Definitions and Background
PFAS encompass a whole family of synthetic chemicals that contain a carbon and fluorine atom backbone. There are hundreds of known PFAS compounds with varying functional groups, which can include other elements such as oxygen, hydrogen, or sulfur.
PFAS compounds became common applications in the 1950s and ’60s and are now part of hundreds of industrial processes and consumer products. They are considered useful because they are resistant to heat, water, and oil. Consumers may be exposed to PFASs in non-stick cookware, grease-resistant paper, fast food wrappers, microwave popcorn bags, stain-resistant carpets and fabrics, water-resistant clothing, cleaning products, and personal care products.
According to the American Cancer Society, Teflon® is a brand name for the human-made chemical known as polytetrafluoroethylene (PTFE), one of the PFAS. It has been in commercial use since the 1940s and has a wide variety of applications due to its stability. PTFE doesn’t react with other chemicals and can provide an almost frictionless surface. Think of it as that non-stick coating surface that you see on lots of pans and other cookware.
PFAS are also used in industrial processes and, notably, in firefighting foams used by the military, airport authorities, and local fire and rescue agencies. The EPA says that it is these foams that are most often implicated when PFAS is found in groundwater or in the environment and that some PFAS take a very long time to break down in the environment and our bodies. As a result, they have the potential to build up in the organs and tissues of humans and animals. Animals further up the food chain — such as humans — may accumulate even more of the chemicals in their bodies when they eat plants or other animals that have been exposed to PFAS.
Research has shown that another type of PFAS, perfluorooctanoic acid (PFOA), can increase people’s levels of triglycerides, which are a type of fat, and cholesterol, both of which can increase the chance of heart disease.
The Toxic Teflon Cover-Up and Its Consequences
3M has downplayed, avoided, and reframed research conclusions about the PFAS it produced. Its happy facade makes the PFAS compounds appear safer than they are, according to the documents made public by Minnesota’s attorney general.
In several cases, 3M appears to have not pursued further research based on discoveries that suggested the chemicals posed harm, and the company also relied on a number of paid scientists who neglected to disclosed their funding from 3M. Several government officials also understood the vast dangers that PFAS posed without informing the general public.
Timeline of Who Knew What & When about Toxic Teflon
Scientists, 3M researchers, and government officials have known about the dangers presented by these industrial PFAS chemicals for decades. The complexity of the coverup is most evident when seen as a timeline of events.
In 1947, the Minnesota Mining and Manufacturing Company (3M) began producing perfluorooctanoic acid (PFOA) by electrochemical fluorination.
In the 1950s, 3M expanded worldwide with operations in Canada, Mexico, France, Germany, Australia, and the United Kingdom.
In 1951, DuPont started purchasing PFOA from 3M for use in the manufacturing of teflon, a product that brought DuPont a billion dollars a year profit by the 1990s. DuPont referred to PFOA as C8.
In the 1970s, 3M had evidence of the compounds’ effects on the immune system. Those studies are just now driving the lower levels put forward by the ATSDR, several states, and the European Union.
In 1993, scientific literature states that goats passed PFOS to their offspring through their milk.
In 1998, a discovery is made that PFOS had found its way into eagles found in the wild.
In 2000, 3M gave the EPA hundreds of documents it had withheld from the agency. This means that these documents were in the EPA’s possession for at least 18 years without the agency taking definitive action. PFAS were allowed to spread into groundwater and then drinking water, families, animals, plants, and the food system, where they remain today.
Since 2000, the number of scientific articles published on the health effects of PFAS has increased more than tenfold. The findings have linked the chemicals to a wide range of health effects in people, including testicular and kidney cancer, obesity, impaired fertility, thyroid disease, and the onset of puberty.
In 2001, 3M staff epidemiologist Geary Olsen wrote a report based on an enormous database of more than 55,000 products and more than 90,000 3M employees. The report stated that a positive association existed between the amount of PFOA in workers’ blood and their levels of cholesterol and triglycerides.
In 2003, Olsen and 3 co-authors — all 3M employees — published an article in the Journal of Occupational and Environmental Medicine that contradicted Olsen’s original research. “There were no substantial changes in hematological, lipid, hepatic, thyroid, or urinary parameters consistent with the known toxicological effects of PFOS or PFOA.” The authors note that PFOA was “positively associated with cholesterol and triglycerides” and that “serum PFOS was positively associated with the natural log of serum cholesterol … and triglycerides” but dismiss these effects as “minimal.” The article omits most of the original information that laid out the increase in cholesterol and triglycerides in exposed workers.
In 2005, many of the 3M documents were placed under seal as a result of a separate lawsuit over PFAS contamination in Minnesota.
In 2006, 3M was slapped with more than $1.5 million in penalties for 244 violations of the Toxic Substances Control Act.
