. The process is likely to take much longer. By that point, Christie may no longer be governor, but DuPont will have succeeded in delaying and perhaps permanently deferring its environmental accountability for contaminating New Jersey waters with C8. The Christie administration did not reply to requests for comment.
DESPITE ALL THESE setbacks, it is still not too late for the EPA to regulate C8 and require companies such as DuPont to pay for cleanup costs. Attorney Robert Bilott clearly hasn’t given up on the cause, though there is a certain pathos in the letter he sent the EPA this January, which begins this way:
We first wrote to US EPA and WVDEP in March of 2001 — over 13 years ago — to alert your Agencies to the imminent and substantial threat to human health and the environment posed by the contamination of human drinking water supplies with perfluorooctanoic acid.
Indeed, there is voluminous, and repetitive, correspondence about C8 between the agency and the lawyer. In 2010, the agency responded to his urging to set a national drinking water level with a promise that it would do so by the end of that year. Then, in 2011, the agency promised to set the level by the end of that year. And, again, in a February 2012 letter, the EPA claimed it would take action in the “next few months” or by “early 2013.”
A February 23, 2015 letter from Susan Hedman, a regional administrator of the EPA, has a similar ring, saying that a lifetime health advisory may be developed “later this year,” at which point the agency might just possibly reevaluate its 2009 consent order with DuPont.
Recent testing by the EPA found C8 in 94 water systems serving a total of 6.5 million Americans. The minimum testing level was .02 ppb, which is far greater than new estimates of an approximate safe level in drinking water. If the EPA does ever decide to regulate C8 and set a national drinking water standard, DuPont might still be able to avoid cleanup costs, since the company has now cut its ties with the chemical. In July, DuPont spun off its chemical division into a separate company called Chemours. DuPont has promised to cover whatever settlements result from the crop of personal injury claims scheduled to come to trial in the fall. But, if they’re ever levied, cleanup costs for the C8 DuPont leaked into the larger environment, which could add up to many billions of dollars, could fall to Chemours, a much smaller company.
Over the years, as letters have flown back and forth between lawyers and various agencies, levels of the chemical in human blood throughout the United States appear to be dropping. That is good news for the people whose systems the chemical is exiting — the chemical has a half-life in humans of about four years — though not necessarily for the planet at large, since the chemical isn’t going away. It’s simply being diffused, spreading throughout the world’s water systems.
Meanwhile, as it was dispensing with its C8 problem, DuPont was busy introducing new chemicals to replace the old one. Since at least 2009, the company has been using what it calls the “Capstone” line of surfactants and repellants, which in July became the property of Chemours. The replacement molecules are reported to have a six or fewer fluorinated carbon chain as their base but little more about them is known since their chemical make-up is proprietary. FDA records obtained by the Environmental Working Group show that since 2005 the agency approved at least 10 “fluorochemicals” that could replace C8 in food packaging, though there is little public record of health risk assessments being performed on them.
This spring, an international group of scientists and environmental advocates issued a public warning about these replacement chemicals. The “Madrid Statement,” as it’s called, noted that while the “shorter-chain” chemicals used to replace C8 may not stay in human bodies quite as long, “they are still as environmentally persistent as long-chain substances or have persistent degradation products.” The statement, which has now been signed by hundreds of scientists, continued: “Because some of the shorter-chain PFASs are less effective, larger quantities may be needed to provide the same performance.”
The Madrid Statement called on governments to require companies to conduct more toxicological testing and to make chemical structures public. And this year, after it banned the chemical, the European Union proposed a global ban on C8, which is now being produced in India, Russia, and China.
The United States has yet to set a level that’s safe to drink. As Mike Romine in West Virginia sees it, there is something terribly wrong with letting people be exposed to a chemical that can hurt them.
Such thinking was the basis for the class-action suit targeting the plant in West Virginia where Romine worked and the subsequent settlement requiring DuPont to provide clean water to tens of thousands of people in nearby water districts. In a few weeks, the first of approximately 3,500 personal injury claims resulting from that class action will come to trial in Columbus, Ohio. We may soon know if a jury will hold DuPont accountable for the lives it has forever altered, through chemistry.
But whatever happens in those claims, the overwhelming majority of Americans have also been exposed. So far, no one has offered them any recourse or offered to ensure that their water is safe to drink.
EDITOR’S NOTE: DuPont, asked to respond to the allegations contained in this series, initially declined to comment due to pending litigation.
In previous statements and court filings, however, DuPont has consistently denied that it did anything wrong or broke any laws. In settlements reached with regulatory authorities and in the class-action suit, DuPont has made clear that those agreements were compromise settlements regarding disputed claims and that the settlements did not constitute an admission of guilt or wrongdoing. Likewise, in response to the personal injury claims of Mike Romine, Jeromy Darling, and others, DuPont has rejected all charges of wrongdoing and maintained that their injuries were “proximately caused by acts of God and/or by intervening and/or superseding actions by others, over which DuPont had no control.” DuPont also claimed that it “neither knew, nor should have known, that any of the substances to which Plaintiff was allegedly exposed were hazardous or constituted a reasonable or foreseeable risk of physical harm by virtue of the prevailing state of the medical, scientific and/or industrial knowledge available to DuPont at all times relevant to the claims or causes of action asserted by Plaintiff.”
Before the publication of this article, DuPont provided the following statement:
DuPont has worked collaboratively with the U.S. Environmental Protection Agency (EPA) to meet and exceed the Agency’s program requirements on PFOA. We have never requested nor have we received special consideration or treatment from the Agency regarding PFOA.
In 2006, EPA and the eight major companies in the industry, including DuPont, launched the 2010/15 PFOA Stewardship Program, in which companies committed to reduce global facility emissions and product content of PFOA and related chemicals by 95 percent by 2010, and to work toward eliminating emissions and product content by 2015.
Prior to the development and implementation of the PFOA Stewardship Program, EPA posted the following statement on the use of consumer products on the Agency’s website. “The information that EPA has available does not indicate that the routine use of consumer products poses a concern. At present, there are no steps that EPA recommends that consumers take to reduce exposures to PFOA.” The statement is the Agency’s recommendation, and DuPont had no involvement in its development.
With respect to Linda Fisher, for over 30 years, she has served with distinction as a leader in environmental protection, health and safety for the EPA and later for private businesses. Throughout her career, Linda has upheld the highest standards of integrity and ethical behavior, and has fully complied with the EPA’s ethics rules since leaving EPA, and later as DuPont’s Chief Sustainability Officer. In her role as Chief Sustainability Officer Linda was instrumental in helping DuPont design and implement its Global Stewardship Program to ensure the company met its commitments with the EPA. Linda has never represented DuPont on PFOA matters with the EPA.
Our work with the Agency has been and remains transparent, and we have cooperated in every way with the spirit and letter of applicable laws and EPA guidelines.
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.
This article was reported in partnership with The Investigative Fund at The Nation Institute.
Ava Kofman and Sheelagh McNeill contributed to this story.
In this series, Sharon Lerner exposes DuPont’s multi-decade cover-up of the severe harms to health associated with a chemical known as PFOA, or C8, and associated compounds such as PFOS and GenX.
The first of 3,500 personal injury and 37 wrongful death claims against DuPont went to trial in Columbus, Ohio, this week.
DUPONT WENT TO COURT this week, defending its use of C8, the chemical that spread from the company’s Parkersburg, West Virginia, plant into the drinking water of some 80,000 people in West Virginia and Ohio. A jury in Columbus, Ohio, is now hearing the case of Carla Bartlett, a 59-year-old woman who developed kidney cancer after drinking C8-contaminated water for more than a decade.
As The Intercept reported in a three-part series last month, Bartlett’s is the first of some 3,500 personal injury and 37 wrongful death claims stemming from the 2005 settlement of a class-action suit filed on behalf of people who lived near the plant. Another trial over the chemical, which for decades was used in the production of Teflon and many other products, is scheduled for November. Together, the “bellwether” cases, six in all, are expected to give attorneys on both sides a sense of whether the rest of the claims will proceed or settle — and for how much.
Bartlett’s attorneys, including Robert Bilott, who has been working on C8 since taking the case of a West Virginia farmer named Wilbur Tennant in 1999, argue that DuPont is guilty of negligence, battery, and infliction of emotional harm for exposing Bartlett to C8 in her drinking water.
DuPont’s attorneys, who summarized their case in opening arguments and will present their witnesses later in the trial, insist that the company bears no responsibility for the kidney tumor for which Bartlett was treated in 1997. “Nobody at DuPont expected that there would be any harm from the extremely low levels of C8 that were reached in the community,” said DuPont’s attorney Damond Mace in his opening argument.
The company’s defense hinges on the contention that company employees did not realize C8 was dangerous at the time Bartlett was exposed — despite hundreds of internal documents detailing DuPont’s knowledge that the chemical posed risks to both animals and humans. When evidence of its harm did emerge, said Mace, it was too late: “Nothing that happened after 1997 would have allowed DuPont to go back and do things any differently than had already been done.”
The particular threats posed by the chemical were detailed by the findings of a panel of scientists, who in 2012 determined that C8 exposure at the level measured in six water districts — at least .05 parts per billion — was “more likely than not” linked with six illnesses: preeclampsia; ulcerative colitis; high cholesterol; thyroid disease; testicular cancer; and Bartlett’s disease, kidney cancer.
“Kidney cancer occurs every day all across this great country of ours.”
The 2005 class-action settlement requires DuPont to accept C8’s links to these diseases, and that agreement forces the company’s attorneys to walk a legal tightrope over causality. While they must admit that C8 can cause kidney cancer, they deny that it caused Bartlett’s particular cancer. As Mace told the jury: “Kidney cancer occurs every day all across this great country of ours.” He then pointed out that Bartlett, who weighs 230 pounds, displayed one of the “major risk factors” for the cancer: obesity.
DuPont also contends that C8 isn’t as toxic as the plaintiffs claim. As evidence, Mace cited a report produced by the West Virginia Department of Environmental Protection, with the help of an industry-funded group and several DuPont employees, that set a temporary standard for drinking water safety that was 150 parts per billion (ppb). Yet the company’s own internal standard for the chemical was 1 ppb.
The DuPont lawyer also told the jury about a study the company conducted that concluded Wilbur Tennant, the West Virginia farmer who sued DuPont over the death of his entire herd of cattle, was responsible for his own cows’ deaths. The report failed to disclose that the company had dumped 7,100 tons of C8-contaminated sludge into a landfill near the stream from which Tennant’s cows drank. Instead, the authors blamed Tennant’s “failure to provide the right supplements for the cattle” — a conclusion Mace repeated in court, adding, “They had pink eye and many other issues.”
If the chemical were really dangerous, DuPont attorneys contend, government agencies would have regulated it. The implication is that the company was within its rights to dump barrels of the stuff into the ocean, as it did in the 1960s. And that it was perfectly fine to emit more than 632,000 pounds of the toxic substance directly into the Ohio River, as DuPont did over the more than 50 years it used C8 in West Virginia. “They were allowed under the law,” Mace said of the plant’s river emissions. “There is a difference between emissions from a plant and what an individual is exposed to. There weren’t people there right at that pipe.”
We’ll soon know which argument a jury finds more persuasive. But even if they decide in Bartlett’s favor, or the company opts to settle the suits, the costs may not fall to DuPont. Facing years of litigation over the chemical and the possibility of federal regulation — and thus enormous cleanup liabilities — in July DuPont spun off its chemical division into a separate company called Chemours.
Settlement costs could force Chemours, whose stock price has fallen 57 percent since June, to the brink of bankruptcy — or beyond.
After less than one full day of deliberation, a jury in Columbus, Ohio, found DuPont liable for $1.6 million in a personal injury claim…
A JURY HAS FOUND DUPONT liable for negligence in the case of Carla Bartlett, taking less than a day to award $1.6 million to the Ohio woman who developed kidney cancer after drinking water contaminated with a chemical formerly used to make Teflon. The jury declined to give Bartlett punitive damages in the federal case. Instead, the award included $1.1 million for negligence as well as $500,000 for emotional distress.
“This is brilliant,” one of Bartlett’s attorneys, Mike Papantonio, said of the verdict. “It’s exactly what we wanted.” Papantonio emphasized that Bartlett’s case, the first of more than 3,500 personal injury and wrongful death suits filed on behalf of people in West Virginia and Ohio who were exposed to C8, had been chosen by DuPont as the first to be tried and involved less egregious injuries than many others yet to be heard.
“They picked this case with the idea that it was the most winnable. Strategically they never dreamed we’d win this case,” said Papantonio, who predicts that other C8 suits in the pipeline will result in punitive damages. “Really, it’s just a matter of time.”
In a statement, DuPont said it expected to appeal the verdict and emphasized that “safety and environmental stewardship are core values at DuPont.”
CARLA BARTLETT LIVED much of her life in Coolville, Ohio, a tiny town a few miles across the Ohio River from a DuPont plant in Parkersburg, West Virginia. After years of drinking water that had been contaminated with C8, Bartlett, who is now 51, was diagnosed with a tumor on her kidney in 1997 and underwent a painful surgery that involved removing part of one of her ribs along with the tumor.
Bartlett’s attorneys argued that while she and tens of thousands of people living near Parkersburg, West Virginia, were drinking water contaminated with C8, DuPont was actively working to ensure they didn’t “connect the dots” about the chemical. One DuPont PowerPoint presented by Papantonio described the company’s strategy of keeping sensitive information from government agencies, community organizations, and “disgruntled employees.”
DuPont’s lawyers, for their part, denied any responsibility for Bartlett’s illness. “Nobody at DuPont expected that Mrs. Bartlett or anyone else in the community would be hurt,” said Damond Mace, who emphasized that the company couldn’t have predicted that scientists would find a probable link between C8 and kidney cancer, as they did in 2012.
Bartlett’s attorneys responded with voluminous internal communications showing the company did in fact foresee the damage they would later inflict. In one DuPont document, a summary of a 1984 meeting about C8, a DuPont employee concluded that “we are already liable for the past 32 years of operation.”
The presentation of historical documents was designed to convince the jury that the company acted irresponsibly, even given the information that was available before Bartlett’s diagnosis. Bartlett’s lawyers laid out a clear timeline that began in the 1950s, when DuPont first learned of the chemical’s potential toxicity. By 1966, some DuPont employees realized that C8 was seeping into groundwater. By 1980, after the company instituted regular testing of its own employees, DuPont had evidence that C8 was present in workers’ blood — and within two more years there was evidence that the contamination persisted in human tissues. By 1984, according to testimony, DuPont’s own testing had established that C8 had leaked into local drinking water. In 1989, DuPont knew that C8 caused testicular tumors in rats — and even classified C8 as a possible carcinogen. But rather than reporting these developments, Mike Papantonio told the jury, “They hid this information from the public for at least 16 years.”
The company could have easily disposed of its C8 waste differently, Bartlett’s attorneys argued. As evidence, they produced a 1985 memo and a manufacturer’s information sheet from 3M, the company that sold C8 to DuPont until 2000, both of which clearly stated that the chemical should have been either incinerated or placed in a landfill designed for hazardous waste. Bartlett’s lawyers also revealed documents showing that DuPont did in fact follow 3M’s directive in its facilities in Japan, China, and the Netherlands, where it burned C8 waste.
In Parkersburg, however, DuPont chose to pump C8 through its smokestacks, bury it in unlined landfills, and dump up to 50,000 pounds a year directly into the Ohio River. The attorneys also presented evidence that switching to incineration would have cost the Parkersburg plant less than .2 percent of its annual operating costs. “The only reason they didn’t do it was because they wanted to save money,” Papantonio told the jury. Later, he added: “We wouldn’t be here today if it were incinerated.”
ARGUABLY THE MOST MOVING testimony came from Bartlett herself, a mother of two who described her daily routine of drinking iced tea that she unwittingly made with contaminated water, the physical pain of her ordeal, and her fear of a recurrence. Bartlett cried while on the stand and traced a huge line across her body where she has a scar from her surgery, saying, “It’s very big, and it’s very ugly.”
But it was testimony from two of DuPont’s own witnesses, who admitted to having high levels of C8 in their own bodies, that may have been even more damaging. Anthony Playtis, who was occupational health coordinator at the DuPont plant in Parkersburg, said that in 1994 C8 was measured in his blood at 400 parts per billion (ppb), a level that is roughly 100 times the national average. The retired DuPont worker went on to dismiss the notion that the measurement was cause for concern. “I knew there were a lot of other people who had much higher levels, and so I didn’t think mine was anything to worry about,” he said. Also, Playtis noted, “Everything is toxic.”
As part of a group of DuPont employees who measured C8 levels in local drinking water, Playtis took a sample from his home in 1988 that measured 2.2 ppb — more than double the safe level the company had set internally. But neither he nor anyone else at DuPont reported the elevated C8 readings to the public or to regulators until 1999. During those years, local children were splashing in backyard pools and community members were watering their vegetable gardens with the stuff.
Another former DuPont employee, Paul Bossert, who served as plant manager in Parkersburg from 2000 to 2005, made a point of mentioning that he drank the plant’s water, which had elevated levels of C8, and acknowledged that the chemical had been measured in his own blood at 85 ppb. Upon cross-examination, however, Bossert admitted that he had high cholesterol and a potentially cancerous “spot” on his kidney. Both conditions are among the six approved by a panel of scientists as grounds for personal injury cases such as Bartlett’s.
The jury didn’t have to make a decision about whether Bossert’s health conditions were caused by C8, but they did have to try to determine if the chemical caused Bartlett’s cancer, and they were given specific instructions about how to do so. According to the terms of a 2005 class-action settlement over the contamination that spawned these cases, they had to accept as fact that drinking C8 for at least a year at the level of .05 ppb or above, as Bartlett did, can cause cancer.
Although DuPont’s attorneys were not permitted to dispute the fact that C8 can cause cancer, they did question whether it had caused Carla Bartlett’s particular illness. “Just because C-8 is capable of causing cancer does not mean that it did cause Mrs. Bartlett’s kidney cancer,” DuPont attorney Damond Mace said. Instead, he argued that Bartlett’s cancer that was caused by her obesity.
The $1.6 million verdict is only one of several problems now facing DuPont. Since March the company’s stock is down more than 30 percent, and on Monday CEO Ellen Kullman announced she was stepping down, leaving DuPont without a succession plan.
Some observers who are familiar with the company’s long history in Parkersburg believe Kullman’s departure is tied to C8. Jeffrey Dugas, campaign manager of Keep Your Promises DuPont, a local nonprofit devoted to holding the company accountable, said the company’s mishandling of the chemical — the contamination, the cover-up, and now the bruising legal fight that just concluded in Columbus — hasn’t served anyone well.
“This whole process of trying to wiggle out of its responsibilities has hurt everyone involved,” said Dugas. “The latest victim is Ellen Kullman. But mid-Ohio residents have been suffering for over a decade.”
As the first of six bellwether cases, Bartlett’s verdict is seen as an important predictor of the thousands of C8 claims that may yet come to trial. The next case, in which the plaintiff has ulcerative colitis, is scheduled to be heard in Columbus in late November. The future of Chemours, the chemical company that was recently spun off from DuPont, may also hinge on the outcome of these trials.
With C8 present in water far beyond the Ohio Valley, where Bartlett and other plaintiffs in the current crop of plaintiffs were contaminated, the implications of the Bartlett case may be far wider. Papantonio, who tried some of the first asbestos cases, sees that litigation, which has cost industry more than $50 billion to date, as a possible model.
“This is starting out just like those cases,” said Papantonio. “If I was in charge of this company, I’d be worried.”
The EPA has yet to regulate the toxic PFCs found in fire-suppressing foam, Teflon, and other products that have contaminated our drinking water.
LORI CERVERA HAD ALWAYS been an active person. She liked camping, playing outdoors with her kids, and practically lived in her running shoes. She didn’t have much patience for illness. So when she developed a dull ache on her right side in May 2014, Cervera took a few Tylenol and did her best to ignore it. But after a few days in which the pain grew sharper and more intense, she went to the hospital, where a CT scan revealed a mass. To her complete surprise, Cervera, a mother of four and grandmother of two who was 46 at the time, was diagnosed with stage 2 kidney cancer. That July she underwent surgery to remove both the tumor and almost half her right kidney.
Cervera returned to her home in Warrington, Pennsylvania, relieved to be alive but also perplexed. She had no family history of kidney cancer, and the diagnosis felt like it came out of left field. So with 22 staples still in her belly and a drainage tube coming out of her wound, Cervera propped herself up in bed and took to Google, intent on learning more about what might have caused her illness.
Her research quickly led her to a recent report on PFOA, or perfluorooctanoic acid, also known as C8, a chemical that for six decades was used by DuPont in the production of Teflon and other products. Research on people in West Virginia and Ohio who had consumed water contaminated by leaks from a nearby DuPont factory showed probable links between the chemical and six diseases, including kidney cancer.
Cervera soon discovered that the very same chemical, as well as a related one, PFOS, had been found in drinking water in her area. Both were part of a larger class known as perfluorinated chemicals, or PFCs, “emerging contaminants” that were still being studied — and had yet to be regulated. And, according to public notices from the local water and sewer authorities, both had come from foam that was used to put out airplane fires and train soldiers at two nearby military bases — the Naval Air Warfare Center in Warminster and a former naval air station at Willow Grove, now owned by the Pennsylvania Air National Guard.
Cervera knew the bases well. One of her daughters works across the street from the Naval Air Warfare Center, which everyone calls Johnsville. Willow Grove is only about a mile south of her house; she drives by it practically every day. The Wawa convenience store where she buys milk and gas is directly across the street from Willow Grove, which the Navy shut down in 2011. It wasn’t hard to imagine how water from that former base would make its way to her home. The road that runs between the two parallels a creek that floods practically every time it rains.