In 2010, the Minnesota attorney general filed a lawsuit that charged that 3M polluted groundwater with PFAS compounds and “knew or should have known” that these chemicals harm human health and the environment and “result in injury, destruction, and loss of natural resources of the State.”
In 2012, Robert Delaney, a Minnesota state scientist who tried to raise alarms about the chemicals, was largely ignored. Now Delaney, who delivered a report to his superiors about high levels of the chemicals in fish and the dangers they presented to people, has been “heralded as prophetic.”
In February, 2018, 3M settled the suit for $850 million, in essence admitting that they “acted with a deliberate disregard for the high risk of injury to the citizens and wildlife of Minnesota.” The Minnesota Attorney General’s Office released a large set of documents — including internal studies, memos, emails, and research reports — detailing what 3M knew about the chemicals’ harms.
The EPA says it remains committed to evaluating PFOA and PFOS under the regulatory determination process using the best available science. As a part of the evaluation, EPA will be reviewing all newly available scientific information including the Agency for Toxic Substances & Disease Registry (ATSDR) report. (Their 2-page fact sheet is quite helpful.)
The EPA says it is taking steps to accelerate the determination process before the existing statutory deadline, which is 2021.
Lerner’s investigation has uncovered how the EPA pressured the federal ATSDR to suppress a study showing PFAS chemicals. The delay is another in a series of blatant missed opportunities for the government to get critical health information to the public.
Yes, 3M paid its fines, but the decades of secrecy have allowed PFAS chemicals from the company’s facilities to enter the water in Minnesota, Alabama, and elsewhere. PFOS and PFOA were accumulating in the environment and in people, the vast majority of whom now have the chemicals in their blood.
The lag in getting scientific information to regulators resulted in prolonged public exposure to the chemicals, as Philippe Grandjean argues in an editorial in the journal Environmental Health. A physician and environmental health scholar who has studied the immune effects of PFAS and provided expert testimony for Minnesota in the 3M case, Grandjean argues that regulators should learn from this massive misstep, and that substitutes for PFOS and PFOA “should be subjected to prior scrutiny before widespread usage.”
3M’s fluorochemicals helped the company expand into a multibillion dollar entity it is today. Lerner argues that “the real-life implications of this careful curation of the scientific record on PFAS is still coming into relief as the public begins to grapple with the likelihood that the EPA’s safety levels for these two chemicals are far too high.” She points to a study released by the ATSDR in June that calculated the limit for PFOS and PFOA in drinking water ought to be around 7 and 11 parts per trillion or ppt, respectively, just a fraction of the 70 ppt that the EPA set for the chemicals in 2016.
The number of people thought to be affected by this contamination continues to expand as the scientific information is refined. In Minnesota, where 3M is headquartered and the lawsuit was filed. PFAS water contamination is now a national — and international — issue. Using data collected by the EPA, the Environmental Working Group calculated that more than 100 million Americans may be have some level of PFAS in their drinking water.
Philippe Grandjean, who has been a physician and environmental health researcher for more than 40 years, has also been affected by the realization of just how long he and others were kept in the dark about the harms of the chemicals. “I lost my confidence in the scientific literature,” said Grandjean. As he sees it, his whole profession has been stained by the experience. “We in my field have failed.”
Photo by JPC24M on TrendHype / CC BY-SA
The Teflon Toxin Internal studies and other documents show that 3M knew by the 1970s that PFOA and PFOS were toxic and accumulating in people’s blood.
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.
The best evidence of how C8 affects humans has also come out through the legal battle over the chemical, though in a more public form. As part of a 2005 settlement over contamination around the West Virginia plant where Wamsley worked, lawyers for both DuPont and the plaintiffs approved a team of three scientists, who were charged with determining if and how the chemical affects people.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.
3M Knew About the Dangers of PFOA and PFOS Decades Ago, Internal Documents Show
PFOA and PFOS Are Only the Best-Known Members of a Very Dangerous Class of Chemicals
The U.S. Military Is Spending Millions to Replace Toxic Firefighting Foam with Toxic Firefighting Foam
EPA Orders Testing for GenX Contamination Near Chemours Plant in West Virginia
Citizen Groups Will Sue DuPont and Chemours for Contaminating Drinking Water in North Carolina
New Teflon Toxin Found in North Carolina Drinking Water
The Teflon Toxin Goes to China
DuPont May Dodge Toxic Lawsuits By Pulling a Disappearing Act
Teflon Toxin Contamination Has Spread Throughout the World
How DuPont Concealed the Dangers of the New Teflon Toxin
New Teflon Toxin Causes Cancer in Lab Animals
Toxic Firefighting Foam Has Contaminated U.S. Drinking Water
DuPont Found Liable in Teflon Toxin Trial
The Teflon Toxin Goes to Court
How DuPont Slipped Past the EPA
The Case Against DuPont
DuPont and the Chemistry of Deception
NEWS THAT THE Environmental Protection Agency pressured the federal Agency for Toxic Substances and Disease Registry to suppress a study showing PFAS chemicals to be even more dangerous than previously thought drew outrage this spring. The EPA pressure delayed the study’s publication for several months, and a similar dynamic seems to have been in play this July in Michigan, where Robert Delaney, a state scientist who tried to raise alarms about the chemicals six years ago, was largely ignored. Delaney, who delivered a report to his superiors about high levels of the chemicals in fish and the dangers they presented to people, has been heralded as prophetic. And both delays are being lamented as missed opportunities for getting critical information to the public.