When they moved 25 miles north to Warrington from Philadelphia in 2000, the Cerveras had found the well at their new home charming. Now, after reading about the contamination, she regarded it with suspicion. Had the water she drank and used to make coffee, brush her teeth, fill kiddie pools, and mix infant formula for her grandchildren over the years contained chemicals from the military bases?
In August 2014, she decided to find out and requested a free test of the well water, which the local EPA office was offering to families living close to the bases. Three months later, an agency staffer rang her bell to hand-deliver the results: Though the chemicals were present in their well, they weren’t at levels of concern, he assured her. “We were so relieved,” said Cervera, who went on drinking and cooking with the water.
However, EPA monitoring done around the time of Cervera’s surgery showed that the Warminster municipal water authority, which provides water to the township adjacent to Warrington, had the third-highest level of PFOS of all public drinking water systems tested in the entire country — 1.09 parts per billion — as well as a very high rate of PFOA, .349 ppb. The Warminster water authority stopped using two of its public wells last year because of the contamination. Warrington Township, where the Cerveras lived, found PFCs at elevated levels in three of its public supply wells and also shut them down. The chemicals had spread into some private wells, too. By June 2015, 45 had been identified with either a PFOA or PFOS level above the safety threshold set by the EPA. The chemicals were also present at lower levels in more than 100 other wells.
In late January 2015, a second test of the Cerveras’ well showed higher levels of contamination, but they were given no indication that they should stop drinking the water. Then, in August, a few weeks after a third test of their well water, a worker from the lab that processed their sample called to tell them to stop drinking it immediately. A few days later, several 5-gallon jugs of water arrived at their home. Cervera noticed the same plastic jugs began to appear outside many of her neighbors’ homes as well.
IN MAY 2014 when Cervera was first noticing the pains in her side, Andrea Amico read in her local paper that PFCs had been found in the water on the former Pease Air Force Base near her home in Portsmouth, New Hampshire. The level of PFOS in one of the wells serving Pease was 12 times a provisional safety level set by the EPA — so high, in fact, that the city promptly decided to shut it down.
Pease, which was a Strategic Air Command facility and Air Force base until 1991, is now home to a golf course, a commercial airport, and more than 250 businesses employing some 9,500 workers. Amico works as an occupational therapist for a hospital that’s based there, and her husband, a graphic artist, worked at Pease for more than eight years. But when she heard about the contamination, Amico’s thoughts immediately turned to her son and daughter, ages 2 and 4, who have attended Great Bay Kids’ Company, one of two childcare centers at Pease, since they were 12 weeks old.
“I was like, oh my God, my children are in daycare there,” she said. “What are these chemicals?”
The answers she has received over the past several months have often contradicted one another, sending Amico on a journey through medical journals, doctors’ offices, and public forums. What is indisputable is that PFOA and PFOS are part of a group of man-made chemicals that have been tied to a range of health effects, from obesity in children to reproductive problems and cancers. Used to make Teflon, stain- and water-resistant coatings, cosmetics, and hundreds of other products, PFCs persist in the environment and are easily absorbed by the human body. Both PFOS and PFOA, the best studied of these chemicals, have been shown to be “endocrine disruptors,” tiny amounts of which can interfere with the hormonal system.
What was less clear to Amico was how being exposed to these contaminants would affect her family. PFCs, she knew, can cross the placenta, showing up in cord blood and newborns. They also accumulate in breast milk. And several studies have shown children to be particularly vulnerable to their effects.
Yet some state officials she encountered at community meetings seemed more interested in calming her down than giving her an honest picture of the dangers of PFCs. “They weren’t giving us the whole story,” said Amico. “There’s this apprehension that we’re going to freak out.”
Nor were the local authorities of much help when it came to finding out how much of the chemicals her family members had in their bodies. Right after the contamination was discovered, Rick Cricenti, director of the Emergency Services Unit at the New Hampshire Department of Health and Human Services, promised to help Amico get blood tests, she said. But eventually he stopped replying to her emails and returning her calls, and Amico spent more than seven months trying to find anyone to help her determine the level of PFCs in her family’s blood.
Jet fuel is made to burn. When airplanes crash, the reserve of the hydrocarbon liquid can produce a massive, violent fireball. Water, which doesn’t mix with the fuel, does little to extinguish these explosive fires, often just boiling off or sinking ineffectually under the fuel itself. So, about 50 years ago, the Minnesota-based chemical manufacturer 3M, in conjunction with the Navy, developed a product that would help extinguish such fires.
The sudsy liquid, dubbed “Aqueous Film-Forming Foam,” or AFFF, put out hydrocarbon fires more quickly and effectively than ever before by smothering them. Since it was developed, the military has been using huge quantities of the foam, which has been heralded for saving firefighters’ lives. Unfortunately, 3M’s miracle product also contained PFOS. And the other official formulation of the foam purchased by the Department of Defense contains “telomers,” compounds that can break down into PFOA and other PFCs. In addition to being linked to health problems, PFOA and PFOS stay in the human body for years and, unless they are removed, persist in the environment indefinitely.
The extent of contamination would no doubt be far less if the military had just used the foam to put out crash fires, which are fairly rare. Between 1979 and 2000, for instance, there were only four plane crashes near Willow Grove. But the foam is also used to teach soldiers to put out fires, and those training exercises are common. A typical exercise, which has been conducted by various branches of the military many thousands of times since the 1960s, involves flooding a fire pit with flammable liquids, lighting them on fire, and then putting out the flames with between 75 and 100 liters of firefighting foam. For decades, no one thought to construct barriers at these sites to contain the foam, which sank down through the earth into the water table.
CONTAMINATION FROM THIS frequent dousing with PFC-laced foam is a far bigger problem than either Amico or Cervera imagined. Water testing done in or near military bases, which isn’t yet complete, has already shown that the chemicals spread into public drinking water systems around Willow Grove, Pease, and a third base — Eielson, in Alaska. PFCs have also been detected in the ground water at many more bases, including the Air National Guard base in Delaware; the Grissom Air Reserve Base in Indiana; and the Naval Air Station in Fallon, Nevada. Indeed, according to a 2013 presentation by the Air Force, PFCs were found at every Air Force base that had been tested, which so far includes Randolph in Texas; Robins in Georgia; Beale and McClellan in California; Eglin in Florida; Ellsworth in South Dakota; and F.E. Warren in Wyoming.
In some of these places, huge amounts of chemicals from the foam have been found in soil and water. At Tyndall Air Force Base in Florida, for instance, one of the telomers that can decay into a chemical similar to PFOA was found at 14,600 ppb. Near the Naval Air Station in Fallon, Nevada, where fire-training exercises were conducted for more than 30 years, PFOA has been recorded in the groundwater at levels as high as 6,720 ppb. And, at the former Wurtsmith Air Force Base in Michigan, where crash trainings also took place for more than three decades, one plume of groundwater had concentrations of total PFCs between 100,000 and 250,000 ppb.
It’s clear that the full extent of the contamination will be much bigger still. As of 2014, there were 664 current or former military fire- or crash-training sites in the U.S., according to a statement from the Office of the Secretary of Defense. The Air Force and Navy have the largest number of these spots. Although the DOD has said it’s too early in the cleanup process to know how many of these sites have been contaminated with PFCs, it is likely that all of them have, said Jennifer Field, a professor of environmental and molecular toxicology at Oregon State. Field has been studying the environmental fate of the chemicals used in firefighting foam and has yet to see an area where the foam was used in which PFCs have not been detected.
“We’re batting 100 on the bases where they’ve had fire-training sites,” Field told me. “Even one crash site can leave a fingerprint.” No one yet knows the full extent of the emerging environmental contamination caused by the firefighting foam. But according to Field, “It’s going to be big.”
The U.S. military, which has been using the foam in fire-training exercises since the 1960s, is the biggest user — and polluter — by far. But commercial airports, airplane hangars, oil refineries, fire departments, petrochemical transfer and production sites, and heliports have also used firefighting foam containing PFCs for decades, which likely pushes the total number of contaminated sites into the thousands, according to Thomas Bruton, a PhD candidate in environmental engineering at Berkeley who is studying PFC contamination.
There’s little doubt that, together, widespread use of firefighting foam has contributed to the exposure of huge numbers of people to PFCs. EPA monitoring begun recently found PFOS in water systems serving almost 10 million Americans, most of whom have no idea they’re drinking it. The number of potentially exposed people climbs to more than 14 million when the other five PFCs now being monitored by the EPA are included. And those six chemicals are only the tip of the iceberg; more than 2,000 PFCs have already been identified on the global market, and scientists expect that number to climb to 4,000.
Even as the Air Force, Navy, and the Department of Defense struggle to clean up this massive environmental mess, the military continues to use PFC-containing firefighting foam for both training purposes and emergencies. The military has the largest stockpile of PFOS-containing firefighting foam in the United States, with around a million gallons, according to a 2011 estimate by the Fire Fighting Foam Coalition, an industry group. While the EU and Canada have banned the use of stockpiled foam containing PFOS, the U.S. has no restrictions on its use.
In fact, the current military specifications for firefighting foam require that the product contain PFCs. In response to a list of questions provided by The Intercept, a military spokesperson wrote: “Until non-PFC formulations are certified, DOD is implementing measures to prevent uncontrolled releases of firefighting foams during maintenance and firefighting training exercises. Additionally, DOD will be removing stocks of PFOS-based foam where practical.” While the military can still use the stockpiled foam, according to the DOD response, “Non-PFOS based foams, which do contain shorter-chain PFCs, will continue to be the main product used for firefighting until non-PFC formulations can be tested and certified to meet the military performance specifications.”
These products using “shorter-chain” PFCs, which manufacturers have been shifting to in recent years, consist mostly of molecules with either four- or six-carbon bases, as opposed to eight, like PFOS and PFOA. Industry has claimed that the new compounds are safer, because the shorter-chain molecules have a shorter half-life. But since long-chain chemicals persist indefinitely, the practical difference may not amount to much. To date, little research has been completed about the health effects of these chemicals. Experts disagree about their potential to cause harm, but they are suspected to persist in the environment and to accumulate in the human body.
In recent years, biologists have begun to trace the path of chemicals from firefighting foam through the environment, and PFCs from the foam have been shown to accumulate in earthworms. At levels between 10 and 120 ppb, PFOS can damage the worms’ DNA. Fish swimming near the Wurtsmith base had internal PFOS levels as high as 9,580 ppb. Birds that eat these fish have PFCs in them, too.
The chemicals are clearly entering humans’ bodies as well. Before the 1940s, when the first PFCs were developed, no one had them in their blood. Now, it’s virtually impossible to find anyone who doesn’t have at least trace amounts of these man-made substances in their bodies, most of which likely come from exposure to the chemicals in consumer products.