But the dangers presented by these industrial chemicals have been known for decades, not just a few months or years. A lawsuit filed by Minnesota against 3M, the company that first developed and sold PFOS and PFOA, the two best-known PFAS compounds, has revealed that the company knew that these chemicals were accumulating in people’s blood for more than 40 years. 3M researchers documented the chemicals in fish, just as the Michigan scientist did, but they did so back in the 1970s. That same decade, 3M scientists realized that the compounds they produced were toxic. The company even had evidence back then of the compounds’ effects on the immune system, studies of which are just now driving the lower levels put forward by the ATSDR, as well as several states and the European Union.
The suit, which the Minnesota attorney general filed in 2010, charges that 3M polluted groundwater with PFAS compounds and “knew or should have known” that these chemicals harm human health and the environment, and “result in injury, destruction, and loss of natural resources of the State.” The complaint argues that 3M “acted with a deliberate disregard for the high risk of injury to the citizens and wildlife of Minnesota.” 3M settled the suit for $850 million in February, and the Minnesota Attorney General’s Office released a large set of documents — including internal studies, memos, emails, and research reports — detailing what 3M knew about the chemicals’ harms.
Some of the documents had been under seal since 2005 as a result of a separate lawsuit over PFAS contamination in Minnesota. And the documents had been in the EPA’s possession for at least 18 years: In 2000, 3M gave the EPA hundreds of documents it had withheld from the agency, resulting in more than $1.5 million in penalties in 2006 for 244 violations of the Toxic Substances Control Act. Even so, for years the EPA did nothing. Even as a few government officials and company scientists understood the vast dangers they posed, PFAS were allowed to spread into groundwater and then drinking water, into people and their children, into animals, plants and the food system where they remain today.
Suppressing Damaging Data
As a staff epidemiologist at 3M, Geary Olsen has had a wealth of data at his fingertips. The company he’s worked for since at least 1998 makes more than 55,000 products and has more than 90,000 employees. Olsen had access to internal information about both and has been able to combine them to pursue the kinds of scientific questions most researchers can only dream of being able to ask and answer.
In one study, for instance, Olsen looked at blood tests of 3M employees at the company’s plants in Antwerp, Belgium, and Decatur, Alabama, both of which made PFOA and PFOS, among other products. By the late 1990s when Olsen was embarking on this research, these chemicals were known within the company to accumulate in humans and alter cholesterol levels in lab animals. Because the workers had undergone three separate rounds of blood tests, Olsen was able to trace the levels of the chemicals in workers’ blood over time. And by combining his results with various clinical measures the company had been tracking in its workers, he was able to see whether there was a relationship between the chemical and these health outcomes.
Olsen’s findings, written up in an draft report in October 2001, were clear. There was a positive association between the amount of PFOA in workers’ blood and their levels of cholesterol and triglycerides, states the report, on which Olsen is listed as the principal investigator. The report devoted more than 20 tables to triglycerides and cholesterol, detailing a relationship that later studies would confirm: PFOA increased people’s levels of triglycerides, which are a type of fat, and cholesterol, both of which can increase the chance of heart disease. The results were in keeping with rat evidence, as the report noted.
Yet less than two years later, when Olsen and the three co-authors on the report — all 3M employees — published an article based on the same research, it downplayed this key finding. Indeed, according to the study, which ran in the March 2003 issue of the Journal of Occupational and Environmental Medicine, “There were no substantial changes in hematological, lipid, hepatic, thyroid, or urinary parameters consistent with the known toxicological effects of PFOS or PFOA” — a statement that appears to contradict the authors’ earlier finding.
In the 19th paragraph of the 2003 article, the authors note that PFOA was “positively associated with cholesterol and triglycerides” and that “serum PFOS was positively associated with the natural log of serum cholesterol … and triglycerides,” but dismiss these effects as “minimal.” The article omits most of the information that was contained in the draft’s tables and clearly laid out the increase in cholesterol and triglycerides in exposed workers.