The PFCs from firefighting foam can add substantially to this burden, as Andrea Amico now knows. After several months of public meetings, letter writing, and phone calls, she finally managed to get free testing approved not just for her family but also for anyone who drank the water on Pease. Rick Cricenti, the New Hampshire official who stopped responding to Amico’s communications, referred me to a spokesperson for the New Hampshire Department of Health and Human Services, who did not dispute her version of events but said, “I feel good about the department’s response ultimately to this contamination.” Eventually, that response included working with the CDC to offer blood testing to anyone who was affected. So far, 1,600 people have had their blood tested for the presence of nine PFCs. The first of the results, which were released in August and September, showed that the average level of PFOS in children who were exposed to water from Pease was more than double the rate measured in a comparison group of children. Levels of another PFC called PFHxS were particularly high — more than triple the national average among adults and five times higher than a comparison group among children.
Amico’s daughter, who was just 4 when she had her blood tested, had a PFOS level that was more than four times that of a group of children from elsewhere in the country; her PFHxS level was more than 12 times higher.
IN 2006, THE EPA helped broker a deal under which the eight companies in the U.S. that were making or using PFOS and PFOA would stop doing so. As of this year the companies say that they have. But the federal agency dedicated to protecting human health and the environment has yet to set a safe level of lifetime exposure to the chemicals.
As The Intercept reported in August, Robert Bilott, an attorney representing people living in West Virginia and Ohio near a DuPont plant, first asked the EPA to regulate PFOA in 2001 under the Toxic Substances Control Act, “on the grounds that it ‘may be hazardous to human health and the environment.’” Bilott based his plea on decades of research on PFOS and PFOA he had uncovered through his legal work. In one of the many studies he unearthed, which was reported by 3M scientists in 2001, two of six male monkeys exposed to PFOS died. The chemical also caused monkeys to lose weight, increased the weight of their livers, and interfered with various hormones.
Still, the EPA didn’t address the question of how much PFOA or PFOS might be safe until 2009, after the agency discovered that sludge containing high levels of both chemicals had made its way from a wastewater treatment facility in Decatur, Alabama, to nearby fields. For 12 years, it turned out, that contaminated sludge had been spread across 5,000 acres of local grazing land. The fear was that the chemicals would make their way into animals and humans in the rural area. And, in fact, they did. But even so, the EPA didn’t enact binding regulation, which could have been used to force the companies responsible for the chemicals’ presence in water, including 3M, to clean up the contamination.
Instead, the agency came up with a temporary, unenforceable solution to the PFC problem. The Provisional Health Advisory on PFOS and PFOA that the EPA released in 2009 referred to the industry’s monkey research and other evidence of disturbing health effects of PFCs on animals when it calculated the maximum levels of these chemicals that humans should be exposed to through drinking water. For PFOS it was 0.2 ppb; for PFOA, 0.4 ppb. But these levels fall short of enforceable regulations.
And both are for “short-term exposure,” which according to the EPA means they are supposed to apply to periods of exposure that last from “weeks to months.” Yet Andrea Amico’s oldest child was exposed for years — indeed, for most of her life. In all likelihood, Lori Cervera and her family drank contaminated water for as long as 15 years. And many others living near fire-training sites may have been exposed to the chemicals for far longer, since the military has been using the foam for close to 50 years.
Although the EPA has repeatedly said it would update these numbers, it hasn’t done so since 2009. In a written response to questions from The Intercept, Cathy Milbourne, an EPA spokesperson, said the agency expects to finalize health advisories for PFOA and PFOS “this winter.” Once published, those numbers will supersede the provisional health advisories from 2009.
In the meantime, the military continues to use the provisional safety levels to guide its response to contamination from AFFF. One of the agency’s Q&A sheets, for instance, assures people living near Willow Grove that these levels “are intended to ensure protection of public health, with a margin of safety built-in.” Those in charge of the cleanup there use the numbers to determine who receives bottled water and which homes now reliant on contaminated private wells will be connected to public water systems. And residents whose wells contain even slightly less than this amount and who have been drinking the chemicals for years may be reassured, as Cervera was, that their water is safe to drink.
SINCE THE EPA SET these provisional levels, evidence has emerged suggesting that guidelines for safe levels of PFC exposure over the long term should be much lower. In 2009, the same year that the EPA set its short-term level for PFOA at .4 ppb, a group of water experts appointed by New Jersey’s Department of Environmental Protection calculated what they thought should be a safe lifetime limit for drinking water: .04 ppb, one-tenth the EPA’s provisional level. And since then, much evidence has emerged showing that the long-term level should be lower still.
In 2012, data gathered from plaintiffs in a class-action suit Bilott and others filed against DuPont found that exposure to PFOA was likely linked to kidney cancer, testicular cancer, thyroid diseases, ulcerative colitis, high cholesterol, and preeclampsia. The minimum level of contamination in water districts represented in the suit was low — just .05 ppb, a small fraction of the level now being used to guide cleanup — and more recent research suggests maximum levels for drinking water should be even lower than that.
For years, industry did the vast majority of research on PFCs, most of which was never made public. “We didn’t pay attention to the PFCs because it looked like there was nothing,” said Philippe Grandjean, a physician and environmental health researcher at the Harvard T.H. Chan School of Public Health. But in 2000, after conducting a study of the health effects of PFOA on monkeys, 3M announced that it would phase out production of both PFOS and PFOA. “It was when industry said ‘oops,’ that’s when the academics got started,” said Grandjean.
Grandjean himself became interested in PFCs after he noticed a 2008 study in which researchers looked at how the chemicals affected mice. “Animal toxicologists got to the immune system and — bing! — they found these very strong effects.” Grandjean wondered whether the chemicals might have similar effects in children and devised a way to find out: He looked at the blood from group of young children before and after they were vaccinated for tetanus and diphtheria. His findings, which were published in the peer-reviewed Journal of the American Medical Association in 2012, were striking: After being vaccinated, 7-year-olds who had very slightly elevated levels of PFCs in their blood tended to have lower levels of antibodies to those diseases. For each doubling of exposure to the chemicals, the risk that the vaccine didn’t take increased twofold to fourfold.
“I fell off my chair when we got our first results,” said Grandjean, who believes the study has broad implications for overall immune function, which affects the development of allergies, autoimmune diseases, cancers, and a huge range of other illnesses. Indeed, a separate study, published in 2013, bears out his hunch. This one mapped certain illnesses to exposure to very low levels of certain PFCs in Norwegian children. Those who had higher levels of PFOA and another perfluorinated chemical, PFNA, got more colds. And those who had higher levels of PFOA and PFHxS, the chemical found at elevated levels in many of the people near Pease, were more likely to get stomach infections.
Based on his findings — which were corroborated by other research showing an association of very small amounts of PFCs in the blood of pregnant women in Demark with increased risk of miscarriage — Grandjean came up with a maximum level of the chemicals that would be safe to ingest that was much lower than the provisional level set in 2009. “You need to get down to something like several hundredfold less than what EPA originally set,” said Grandjean, who has suggested a safe level should be set below .001 ppb instead of 0.2 or 0.4.
Though it came close, the contamination detected in Lori Cervera’s well never exceeded the EPA’s guidelines for short-term exposure. After years of exposure, though, even tiny amounts of the chemicals can be harmful, according to Grandjean. Because PFCs accumulate in the body — it takes five years for people to get rid of just half of PFOS in their bodies, for instance — for people who have been chronically exposed, like Cervera, “any additional exposure should be prevented,” said Grandjean.
It’s never easy to find and clean up tiny molecules that have been scattered through vast amounts of water and soil.
And the effort to rid the environment of PFCs from firefighting foam promises to be especially messy and difficult. Not only have these chemicals been spread across the entire country, they’re often mixed in with other contaminants, including jet fuel, benzene, and other byproducts of combustion. This is certainly the case at Eielson, Pease, and Willow Grove, all of which were Superfund sites well before they were known sites of PFC contamination from firefighting foam.
So far, the best method for cleaning up PFCs requires putting contaminated water through an “activated” carbon filter, and then burning the chemicals that have been filtered out. The process is expensive, as is the pumping of the water from the ground to a place where it can be treated.
Indeed, in July, the Navy agreed to pay $8.8 million to treat the public drinking water wells of the Horsham Water and Sewer Authority near the Cerveras’ home and almost $4 million to clean the water at the Warminster Municipal Authority in the next town. And those costs are only for cleaning wells that have PFCs above the provisional advisory levels.
Because PFCs are unregulated, the law doesn’t require their cleanup — and the costs of getting them out of the environment aren’t covered by the Superfund program. Nevertheless, the Air Force has decided it will address the contamination on a case-by-case basis, reviewing and addressing requests for action on PFCs when “direct human exposure, and/or off-site migration is identified.”
The consequences of not adequately cleaning the PFCs loom large. At Willow Grove, for example, plans are already underway to develop housing, a school, and a retirement community.
IN OCTOBER, A JURY found DuPont liable for $1.6 million in damages to a woman who had developed kidney cancer after drinking PFOA-contaminated water near one of the company’s plants. Though she developed the same disease after similar exposures, at this point, Lori Cervera is unlikely to have such success in the courts.
In the DuPont cases, the second of which will be tried in March, there is ample evidence the company was responsible for putting the chemical into local drinking water. And, according to the terms of the class-action suit from which the case stemmed, the jury had to accept that PFOA can cause kidney cancer.
If Cervera were to sue, her lawyers would have to sort through a tangle of potentially responsible parties. Over time, the bases near her have been home to several branches of the military, including the Navy, the Air Force, the Air National Guard, and the Army Reserve. Suing any of them is notoriously difficult. And then there is the challenge of sorting out which of several companies made the particular foam in question. Though 3M was the sole supplier of firefighting foam to the U.S. military until 1982 and made about three-quarters of the military’s entire stockpile, six other manufacturers, including Ansul, Chemguard, National Foam, and Buckeye Fire, have also sold firefighting foam to the military. And they bought some of the chemicals used in the foam from other companies.
National Foam, Ansul, and Chemguard declined to comment for this story. Buckeye Fire did not respond to repeated requests for comment. 3M provided the following statement:
“3M’s AFFF products were all sold with material safety data sheets, or MSDSs, that advised how to handle and dispose of the product in a safe and effective manner,” Donna Fleming Runyon, spokesperson for 3M, says. “When used properly, we believe AFFF was safe and effective. In fact, the products are widely credited with benefiting the military and civilian firefighters around the world. They are known in many cases to have saved lives.”
“We believe that PFCs, such as PFOS and PFOA, do not present health risks at the levels they are typically found in the environment or in human blood,” says Carol A. Ley, MD, vice president and corporate medical director, 3M Medical Department. “In more than 30 years of medical surveillance, we have observed no adverse health effects in our employees resulting from their exposure to PFCs such as PFOS and PFOA,” says Ley. “This is important since the level of exposure in the general population is hundreds, if not thousands, of times lower than that of production employees who worked directly with these materials.”
Still, Cervera was considering her legal options — and, for months, waiting for calls back from the Centers for Disease Control, the EPA, and the local base closure office to get more information about her exposure over the years. But at press time, a routine blood test had heightened her doctors’ suspicions that her cancer had returned — and banished, for now, Cervera’s questions about why she got sick.