The minimizing of this bad news is just one of several instances in which 3M seems to have downplayed, spun, and tailored its own research to make these two PFAS chemicals and others it produced appear safer than they were, according to the documents made public by Minnesota’s attorney general.
In some cases, relatively reassuring findings about the chemicals made their way into the scientific literature, while other more concerning ones — like the 1993 observation that goats passed PFOS to their offspring through their milk, or the 1998 discovery that PFOS had made its way into eagles found in the wild, or the association between PFOA and lipids that Geary identified — did so only after many years. In several cases, 3M appears to have not pursued further research based on discoveries that suggested the chemicals posed harm. And the company also relied on several paid scientists, including John Giesy, now a professor at the University of Saskatchewan, who weighed in on the environmental impact of PFOA and PFOS without disclosing their funding from 3M.
In an email, a 3M spokesperson strenuously denied that the company tailored its research around PFAS, writing that “neither 3M nor Dr. Olsen has distorted or suppressed the scientific evidence regarding PFAS in any way.” The email also pointed out that the company eventually gave the EPA Olsen’s 2001 report, which at this point has “been publicly available for well over a decade.” While acknowledging that Olsen found an association between cholesterol levels and PFOA, the 3M spokesperson noted that the effect of PFOA he documented in some workers — increasing cholesterol levels — was inconsistent with those observed in rats, whose levels decreased after exposure to the chemical, and that “the science is complex and neither the study nor the larger body of scientific evidence on this issue establishes causation.”
In a separate email, the 3M spokesperson wrote that “the Minnesota Attorney General released a small set of documents that should not be taken out of context in an effort to distort the full record regarding 3M’s actions with respect to PFOA or PFOS. 3M acted reasonably and responsibly in connection with products containing PFAS, and stands behind its environmental stewardship record.”
Giesy did not respond to a request for comment, but the University of Saskatchewan provided a statement saying that “Prof. Giesy rejects the unproven claims, which were never tried or tested in court.” Giesy “encouraged the company to voluntarily cease production of the chemical,” the university’s statement goes on to say, also noting that it conducted an investigation, which determined that Giesy had not violated university policy. The statement also pointed out that Giesy has not worked for 3M since he began working at the University of Saskatchewan in 2006.
Paul Brandt-Rauf, editor of the Journal of Occupational and Environmental Medicine, declined to comment, citing pending letters to the editor in his journal.
Yet the documents released by the Minnesota Attorney General’s Office demonstrate that 3M’s communications strategy altered the scientific record on PFAS by prettifying the scientific picture of PFOA and PFOS over the more than four decades it produced them.
While 3M readily paid its fines, there was no undoing the delay in regulatory action that resulted from the previous decades of keeping its damning information secret. While the studies sat in 3M’s private files, PFAS chemicals from the company’s facilities were entering the water in Minnesota, Alabama, and elsewhere, and PFOS and PFOA were accumulating in the environment and in people, the vast majority of whom now have the chemicals in their blood.
The lag in getting scientific information to regulators in turn resulted in prolonged public exposure to the chemicals, as Philippe Grandjean argues in an editorial in the journal Environmental Health. A physician and environmental health scholar who has studied the immune effects of PFAS and provided expert testimony for Minnesota in the 3M case, Grandjean argues that regulators should learn from this massive misstep, and that substitutes for PFOS and PFOA “should be subjected to prior scrutiny before widespread usage.”
The Principled Path
The history of PFAS compounds has mostly revolved around DuPont. That giant company also knew for decades that PFOA was escaping its plant, leaching into nearby drinking water, accumulating in the blood of its workers, and harming animals tested in its own labs. Since 2004, DuPont has paid more than $1 billion in class-action litigation and several related suits filed by people living near its plant in Parkersburg, West Virginia — and faced massive public outrage over its actions.
To the extent that 3M has come up in coverage of the fast-growing PFAS story, it’s largely been as a footnote — and a foil. 3M was the company that invented PFOA and sold the toxic stuff to DuPont, whose corporate image was besmirched by the news of its deceptions around PFOA. DuPont has also faced a firestorm of protest over GenX, its similarly toxicreplacement for PFOA.
As 3M executives have pointed out on numerous occasions, their company phased out PFOA six years before DuPont did. (DuPont never manufactured PFOS.) “3M has acted appropriately and on the principled path,” William A. Brewer III, a partner in a law firm representing 3M in perfluorinated chemical-related litigation, told me when I first wrote about Minnesota’s lawsuit in 2016. “They immediately reported it, investigated it, and frankly decided to exit the C8 chemistries in their entirety well more than a decade before anyone else who was a competitor.”
But the documents from the Minnesota suit upend the narrative of 3M as the good corporate citizen.