Back in New Hampshire, Amico is now part of a recently formed community advisory board at Pease that is working with the Agency for Toxic Substances and Disease Registry to design a health study to see how the PFCs in drinking water might have affected the health of people who drank water there. It will likely be years before any results emerge from this research.
The U.S. isn’t the only country contending with the environmental consequences of firefighting foam.
PFC contamination from the foam has recently been discovered in Europe, Japan, and Australia, where TV coverage likened the widespread contamination to “Agent Orange, all over again.”
Perhaps the most instructive response to the problem has been in Ronneby, a small town on the southern coast of Sweden. In December 2013, the level of PFOS in drinking water there was found to be elevated. As in the U.S., the Swedish contamination was tied to firefighting foam used by Sweden’s air force. But unlike in the U.S., the response in Ronneby was thorough, swift, and very open.
As soon as the problem was discovered, it was widely reported to the public and clean water was distributed. Blood sampling of exposed residents got underway by February and initial results from those tests were reported in March. Within months, a Swedish university received an emergency research grant to study the health effects in the population and the government mobilized a network of national agencies to work on the issue.
As in the U.S., plenty of questions remain about the PFCs in Ronneby. Epidemiological studies of the health of the local population, while already funded, won’t get underway until 2016, according to Kristina Jakobsson, a professor of occupational and environmental medicine at Gothenburg University. But the process is clearly already a governmental priority — or as Jakobsson put it simply, “an act of responsibility.”
Research: Danielle Mackey and John Thomason
While touting GenX as being a safe replacement for PFOA, DuPont filed 16 reports of “substantial risk of injury to health or the environment”…
THE CHEMICAL INTRODUCED by DuPont in 2009 to replace the surfactant PFOA causes many of the same health problems in lab tests that the original chemical did, including cancer and reproductive problems, according to documents obtained by The Intercept. PFOA, also known as C8, was a key ingredient in Teflon.
C8 was originally manufactured by 3M, then by DuPont, and was phased out after a massive class-action lawsuit revealed evidence of its health hazards. The new chemical, sold under the name GenX, is used to make Teflon and many other products. While touting GenX as having a “more favorable toxicological profile” than C8, DuPont filed 16 reports of “substantial risk of injury to health or the environment” about its new chemical. The reports, discovered in the course of an investigation by The Intercept, were filed under Section 8 (e) of the Toxic Substances Control Act (TSCA) and submitted to the EPA between April 2006 and January 2013. They cite numerous health effects in animals, including changes in the size and weight of animals’ livers and kidneys, alterations to their immune responses and cholesterol levels, weight gain, reproductive problems, and cancer.
“It’s the same constellation of effects you see with PFOA,” said Deborah Rice, a retired toxicologist who served as a senior risk assessor in the National Center for Environmental Assessment at the EPA. “There’s no way you can call this a safe substitute.”
In one experiment, rats given various amounts of GenX over two years developed cancerous tumors in the liver, pancreas, and testicles, according to a report DuPont submitted in January 2013. In addition to the cancers, some of the GenX-exposed rats in that experiment also developed benign tumors, as well as well as kidney disease, liver degeneration, and uterine polyps.
Satheesh Anand, a DuPont senior research toxicologist who signed the report, concluded that “these tumor findings are not considered relevant for human risk assessment.” Anand dismissed the significance of the results in part by emphasizing that the mechanism associated with the tumor formation in rats might not be the same in humans. DuPont scientists have long made the very same claim about C8 (as in this study from 2004), which caused testicular tumors in DuPont experiments on lab animals before it was linked to testicular cancer in exposed people.
Alan Ducatman, a physician who studies the health effects of perfluorinated chemicals such as C8 and GenX, characterized Anand’s claim as “a partial argument that could be interesting only to those who are not strongly following the literature.” Ducatman, who teaches environmental health sciences at the West Virginia University School of Public Health, is one of several researchers familiar with the health effects of C8 who reviewed the documents for The Intercept. He summarized DuPont’s interpretation of its own data as “cherry picking,” highlighting “species differences only when arguing that a problematic study finding is not relevant.”
DuPont’s reporting on the hazards of GenX “all has an eerie echo,” Ducatman wrote in an email to The Intercept. He noted that the reports show the chemical has the same trio of biological effects — on the liver, immunity, and the processing of fats — seen with similar chemicals, including C8. “This reminds me a lot of a path we have recently traveled. That journey is not ending well.”
Despite the fact that Section 8(e) reports are required only when companies have evidence that their product presents a substantial risk, the summaries of the experiments written by DuPont employees downplay most of their findings.
“There’s a lot of hand-waving sentences, ‘Yeah, this happened, but we don’t think it’s relevant,’” said Rice, the former EPA toxicologist. In one study conducted on rats and mice, for instance, male rats given any dose of GenX had changes in their cholesterol levels, and some also had changes in levels of two blood proteins. But the report, which like many of the others was labeled “Company Sanitized,” simply concluded that “these changes were of uncertain relationship to treatment and considered non-adverse.” It’s impossible for independent reviewers to evaluate these claims because the reports don’t include the data on which they’re based.
As The Intercept reported in August, DuPont scientists in the 1970s chose not to report abnormal liver test results in workers exposed to C8. In a 2004 deposition, the company’s medical director said that the company had not reported the findings because the liver changes weren’t proven to be problematic health effects related to the chemical. In its filings on GenX, DuPont scientists did report increases in the weights of kidneys and livers, and other changes in liver cells, in rats exposed to the chemical, but they again downplayed the results, saying that these changes were “not considered adverse,” according to a July 2010 letter signed by A. Michael Kaplan, DuPont’s former director of regulatory affairs.
Rice took issue with the judgment that such changes won’t cause problems in humans. “These are well-nourished, homogenous animals,” Rice said of the lab rats. “The human population isn’t like that. When you push these things around, you’re going to push some people into disease states.”
GenX also affected reproduction in lab animals, according to the reports. Rats exposed to higher amounts of the chemical were more likely to give birth early and have babies that weighed less. Another study showed that female rats exposed to GenX reached puberty later than the unexposed animals.
While the company also dismissed the significance of many of these effects in the summaries of its experiments, the findings are “suggestive of a reproductive effect,” said Laura Vandenberg, a reproductive biologist at the University of Massachusetts, Amherst. Vandenberg said that the tests described in the reports can’t fully show the extent of the chemical’s reproductive activity because they only look at the effects of very high doses of GenX.
“That might make sense if what we were worried about was whether this chemical maims or kills you outright,” said Vandenberg. “But that’s not what we’re seeing. People don’t cook on Teflon and drop dead. These are chemicals that interfere with normal biological functions at low doses and contribute to disease.” Because hormones act at low doses, “you have to study them at low doses.”
The DuPont studies estimated the lethal dose of GenX in rats as 7500 mg/kg. At such doses or higher, the animals “died within approximately 3 hours of dosing and exhibited discomfort, gasping and/or tonic convulsions prior to death,” according to one report submitted in 2006.
While all the scientists The Intercept asked to review the reports agreed that the issues they raised demanded multiple additional investigations, the EPA did not require any further testing of GenX.
Some of the reports reference a consent order for GenX, a document the EPA issued in 2009, which The Intercept obtained through a Freedom of Information Act request. That document lays out the agency’s many concerns about DuPont’s C8 replacement, including evidence that the chemical and its salt are toxic to lab animals and cause mutations in mammalian and human cells. The document also lays out concerns that the molecules “will persist in the environment, could bioaccumulate, and be toxic to people, wild mammals, and birds”; that “there is high concern for possible environmental effects over the long-term”; and that “EPA has human health concerns.”
Such orders are issued when the EPA requires more information in order to evaluate a new chemical’s safety. Although the DuPont studies show many significant findings and clearly raise questions about the health and developmental effects of GenX, the lack of a strong regulatory response to them isn’t unusual, according to one EPA official.
“A lot of them do just get filed away,” Vincent Cogliano, director of the Integrated Risk Information System at the EPA, acknowledged of studies industry submits to the agency.
The EPA has a number of options once it has evidence that a chemical is hazardous. The agency could use its statutory authority to regulate the chemical, setting limits on its use or even banning it and requiring companies to clean up contaminated areas. While the EPA has yet to take any of those actions on C8, which has been shown to be hazardous over the past decade, it has added that chemical to the list of substances regularly monitored in drinking water.
The EPA could also add GenX to that list, but such efforts are often met with resistance from industry. “Companies fight them,” Cogliano said, “and bring in other scientists who debunk the studies that show there are health hazards.”
For now, GenX is neither regulated nor tracked, even as Chemours (the chemical company spun off by DuPont in July 2015) produces the chemical and releases it into the environment in undisclosed amounts. Chemours declined to reveal production quantities for GenX, but said that emissions are 1 percent or less of the quantities used. Yet according to one of the hazard reports DuPont sent the EPA in March 2010, “The biodegradation of the test substance was 0%.” So GenX, like C8, is likely to be with us forever.
In response to inquiries from The Intercept, DuPont declined to comment, noting that GenX is now a product of Chemours.
Chemours responded with the following statement:
Chemours was created in July 2015 through the spin-off of the DuPont Performance Chemicals unit, which included the fluoropolymers business. Before this, in 2013, DuPont stopped making or using PFOA, replacing it with a new polymerization aid for use in the manufacture of fluoropolymers.
Extensive health safety testing was conducted on the new polymerization aid, and the data has been shared with regulatory agencies around the world as well as published in peer-reviewed scientific publications. The full body of testing data indicates that the polymerization aid can be used safely in the manufacture of fluoropolymers. It is rapidly eliminated from the body with low bioaccumulation potential. It has low acute toxicity in mammalian and aquatic testing, low repeated-dose toxicity in mammalian testing, and is not a skin sensitizer. Data suggests that it is not a developmental, reproductive, or genetic toxicant, or a human carcinogen. In addition, the new chemistry is used in conjunction with environmental exposure control technologies that reduce potential for environmental release and exposure.
Studies to evaluate chemical safety are designed to find health effects through the use of very high doses, in order to establish acceptable exposure limits with appropriate margins of safety. Therefore, finding such effects is important in effectively managing chemical safety. The level of potential worker or public exposure to this chemical is orders of magnitude below the levels at which any effects have been seen in our testing.
Regulatory authorities in the U.S., Europe, China, Japan and Taiwan have reviewed the testing data on our new polymerization aid and have given permission for its manufacture and use.
Chemical companies are using a trade secrets loophole to withhold the health effects of new products, preventing scientists from identifying emerging environmental threats.
MARK STRYNAR AND Andrew Lindstrom walked down the muddy bank of the Cape Fear River toward the water, sampling equipment in hand. It was the summer of 2012, and the scientists, who both work for the Environmental Protection Agency, were taking the first steps in what would be more than two years of detective work. The Cape Fear winds its way for over 200 miles through North Carolina before flowing into the Atlantic, but Strynar and Lindstrom were focused on a 20-mile stretch that runs from a boat dock outside Fayetteville south to the little town of Tar Heel. About halfway between the two points, on the western bank of the river, sits a large plant built by DuPont.