In 1948, 3M, or the Minnesota Mining and Manufacturing Company, as it was then called, acquired the patent for a process of creating compounds out of fluorine. Manhattan Project scientists — several of whom landed at 3M after the war — had already used fluorine to separate the uranium used for the atom bomb. Their new method bonded carbon to fluorine atoms, creating novel materials such as an extraordinarily stable fluid called PFOA. 3M executives believed that the substance might have commercial applications, though they didn’t at first know what those might be. In 1950, after two years of conferring with various companies, 3M landed a deal to sell PFOA to DuPont to make Teflon. After that, “we were in business,” a 3M executive later recalled.
3M would continue to sell PFOA to DuPont for more than four decades. Starting in the early 1950s, the company also made PFOS, a closely related compound that wound up in hundreds of products, including the company’s own Scotchgard fabric protector, which, by the end of the 1950s, was being applied to both upholstery and clothing; and firefighting foam that 3M provided exclusively to the U.S. military for decades. 3M went on to market some of these its fluorochemical products as “the solution for your problems.”
3M’s fluorochemicals helped the company expand into a behemoth worth more than $120 billion. But the story of 3M “is clearly not a story of molecules, compounds, good science or technology,” as the company’s own corporate history explained in 1991. “It is a story of people.” Indeed, while 3M was distinguished by both its industrial chemistry and occupational health, it was individuals who made the fateful choices about which lines of scientific inquiry to pursue — and which to share with the public.
A Medical Mystery
The first scientists to raise the alarm about the fluorine-based chemicals didn’t work for 3M. In August 1975, a University of Florida researcher named Warren Guy called the company to get help with a medical mystery his colleague, Donald Taves, had stumbled upon. Taves had detected a form of fluoride in his own blood that hadn’t been found in blood before. The fluorine didn’t break down and appeared to be part of a large and stable molecule. The discovery sparked the scientists to look for and find fluorinated compounds in other blood samples, as they described in a 1975 paper. Guy was calling 3M to ask whether Teflon and Scotchgard might be the source of the compounds.
“We plead ignorance,” one of 3M’s chemists, G. H. Crawford, recounted in a summary he wrote up after the call. But within a few months, staff scientists knew quite a bit about the fluorinated compound found in blood. They compared the unique spectrum of its own patented compound, PFOS, with that of the chemical identified by Taves and Guy and found that they matched, according to a timeline the company compiled in 1977.
During the phone call, Crawford also suggested that Guy check blood samples from “uncivilized areas, e.g. New Guinea” where Teflon and Scotchgard weren’t in use. Later testing of historical blood samples would show Crawford’s suspicion to be spot on. After their introduction into consumer products in the 1950s, the fluorinated compounds began to appear in blood samples from around the world going as far back as 1957.
Closer to home, the chemicals were clearly accumulating in their own factories. By 1976, 3M measured fluorochemicals in the blood of workers at its plant in Cottage Grove Minnesota at “1,000 times normal.” The chemical appeared to accumulate in animals, too. Mice fed “Scotchban,” a grease-proofing 3M product that contained PFOS, had “4,000 times normal organic fluorine compound,” in their blood, the timeline also noted. By 1979, the company noted that samples from Red Cross blood donors also contained trace levels of the fluorinated chemical.
But it’s clear that the scientists’ fielding Guy’s phone call had yet to grasp the implications of the situation. After the call, Crawford tried to put a positive spin on the dawning realization that their chemical had found its way into Americans’ blood.
“If it is confirmed to our satisfaction that everybody is going around with fluorocarbon surfactants in their bloodstreams with no apparent ill-effect, are there some medical possibilities that would bear looking into?” Crawford asked in his notes. Perhaps PFOS might help with hardening of the arteries, “kidney blockage, senility and the like,” Crawford mused, going on to suggest animal experiments “both from a defensive point of view and for the above (to me) intriguing reasons.”
While the company was pondering the possibility that the massive human experiment it had launched might have some positive outcomes, it was becoming clear that it would almost certainly have some negative ones. According to minutes from a 1978 meeting about 3M’s experiments on rats and monkeys, PFOA and PFOS “should be regarded as toxic.” Disturbingly, PFOA caused changes in rats’ livers at levels lower than that measured in one of its workers, according to the memo, which described the finding as suggestive of “a possible human health problem.” Nevertheless, the eight staff members present at the meeting decided that the toxicity “does not constitute a substantial risk and should not be reported [to the EPA] at this time.”
Two studies on monkeys done later that year might have been seen as even more alarming — and worth sharing with the public. One had to be stopped because all the monkeys given PFOS died (“Incorrect (too high) feeding levels were used and all animals died within the first few days”). In the other, monkeys given PFOA developed tiny lesions on their spleen, lymph nodes, and bone marrow — organs central in maintaining the body’s immune defenses.