Perfluorooctanoic acid, commonly known as PFOA or C8, is a “perfluorinated” chemical, which means that its base includes carbon chains attached to fluorine atoms. Because the fluorine-carbon bond is one of the strongest in chemistry, these compounds are incredibly stable, which makes them useful in industry. But that stability also makes them endure in the environment. Indeed, C8, which has recently been detected in upstate New York, in Vermont, and in Michigan’s Flint River, among other places, is expected to remain on the earth long after humans are extinct. And evidence suggests that many of its replacements are just as persistent.
The potential permanence of the problem was only one reason the EPA team was mucking around on the banks of the Cape Fear River. There were short-term dangers, too. Strynar and Lindstrom knew well that the Cape Fear is a source of drinking water and that if perfluorinated chemicals — known as PFCs — had contaminated the river, they would soon make their way into human bodies. Strynar had spent eight years documenting the presence of these molecules in fish, food, air, house dust, and humans. Lindstrom, an expert on measuring PFCs in the environment who has worked for the EPA for more than two decades, had also been documenting the steady proliferation of the chemicals. Both knew that the potential for contamination around the plant was great, because C8 had spread into the water around many of the facilities that made and used it, including plants in West Virginia, Minnesota, New Jersey, Alabama, Germany, and Japan. According to data from the Centers for Disease Control, 99.7 percent of Americans already had C8 in their blood.
What Lindstrom and Strynar didn’t know was exactly what DuPont had used to replace C8 and whether it was escaping the plant. The river water was their key to finding out. By comparing the samples from above and below the plant’s outflow, they could determine which chemicals may have entered the river at that point.
Strategic sampling was the easy part. Figuring out the exact chemical structure of those molecules would require more ingenuity. Ultimately, it would take a team of 10 scientists from five different institutions more than a year to figure out the structure of the PFCs they found in the river — using a mass spectrometer, which produced spiky graphs depicting the exact weight and features of each molecule, software that uses the masses of compounds to generate likely chemical formulas, and painstaking searches of chemical databases and public records for descriptions of new PFCs to compare against their findings. Altogether, the scientists found 12 new PFCs, including one discovered in the files of the West Virginia Department of Environmental Protection, which in 2011 approved DuPont’s use of a C8 replacement at its Washington Works factory in Parkersburg. That was the same facility that had caused massive C8 contamination of drinking water linked to severe health problems among the local population.
After analyzing the molecules, Strynar and Lindstrom concluded that “a new generation of replacement compounds is now out in the environment,” they wrote in response to questions from The Intercept. These new chemicals likely had “the same chemical performance properties” as the older generation of PFCs, like C8. “This would also suggest,” they wrote, “that their toxicity and environmental persistence are likely to be similar as well.”
When companies want to begin making and selling a new chemical, they are required to file a written notice with the EPA. But current regulations do not mandate that any particular health or safety studies be performed, and according to a 2007 report from the EPA, only 15 percent of new chemical notices contain any information about the materials’ impact on health. Moreover, chemical manufacturers are permitted to claim that various parts of the information they give the EPA are “confidential business information,” or CBI. About 95 percent of new chemical notifications, according to a 2005 Government Accountability Office report, include information that is protected as a trade secret, a figure the EPA confirmed as still “generally accurate.”
Even the very name and structure of a chemical, which are essential to tracking its presence in food, water, and the rest of the environment and determining how it affects humans, can be claimed as CBI. The 12 chemicals Strynar and Lindstrom’s team painstakingly identified are just the tip of a mysterious and dangerous iceberg. Manufacturers have used the CBI shield to withhold the names and identities of 17,585 of the chemicals now registered with the EPA.
The allowance for certain confidentiality claims, which is written into the law, is based on the idea that if companies are forced to reveal the exact nature of a chemical, other companies will be able to duplicate it, depriving the original manufacturer of the opportunity to profit from its research and development investment. In response to past criticism of CBI claims, the American Chemistry Council has said that “balanced confidentiality laws help protect the trade secrets that foster innovation and create jobs.”
“CBI hinders our ability to capture emerging pollutants and make sure the public is safe,” said David Andrews, senior scientist at the Environmental Working Group, whose 2009 report publicly raised the problems posed by the growing list of secret chemicals. “Scientists can’t search for contaminants if they don’t know what they’re looking for.”
The secrecy surrounding DuPont’s C8 replacement, which is sold under the commercial name GenX, left Strynar and Lindstrom in a bizarre situation. Although they work for the EPA’s National Exposure Research Lab, they didn’t have access to all the information they needed to determine whether people were being exposed to the chemical and, if so, whether that exposure posed an environmental risk. They might have applied for CBI clearance, but because those privy to such business secrets are by law forbidden from sharing them, they wouldn’t have been able to reveal what they learned. Compounding the absurdity of their situation, a recent records search has revealed that although the chemical identity of the replacement was initially shielded as CBI, DuPont had declassified it by 2011. As a result, its generic identification number was switched to a traceable number, and information about the chemical was theoretically public. But because there had been no announcement of the declassification and no publication of the traceable number until after Strynar and Lindstrom began their research, no one — including the two EPA scientists — was able to access information about it. And so they had to spend many months and many taxpayer dollars sleuthing out information that was readily available to some of their colleagues within the EPA.
As it turned out, GenX was present in the river.
After a manufacturer tells the EPA about a new chemical it would like to introduce, the agency has 90 days to respond. While it most often simply accepts these new creations and rarely forbids companies from bringing them to market, in about 10 percent of new chemical applications since 1979 and about 40 percent of the notices submitted last year, the agency gave its version of a yellow light, requiring some sort of testing or restrictions on the production of the substance. These requests often take the form of consent orders. Publicly available versions of these documents are often riddled with redactions meant to protect confidential trade secrets.
For instance, a consent order for three PFCs issued in 2006, after the phase-out of C8 was announced, bears the stamp, “EPA SANITIZED,” and notes that critical details such as “company identity, specific chemical identities, production volumes, manufacturing process, processing and use information, and other information” have been scrubbed from it on the grounds of CBI.
The absence of this information makes what does come to light in the rest of the document particularly disturbing. The consent order for the three chemicals acknowledges that the EPA is concerned they “could cause lung effects” and notes that they may degrade into substances that “will persist in the environment, could bioaccumulate or biomagnify, and could be toxic (“PBT”) to people, wild mammals and birds.” These factors taken together, the consent order concludes, “raise concerns for potential adverse chronic effects in humans and wildlife.”
Despite these concerns, the EPA allowed the three replacement chemicals to enter the market in 2006 with the provision that the company perform reproductive, toxicity, and carcinogenicity tests of the chemicals’ effects on rats. Because the testing was required only if the company made or imported more than a certain amount of the chemicals — and because that “trigger amount” was withheld as CBI — it’s unclear if the company ever reached that limit or if the testing was ever done.
When asked about this document, the EPA provided the following response: “Based on concerns raised during the review of three alternative chemicals, a consent order was put in place (and later modified) that requires certain fate testing (i.e., hydrolysis, photolysis and biodegradation studies) to be completed in 2016 and 2017. The data will allow us to better understand the degradation rate of the chemicals.”
Several dangerous chemicals have been replaced by what environmentalists call “regrettable substitutions,” molecules that are often just slightly tweaked versions of the originals and pose similar problems. After PCBs were associated with health problems, including lowered immune response and developmental issues, the chemicals that replaced them also proved to be toxic. And in perhaps the most notorious recent example, bisphenol S (BPS), an additive to plastic used for water bottles and sippy cups, turned out to have many of the same dangerous characteristics as the close chemical cousin it replaced, bisphenol A (BPA).
But while PCBs had only a handful of replacements, and BPA had one primary substitute, the phasing out of PFOA and other PFCs based on 8-carbon chains has led to the introduction of a much larger number of chemicals.
Between 2006 and 2011, after manufacturers agreed to phase out longer-chain PFCs, chemical companies notified the EPA of their intent to introduce some 150 chemicals to replace them, according to research conducted by the Environmental Defense Fund in 2012. At least 125 of those chemical names were claimed as confidential.
Over the past decade, the EPA has reviewed more than 300 proposed alternatives to C8, according to a written response the agency provided to questions from The Intercept. Of those applications, 0.9 percent were not accepted; 67.1 percent were subject to consent orders, which often require additional testing of the chemical; and 18.5 percent were withdrawn by the submitter, “often in the face of regulatory action.”
The manufacture of just one of these compounds can result in many byproducts, which themselves can be dangerous. Several of the 12 PFCs Strynar and Lindstrom found in the Cape Fear River may have been created through the process of making GenX.
While Strynar and Lindstrom were searching the river for signs of DuPont’s C8 replacement, a PhD student in Europe confirmed the chemical structure of GenX in a surprising place. Zhanyun Wang, whose dissertation focused on PFCs, was at a conference in Munich in 2012 when he met a DuPont employee who told him that the formula for GenX had been printed in a brochure.
When Wang, now an environmental scientist who spends much of his professional life tracking down and sharing hidden information about dangerous chemicals, got home from the conference, he easily found a copy of the brochure on the DuPont website. The formula of GenX — CF3CF2CF2OCF(CF3)COOH.NH3 — was right there on Page 2. He told me he assumed that its publication was a mistake but went ahead and included the formula in a 2013 paper that included a roundup of replacements for long-chain PFCs.
Shortly after his paper came out, Wang ran into some colleagues who worked for DuPont. “They were not happy,” Wang recalled. “But then they found out it was from their documents so there was nothing they could do.”
Recently, CBI claims have hobbled the EPA’s efforts to move forward with the regulation of a group of flame retardants known as brominated phthalates clusters (BPCs). These chemicals were introduced to replace older flame retardants that accumulate in humans and the environment, and were banned in some states after being linked to developmental problems, hormone disruption, and cancer.
Like the older flame retardants, BPCs are present in furniture, electronics, and some baby items. Although researchers have only recently begun studying BPCs, they have already raised some of the same red flags, and have linked the newer flame retardants to DNA damage and hormone disruption. Chemtura, one of the companies that made the previous generation of flame retardants, is also producing at least two of these new chemicals and together with two other manufacturers made somewhere between 1 and 10 million pounds of one BPC in 2011, according to the Chemical Data Reporting Database.
In 2013, the EPA began to officially assess the risks posed by BPCs, but in August 2015 it published a document known as a “data needs assessment,” which concluded that the agency still needed more data. The report reveals how much information the flame retardant industry has withheld from the scientific community. Consider two of the chemicals, listed in the August report only as “Confidential A” and “Confidential B.”
The consent order for Confidential A sums up the problem well: As with other consent orders, this document is heavily redacted, with the name of the chemical, its manufacturer, intended uses, and production quantities all withheld as confidential business information. The few details that do emerge are alarming. For instance, the document notes that the chemical raises concerns about “liver and kidney toxicity” and carcinogenicity in humans, as well as toxicity to fish and aquatic life, while also acknowledging that Confidential A will be used in consumer goods and may be “persistent, bioaccumulative, and toxic.”