The next year, a review of the internal studies described PFOS as “the most toxic” of three compounds studied, “certainly more toxic than anticipated,” and recommended that “lifetime rodent studies should be undertaken as soon as possible.” But from the documents released and a search of the medical literature, 3M appears not to have undertaken the studies suggested in the review. Nor did it publish either of the monkey studies. And the company waited 22 years before giving the troubling studies to the EPA or reporting the evidence that the chemical was in the blood of the general public.
Still, 3M appears to have been worried enough about the implications of the studies to seek advice from a well-known toxicologist named Harold Hodge. At a confidential meeting with company executives held in San Francisco in June 1979, Hodge noted that the company’s research on exposed workers showed “indications of liver effects.” Because both PFOS and PFOA also caused liver changes in rats, Hodge suggested that 3M find out whether PFOS “or its metabolites are present in man, what level they are present, and the degree of persistence (half-life) of these materials.” If the levels were high and widespread and the half life long, he said, “we could have a serious problem.”
In a phone call a week after the meeting, Hodge asked that a note be added to the minutes to stress that the research he was proposing was “of utmost importance.” Later that year, another 3M scientist, M. T. Case, underscored Hodge’s suggestion, writing in a memo to his colleagues that “it is paramount to begin now an assessment of the potential (if any) of long term (carcinogenic) effects for these compounds which are known to persist for a long time in the body and thereby give long term chronic exposure.”
In 1980, the company came close to disclosing how widespread its chemicals had become, according to questions drafted in anticipation of the news reaching the general public. “I have heard that fluorochemicals are persistent. Does this mean that [they] are like PCBs and DDT?” one sample question asked, referring to chemicals widely used in electrical equipment and pesticides, respectively, that accumulated in the environment and increased cancer rates. The proper answer, according to the company’s guide was “NO.” But it turned out no rehearsal was necessary. 3M didn’t announce the presence of PFOS or PFOA in human blood — nor did the bad news leak out. And for more than 20 years, as evidence emerged that tumors in exposed lab animals were related to PFOA exposure, that the levels of the chemicals in 3M workers’ blood rose over time, and that their cancer rates were elevated compared to the general population, the questions about the environmental and health consequences of the secret were neither asked nor answered.
What Immune Impact?
The real-life implications of this careful curation of the scientific record on PFAS is still coming into relief as the public begins to grapple with the likelihood that the EPA’s safety levels for these two chemicals are far too high. A study released by the Agency for Toxic Substances and Disease Registry in June calculated that the limit for PFOS and PFOA in drinking water ought to be around 7 and 11 parts per trillion or ppt, respectively, just a fraction of the 70 ppt that the EPA set for the chemicals in 2016.
ATSDR and the state of New Jersey, which has calculated similar safety levels for both chemicals, arrived at the lower number for PFOS in part by including studies showing that very low levels of the chemical affect the immune system. The European Food Safety Authority also recently considered evidence of their immune effects when calculating even lower safety levels — 6.5 ppt for PFOS and just 3 for PFOA. And Philippe Grandjean, a physician and environmental health scholar who has studied the immune effects of PFAS and provided expert testimony for Minnesota in the 3M case, calculated that the safety levels for both PFOS and PFOA should be less than 1 ppt.
In contrast, the EPA did not include studies showing immune effects in its calculations. When asked why it didn’t include these studies when devising its health advisory levels for PFOS and PFOA, the EPA did not respond. The agency instead provided the following statement:
EPA remains committed to evaluating PFOA and PFOS under the regulatory determination process using the best available science. As a part of the evaluation, EPA will be reviewing all newly available scientific information including the ATSDR report. EPA is taking steps to accelerate the determination process before the existing statutory deadline.
The statutory deadline is 2021.
While the immune effects of PFOS and PFOA have entered the public conversation only in recent years, 3M has possessed evidence suggesting that its signature chemical affected the immune system as far back as 1978, when its monkey study showed the tiny lesions on immune organs. An internal summary of research noted both PFOA’s liver and immune effects. At a 1983 meeting of the company’s Fluorochemical Study Committee, a member of the toxicology team listed “immunosuppressive effects” as one of three areas of follow-up research given the highest priority, according to meeting notes.
Yet the company didn’t publish anything about how PFOA affected the immune system, even as it was internally gathering more damning evidence. In 1991, a physician named Frank Gilliland came to work at 3M for a year while he was getting his Ph.D. in environmental health. Gilliland wrote his thesis on the health effects of PFOA in 3M workers in 1992, looking at the effects of the chemical on 115 male workers at one of the company’s plants.
The paper describes his finding that the amount of PFOA in workers’ blood correlated to levels of various hormones. Gilliland also calculated that workers in one of 3M’s plants who had at least 10 years of exposure to PFOA had a death rate from prostate cancer that was three times that of workers who weren’t exposed to PFOA. And his thesis explained that the chemical affected the immune response to foreign chemicals.
While Gilliland went on to publish the prostate cancer finding, an internal paper he wrote that further explored PFOA’s effects on the workers’ immune system never saw the light of day. His draft explained that the level of critical immune cells in workers was “significantly correlated” with their total fluoride levels, “suggesting that cell-mediated immunity may be affected by PFOA.” Gilliland’s paper also noted the company’s 1978 monkey studies — and that “no follow-up studies of these observations have been reported.”
But the company didn’t publish or follow up on Gilliland’s work either, based on the documents released. In a 1993 memo, 3M’s medical director, Jeff Mandel, wrote to the company’s Fluorochemical Steering Committee members that Gilliland had three research papers in the works, all of which were “negative for the most part.” Mandel wrote that “we’re working with him regarding some of the wording.” But none of the papers in the memo came out in any form. And 15 years would pass after Gilliland’s finding that PFOA affected immunity — and 30 years after the monkey study suggested a similar impact — before independent scientists documented the effect of PFOA in humans.
One of the reasons scientists in the field didn’t explore whether PFOA, PFOS, and other chemicals in their class could affect the body’s ability to fight off infection and toxicity was because they believed they couldn’t affect the human body. “Word was that the compounds were inert,” said Grandjean, who considered and rejected the idea of researching how the chemicals affected immunity when 3M took the compounds off the market in 2000.
It was only in 2008, after a study showed that PFOA affected the immune systems of mice, that Grandjean and his team went back to study the chemicals’ impact on humans. “We were already looking at PCBs, which we know are immunotoxic, to see if they affected how children responded to vaccines,” said Grandjean. When his team did the same research with PFAS, they noted a dramatic effect. “These responses were much stronger than anything we can attribute to PCBs.”
Eagles, Fish, and Rats
Another 3M scientist made discoveries about PFAS that the company didn’t readily follow up or publish. In the 1990s, Rich Purdy, an environmental scientist at 3M, detected PFOS in the blood of eagles. He also found that rats that hadn’t been purposely exposed to the chemical had it in their liver, likely because their food was made from fish that had been exposed. (3M had already measured the chemicals in fish in the Tennessee River near its Decatur, Alabama plant back in 1979.) Alarmed, Purdy reasoned that whales, seals, and other fish-eating animals might also be contaminated and urged the company to sample a few species to find out. But his superiors didn’t share his urgency.
“I’m not sure there is a need to support or refute the hypothesis within any particular time frame,” a 3M attorney named Thomas DiPasquale wrote to his colleagues in the company’s corporate division in a 1999 email. Purdy had also suggested alerting the EPA to his concern that PFOS was spreading through the food chain, but his bosses came up with a slower and more measured response.
The year before, the company had laid out its strategic plan for releasing scientific information. In 1998, it had finally provided the EPA with some of the evidence that its chemicals were in blood samples from the general public. In anticipation of the public release of that information, 3M devised a schedule of publications that would “allow the serum level findings to be placed in an understandable, credible context which demonstrates that there is no medical or scientific basis to attribute any adverse health effects to 3M products.”
Purdy believed that the plan to delay the follow-up was another instance of putting the company’s need to protect its self-interest over the environment:
Plan! That is the same stalling technique you have been using for the last year. There is a high probability that PFOS is killing marine mammals and you want another plan when we could have had data to support the risk assessment long ago. You were given a plan in 1983. Again in the early 90s. And you authorized no testing …
You continually ignore our plans and start new plans that slows the collection of data essential for our risk assessments. You slow our progress in understanding the extent of PFOS pollution and damage. For 20 years the division has been stalling the collection of data needed for evaluating the environmental impact of fluorochemicals.
Shortly afterward, Purdy reached his limit, according to a resignation letter he sent in 1999. In it, he explained that his decision to leave was “prompted by my profound disappointment in 3M’s handling of the environmental risks associated with the manufacture and use” of PFOS. While, years before, the company’s planned questions and answers had sought to dispel any comparison to PCBs, Purdy described PFOS as “the most insidious pollutant since PCB.”
I have been assured that action will be taken — yet I see slow or no results. I am told the company is concerned, but their actions speak to different concerns than mine. I can no longer participate in the process that 3M has established for the management of PFOS and precursors. For me it is unethical to be concerned with markets, legal defensibility and image over environmental safety. …
3M told those of us working on the fluorochemical project not to write down our thoughts or have email discussions on issues because of how our speculations could be viewed in a legal discovery process. This has stymied intellectual development on the issue, and stifled discussion on the serious ethical implications of decisions.
I have worked within the system to learn more about this chemical and to make the company aware of the dangers associated with its continued use. But I have continually met roadblocks, delays, and indecision. For weeks on end I have received assurances that my samples would be analyzed soon — never to see results.