Nevertheless, the EPA allowed Confidential A to enter the market in 2009 with the provision that the unnamed company perform additional tests to determine whether the chemical affects reproduction and development in rats. These tests, too, were tied to a trigger level that was claimed as a secret. (According to EPA documents, as of August 2015 the trigger level had not been reached.) The consent order for Confidential A also warns the manufacturer against making “predictable or purposeful release” of the chemical into “the waters of the United States.” But, as we know from Strynar and Lindstrom’s experience, the ability to determine whether the chemical has in fact been released hinges on first figuring out what it is.
Perhaps more disturbing is what happened with Confidential B, a chemical that “sailed through the New Chemicals program,” according to comments on the report that the Environmental Defense Fund submitted to the EPA on January 20, 2016. Despite the fact that the unknown chemical is so worrisome that it made it onto a shortlist of chemicals the EPA is investigating, the agency apparently didn’t require its mysterious manufacturer to perform any health testing. In 2015, according to the EPA’s August data needs assessment, Confidential B was grouped among chemicals that were produced in volumes greater than 1 million pounds.
When asked for comment, the EPA noted that it hasn’t received any new test data on Confidential B “because the production volumes are too small” and pointed out that the agency now typically bans the manufacture and import of new BPCs “until up front testing can be conducted and reviewed.” Asked to resolve the inconsistency, the EPA insisted that “for Confidential B, the production value is not greater than 1 million pounds.”
We don’t know much more about the named BPCs. For instance, the production data entry for a chemical known as TBB, one of the seven flame retardants listed in a supplement to the EPA’s report, is essentially devoid of information. The name of the production site, the amount produced domestically, the amount exported, and, as with Confidential A, the amount produced overall, have all been claimed as CBI.
“By calling production volume data CBI, they’re obscuring the extent of how prevalent a chemical is — and how prevalent exposure is,” said Eve Gartner, a staff attorney at Earthjustice, who submitted comments about the BPC data needs assessment to the EPA on behalf of the Natural Resources Defense Council, the Washington Toxics Coalition, and Earthjustice in January. Without this data, said Gartner, the EPA can’t do its job.
“EPA had a legal obligation to find out more about the toxicity of these chemicals and it failed to do that,” said Gartner. “And now it can’t do a risk assessment that might lead to regulation. That means many more years in which people, children, firefighters — everyone — is being exposed to toxic chemicals.” Indeed, while the regulatory process has been stalled, the environmental concentration of two BPCs known as TBB and TBPH has been doubling every year in urban areas and every 1.6 years in rural areas, according to a 2012 article in Environmental Science Technology.
While Gartner admits that some confidentiality claims, including those for the production volume, may fall into a legal gray area, others are plainly violations of the law. The Toxic Substances Control Act (TSCA), which lays the groundwork for chemical regulation, makes it clear that health studies cannot be protected as CBI. Yet, in 2012, Chemtura submitted more than 12 health studies to the EPA that it claimed as CBI.
The EPA did not dispute that it allowed health studies to be submitted as confidential business information, but wrote in a response to questions from The Intercept that it made summaries of the studies public. The agency statement also noted that “EPA is currently following our established process to review these and other submissions and declassify unwarranted CBI claims.”
When asked for comment, Chemtura did not dispute that it claimed the studies as confidential, but said in a statement that “providing information as Confidential Business Information to protect proprietary technical information is in full legal compliance with what is allowed under Federal regulations.” Chemtura also wrote that it strongly disagrees “with the characterization that there is something wrong with confidentiality claims.”
The law allows us to make a claim of confidentiality in order to protect our investments. Companies invest a lot of money in the development and manufacture of its products. This investment comes in many forms: research, physical testing, construction of manufacturing plants, product registrations, toxicology testing, marketing and advertising are among the many investments a company can make. These investments form proprietary information which is a barrier to entry for other companies. Giving away your investments to competitors is an unsustainable business practice for companies who seek to be successful. In the case of toxicology data, competitors have and do use public information they obtain to register competing “copycat” products against the data originators. Technical data is a valuable asset, and care should be taken in how companies distribute that intellectual property.
Gartner worries that the agency’s acceptance of Chemtura’s inappropriate CBI claim — and apparent failure to notice that the EPA itself was violating the law — signals a much bigger problem. “Nobody blinked an eye at EPA,” said Gartner. “It raises a lot of questions. How many other health and safety studies have been submitted to the agency and claimed as CBI?”
It’s impossible to answer Gartner’s question, since the information needed to determine whether a CBI claim is justified is itself often confidential.
Part of the problem is the weakness of the law. TSCA indicates that companies should have to prove that disclosure of the information they’re claiming as CBI would likely “cause substantial harm to the business’s competitive position.” But while the EPA can face hefty fines if it violates a company’s confidentiality, TSCA offers no way to penalize companies that make false confidentiality claims. The EPA has helped companies declassify documents and encourages them to review their confidentiality claims through “the CBI Voluntary Challenge” and, in 11 cases, has disallowed CBI claims, according to an agency spokesperson. But it has never punished a company for a false claim.
Environmental researchers need to be resourceful — and lucky — to penetrate the obscurity created by CBI. Heather Stapleton, a scientist at Duke University who studies household dust, was able to show that two of the BPC flame retardants were widespread in the environment only because one of her colleagues happened to suggest that a new chemical she noticed in a dust sample might be a component of Firemaster 550, a flame retardant made by Chemtura. Luckily for Stapleton, the colleague happened to have — and share with her — a sample of the product, which isn’t readily available to scientists. Stapleton was able to match the molecules in it to those in the product sample.
Stapleton’s discovery might have ended there. But after giving a talk about her research, a furniture manufacturer who was in the audience gave her a letter from Chemtura saying that the company’s prenatal development studies of its product had found “some effects.” The letter went on to assure the manufacturers that the risk was “negligible,” despite the findings, since the product didn’t leak into the environment.
But Stapleton’s work proved otherwise. The chemical was clearly making its way into the environment if it was showing up in dust samples. Alarmed, she asked Chemtura for its health studies of Firemaster 550. Stapleton said the company declined to supply them (Chemtura told me that it has no record of Stapleton requesting the studies), and so she asked the EPA for any data it had on the product. “They mailed me a CD that had 800 pages and 90 percent was blocked out for CBI,” Stapleton told me recently. “I couldn’t make heads or tails of that document.”
According to a statement from the EPA, the agency declassified the company name, chemical names, and individual ingredients of Firemaster 550 in 2010, and this information is now available in the public docket.
So Stapleton decided to use some of her remaining Firemaster 550 sample to study the product’s health effects, exposing pregnant rats to varying doses of the substance and observing the health of their offspring. She found that exposure could have clear effects on the rats’ babies, which were more likely to become obese and show signs of anxiety. Female rats whose mothers were exposed to Firemaster 550 were more likely to experience early onset of puberty, and males whose mothers were exposed at levels lower than the company deemed safe had an increased rate of heart defects. Stapleton also concluded that Firemaster 550 is an endocrine disruptor.
Independent research on the health effects of the replacements for C8 and longer-chain perfluorinated compounds has only recently begun in earnest. But several studies already indicate problems similar to those linked to C8, which include immune disorders, reproductive problems, and two kinds of cancer.
The most worrisome health information comes from industry itself. Chemical manufacturers are required by Section 8 (e) of the Toxic Substances Control Act to report any information to the EPA that “reasonably supports the conclusion that” a substance they make or use “presents a substantial risk of injury to health or the environment.” But the critical information in these 8 (e) reports can also be claimed as confidential. Last year, the Environmental Working Group reviewed more than 100 Section 8 (e) reports that had been submitted for perfluorinated chemicals between 2007 and 2015 and found that, among the 85 percent in which the chemical’s name was withheld, “reported health effects of exposure included death; maternal and developmental toxicity; degeneration and necrosis of the kidneys; chromosome aberrations; changes to the weight of the heart, kidney, liver, thymus, spleen, prostate, ovaries and adrenal glands; lethargy; and irregular breathing.”
The EPA has possessed evidence of the health effects of DuPont’s C8 replacement, GenX, since at least April 2006, when DuPont filed the first of 16 Section 8 (e) reports about the chemical. Some of those reports reference a 2009 consent order, which The Intercept obtained through a Freedom of Information Act request. That document — in which the specific identity of the replacement chemical and a closely related salt molecule, their production volume, manufacturing process and sites, processing, use, and other information have been withheld as CBI — lays out the agency’s many concerns about DuPont’s C8 replacement. It notes, for instance, that it has evidence that the chemical and its salt are toxic to lab animals and cause mutations in mammalian and human cells. The document also lays out concerns that the molecules “will persist in the environment, could bioaccumulate, and be toxic (“PBT”) to people, wild mammals, and birds”; that “there is high concern for possible environmental effects over the long-term”; and that “EPA has human health concerns for the PMN substances.”
An analysis of the 8 (e) reports, which are based on DuPont’s experiments on lab animals, shows that GenX presents some of the very same health problems that C8 does, including changes in the size and weight of animals’ livers and kidneys, alterations to their immune responses and cholesterol levels, weight gain, reproductive problems, and cancer.
In response to inquiries from The Intercept, DuPont declined to comment, noting that GenX is now a product of Chemours. Chemours responded that “extensive safety testing was conducted” on GenX. “Data suggests that it is not a developmental, reproductive, or genetic toxicant, or a human carcinogen.” (See “New Teflon Toxin Causes Cancer in Lab Animals” for the complete text of Chemours’ response.)
Due to CBI claims, it’s impossible to determine the amounts of the new PFCs that are being manufactured and used in the United States. Without this information and with little monitoring of their presence in the environment, exposure levels are similarly indeterminate. DuPont’s filings in Europe estimate production of GenX at between 10 and 100 tons each year. GenX, however, is only one of the company’s new PFCs. Chemours, the chemical company spun off by DuPont in July 2015, has many additional new formulations of surfactants and repellents for use in textiles, firefighting foam, and leather. Other chemical companies have developed their own substitutes. 3M, which supplied C8 to DuPont for many years, uses a product called ADONA. Solvay, Asahi, Dow Corning, and numerous companies in Japan and Europe have also come up with their own formulations. Zhanyun Wang estimates that tens of thousands of tons of fluorinated alternatives are now produced worldwide.
In May 2015, a group of scientists issued the Madrid Statement, which called for limiting production of all perfluorinated chemicals (regardless of the length of their molecules) based on their persistence and toxicity. The scientists noted that little information has been made public about how poisonous the replacement chemicals are to humans or animals, but that longer-chain PFCs have been shown to cause “liver toxicity, disruption of lipid metabolism, the immune and endocrine systems, adverse neurobehavioral effects, neonatal toxicity and death, and tumors in multiple organ systems” in lab animals and are associated with “testicular and kidney cancers, liver malfunction, hypothyroidism, high cholesterol, ulcerative colitis, lower birth weight and size, obesity, decreased immune response to vaccines, and reduced hormone levels and delayed puberty” in people. And a 2014 study in Environmental Research has already linked one of the C6 replacement molecules, PFHxA, with a health problem that does not seem to be linked to other PFCs — a liver disorder known as Gilbert Syndrome.
There is one way these “shorter-chain” variations seem to be better than the originals they’re replacing. Many of them, though not all, remain in the human body for less time. According to one 2011 document from the European Food Safety Authority, 3M reported that the half-life of its chemical ADONA was between 12 and 34 days in the bodies of three workers. In contrast, it takes humans about four years to clear half of the C8 from their bodies. Although it takes months for lab animals to rid themselves of C8, DuPont has claimed that with GenX, “virtually complete elimination from the body occurs in 12-24 hours.”
But as C8 replacements become increasingly ubiquitous, this improvement may be moot. “Even if it stays for just days,” said Wang, a chemical “still has possibility to cause damage.” Because the replacements are already so widespread, he said, “we’ll keep eating them and drinking them, so we’ll have continuous exposure. And if the environmental concentration in food and water keeps going higher because of increased use, then concentrations in our bodies will also go up.”
Asked for comment, 3M provided the following statement: “We believe that these shorter-chain compounds do not present health risks at the levels they are typically found in the environment.”
In terms of how long they’ll persist in the environment, the new chemicals are just as bad as the C8 they’re meant to replace. Like C8, GenX is extremely stable and will likely persist indefinitely. As A. Michael Kaplan, DuPont’s then-director of regulatory affairs, put it in one of the 8 (e) reports the company submitted to the EPA in 2010, “The biodegradation of the test substance was 0%.”
“It will take thousands of years to break down — or maybe longer,” Wang said of GenX. 3M’s ADONA, he said, will also endure indefinitely. “The company claims that this replacement degrades, but actually it doesn’t.” Indeed, most of the new replacement PFCs — or, in the case of the longer-chain molecules, the substances they degrade into — won’t ever break down. “We’re replacing a super-persistent chemical with super-persistent chemicals.”
It took half a century from the introduction of C8 into commercial use for the public to catch on about its dangers. In part because the EPA has yet to issue binding regulation that could require polluters to be held financially responsible for their mess, most of the contamination from that chemical is still in our environment. The earlier flame retardants that BPCs are replacing — and the dangerous chemicals they degrade into — also remain with us.
Now, with the introduction of next-generation replacement chemicals, industry has reset the clock. In addition to the C8 and the phased-out flame retardants in our water, soil, and air, we are being exposed to hundreds of other chemicals, many of which could endure forever.
DuPont referred to C8 as an “essential processing aid.” Chemours, which has inherited DuPont’s PFC business, notes that its newer generation of fluoropolymer resins, manufactured using GenX, is “critically important.” The company website points out that its products are used to provide cable and internet service, more efficient cars, and “insulation for cabling that is essential for safety, security and performance in buildings, data centers, ships and aircraft.”
But while PFCs are used to make some very useful products, they’re also in many others that are not essential, including food packaging, clothing, make-up, workout gear, and outdoor equipment, such as hiking clothes and tents, which means that nature lovers may be unwittingly spreading the contamination to remote places when they travel. Clearly, many if not all of these products could be manufactured without using PFCs.
The American Chemistry Council insists that “flame retardants provide an important layer of fire protection and help save lives.” But as the Chicago Tribune has reported, the trade organization has used phony customer watchdog groups and bogus claims to make the case for the necessity of flame retardants. Not only do the chemicals provide no meaningful protection from fire, as the Tribune’s reporting made clear, they can actually increase smolder propensity, as California officials noted when the state was doing away with its requirement that furniture makers inject the flame retardants into cushions. Some scientists also insist there is no scientific justification for the current practice of putting flame retardants in electronics. The American Chemistry Council did not respond to our requests for comment.
Although it’s technically possible to rid the environment of some PFCs, the process of finding, extracting, and disposing of them is practically out of reach in most of the world. Most countries won’t be able to pay for it, and the few that can, including the U.S., are unlikely to undertake this incredibly difficult and expensive task.
This should be the ideal time to be grappling with the enduring impact of unsafe chemicals. Congress is in the midst of revisiting our lax national chemical safety law, the Toxic Substances Control Act, and reform bills have passed both the House and the Senate. But lawmakers have already missed the opportunity to close one gaping legal hole that allows unsafe chemicals to enter the market, since neither of the bills now being considered would require companies to submit specific safety data before new chemicals are approved for use.
Nor does either bill really fix the confidentiality problem. The Senate’s bill would make some improvements on CBI, requiring the EPA to review past and future confidentiality claims that mask a chemical’s identity, as well as at least a quarter of the CBI claims for other types of information. But the House bill does not mandate any CBI review or lay out penalties for companies that make false claims. And in one important respect, TSCA “reform” could be a step backward: The House bill would allow companies to claim chemical identity in health studies as CBI.
As Congress dickers over reconciling the two TSCA reform bills, the regrettable replacements are accumulating all around us. The researchers who have made it their business to chase after those chemicals meanwhile struggle to keep pace. Stapleton, the researcher at Duke, is raising money to conduct a larger version of her experiment with Firemaster 550, which was criticized for its small sample size. Stapleton’s lab at Duke also runs a public testing program so that people can send in foam samples from their furniture to determine whether it contains dangerous flame retardants.
Wang, for his part, has become increasingly frustrated with the lack of awareness of the irreversible PFC contamination. Time, he says, is running out. “We need to reduce the emissions as fast as possible and evaluate whether uses are essential.” To his great frustration, however, most of his colleagues who work with PFCs are still focused on C8.
Strynar and Lindstrom, the EPA researchers in North Carolina, are hoping their discoveries will spur medical researchers to investigate the health effects of the PFCs they discovered in the Cape Fear River. They themselves have begun to work on developing methods to measure the chemicals, and to test methods for removing them from drinking water. Their research will likely continue for years.
Although PFOA was originally developed and manufactured in the United States, it’s not just an American problem.
IN RECENT MONTHS, PFOA, the perfluorinated chemical formerly used to make Teflon, has been making news again. Also known as C8, because of its eight-carbon molecule, PFOA has been found in drinking water in Hoosick Falls, New York; Bennington, Vermont; Flint, Michigan; and Warrington, Pennsylvania, among many other places across the United States. Although the chemical was developed and long manufactured in the United States, it’s not just an American problem. PFOA has spread throughout the world.
As in the U.S., PFOA has leached into the water near factories in Dordrecht, Holland, and Shimizu, Japan, both of which were built and operated for many years by DuPont. Last year, the Shimizu facility and part of the Dordrecht plant became the property of DuPont’s spinoff company, Chemours. Just as it did in both New Jersey and West Virginia, DuPont tracked the PFOA levels in its workers’ blood in Holland and Japan for years, according to EPA filings and internal company documents. Many of the blood levels were high, some extremely so. In one case, in Shimizu in 2008, a worker had a blood level of 8,370 parts per billion (ppb). In Dordrecht in 2005, another worker was recorded with 11,387 ppb. The national average in the U.S., in 2004, was about 5 ppb.
Water contamination was also a problem in both locations. In Shimizu, PFOA was detected in 10 wells at the site, with the highest level of contamination measuring 1,540 ppb. Groundwater in Dordrecht, which is about an hour south of Amsterdam, was also contaminated, with 1,374 ppb of PFOA at one spot near the factory in 2014.
But there has been little discussion of the problems at these two sites, at least until recently, when the PFOA contamination became news in Holland. In March, the Dutch National Institute for Public Health and the Environment released a report finding that levels of PFOA in water were elevated at least until 2002 and that residents of Dordrecht had been exposed to airborne PFOA for years.
In early April, a contingent from Keep Your Promises DuPont, an activist group representing residents of West Virginia and Ohio, traveled to the Netherlands and met with local politicians, scientists, Dordrecht residents, and the union representing workers at the plant.
“They’re pissed off,” said Paul Brooks, a physician from West Virginia who went to Holland and told people about the research that enabled epidemiologists to link PFOA to preeclampsia, ulcerative colitis, and two types of cancer, among other conditions. “They knew absolutely nothing about the links to disease, nothing,” said Brooks.
But the Dutch are learning quickly. On April 7, the Dutch newspaper Algemeen Dagblad announced the results of blood tests of two Dordrecht residents who had high blood levels of PFOA. One former DuPont worker had 28.3 ppb in his blood, while his wife, who didn’t work at the plant, had 83.6 ppb. In contrast, the blood level of Carla Bartlett, an Ohio resident who was awarded $1.6 million in the first of 3,500 cases against DuPont, was just 19 ppb in 2005.
Now at least 1,000 Dordrecht residents have requested testing, according to Ingrid de Groot, an investigative journalist for Algemeen Dagblad. De Groot said residents of Sliedrecht, a small town across the river from the Dordrecht, are also worried about airborne C8 contamination “because the wind 90 percent of the time blew in their direction from the Teflon plant.”
DuPont referred questions about its Dordrecht and Shimizu sites to Chemours, the company that has inherited its perfluorinated chemical (PFC) business, which now uses shorter-chain molecules. Chemours offered a statement saying that the area around the Shimizu site, which “was created decades ago” by DuPont and the Japanese company Mitsui, is “highly industrialized and the groundwater is brackish, and not a source of drinking water.” The statement also noted that PFOA has been used by a number of companies in Japan and that “Chemours has never used PFOA.”
Regarding Dordrecht, Chemours wrote that “there is no increased exposure of surrounding residents to PFOA via drinking water for the area surrounding the Dordrecht plant” and that the company “is confident that DuPont acted reasonably and responsibly during the years it used PFOA at Dordrecht, placing high priority on the health of its employees and the community. We believe DuPont went beyond what was required, and what other companies did, to manage PFOA in order to protect the health and safety of its workers and neighbors.” The statement also noted that by 2010, DuPont had reduced its PFOA emissions at the Dordrecht site by more than 90 percent of their level in 2000, and by 2012 the company had phased out the chemical entirely.
ENVIRONMENTALISTS HAVE BEEN pushing to tamp down on the worldwide use of PFOA and PFOS, both of which have been detected all over the world, including in Germany, Canada, Greenland, Spain, Italy, Norway, Sweden, Denmark’s Faroe Islands, France, Vietnam, South Africa, India, England, and Australia, where a governmental inquiry is underway. In 2014, PFOS was listed as one of the persistent organic pollutants to be phased out under the Stockholm Convention, the international treaty ratified by 179 countries (though not the U.S.). Last year, the EU proposed adding PFOA to the agreement.
But as some countries phase out the production of PFOS and PFOA, others are ramping it up. Perhaps the best example is China, where at least 56 companies produce PFCs, according to data collected by the Stockholm Convention. Without drinking water standards for PFOA and PFOS, or restrictions on their use, contamination is spiking there. A comparison of Chinese and European rivers published last year found that concentration of PFCs in the Xiaoqing River was more than 6,000 times higher than in the Scheur River, near DuPont’s Dordrecht plant. In a recent study, scientists tested the blood of fishery workers at Tangxun Lake in China’s Wuhan region. One employee was found to have the highest level of PFOS ever detected in human blood: 31,400 ppb.