Purdy later changed his mind and returned to work at the company, according to a letter from his wife, who was clearly troubled by his decision. He didn’t respond to requests for comment. In any case, within a year of his letter, everything had changed. In 2000, after giving the EPA hundreds of its studies, 3M announced it would cease production of PFOS and PFOA. While the company claimed it made the decision voluntarily, an EPA official at the time said that the agency was prepared to remove PFOS from the market based on research that “suggests to us is that there are potentially long-term consequences.”
Subsequent research has validated the EPA’s suspicion. Since 2000, the number of scientific articles published on the health effects of PFAS has increased more than tenfold. The findings have linked the chemicals to a wide range of health effects in people, including testicular and kidney cancer, obesity, impaired fertility, thyroid disease, and the onset of puberty. The increased cholesterol and lipids in blood that Olsen noted in his 2001 paper have also been identified in several recent studies. And the immune effects have also been borne out, with one recent study by Grandjean showing that levels of the chemicals in infants’ blood were related to their immune response at age 5.
But the lag in awareness of these problems makes addressing them infinitely harder than it would have been when they had first surfaced. It’s now too late to contain the chemicals that originated in 3M’s laboratories. Since PFAS compounds were first traced in a few workers and animals, the chemicals have gone from being an occupational hazard to one shouldered by everyone. Blood testing done in 2003 found PFOA in 99.7 percent of more than 2,000 samples in the U.S. PFOS was in 99.9 percent. And it’s not just those two chemicals. In 2005, 3M tested human blood from around the country for 15 different PFAS — and found 14 of them.
The number of people thought to be affected by this contamination continues to expand as the scientific information is refined. In Minnesota, where 3M is headquartered and the lawsuit was filed, the plume of PFAS that was first detected in the 1960s as leaching from a few landfills now covers 100 square miles of groundwater and affects the drinking water of some 125,000 people in the Twin Cities area.
PFAS water contamination is now a national — and international — issue. Using data collected by the EPA, the Environmental Working Group calculated that more than 100 million Americans may be have some level of PFAS in their drinking water.
3M insists that “the presence of PFAS in blood does not mean that an individual’s health has been harmed and does not mean that there is a risk of adverse health effects. While the science behind PFASs is complex, the vast body of scientific evidence, which consists of decades of research conducted by independent third parties and 3M, does not show that PFOS or PFOA negatively impact human health at the levels typically found in the environment,” according to a statement the company provided in response to questions for this story.
But even as the company has continued to defend its chemicals, 3M’s legal problems have mounted along with the scientific evidence. States, counties, and individuals have filed dozens of suits against the company over the past two years, many of them based firefighting foam that contain PFAS chemicals.
Even if victory awaits those plaintiffs — as a form of it did in Minnesota — it’s not clear that justice will be done. The state will be using its $850 million settlement from 3M to address its massive water contamination problem. But it will be impossible to fully remove the chemicals from the groundwater or lakes or the Mississippi River, or any of the areas where it’s contaminated groundwater.
The people living in these places — and grappling with the realization that they have been ingesting these chemicals for years — have no recourse. “We don’t have some wonder medicine,” said Grandjean. “When I talk to residents about this, I convey the bad news. I’m a physician. I thought I was getting into medicine to solve problems. But all I can do is say, you’ve got this stuff in your body and it’s going to stay there for a long time and there’s nothing we can do about it.”
While there’s no way to go back and undo the environmental and health damage that’s already been done, criminal prosecutions could help prevent a similar situation in the future, according to Rena Steinzor, a professor at the University of Maryland School of Law and author of “Why Not Jail? Industrial Catastrophes, Corporate Malfeasance, and Government Inaction.”
“Criminal law allows us to go after people right now who withhold information they’re supposed to give the government,” said Steinzor. “If lying to the government is prosecuted as a crime with respect to the chemical industry — as it should be — things will get better quick.”
Whether such environmental misconduct might be taken more seriously in the future, 3M’s failure to act sooner on the danger of PFAS still has yet to be fully addressed. Geary Olsen, whose published paper omitted the finding detailed in his internal study, continues to work at 3M. 3M declined to make Olsen available for comment. John Giesy has stayed on as a professor at the University of Saskatchewan, even after it was revealed that he spun the science on PFAS after receiving more than $2 million in grants from the company. And Rich Purdy, who was so distraught by the company’s delays in releasing his research, recently prepared to testify for 3M, according to his wife.
Some researchers, like Frank Gilliland, who detailed the immune impacts of PFOA in his graduate thesis, left 3M “less idealistic” than when he began his work there, he told me in a recent interview. Reached at the University of Southern California, where he is now a professor of medicine, Gilliland said that PFOS and PFOA “should have come off the market sooner.” He said his current academic setting, in contrast to 3M, was a place of “free-ranging scientific inquiry.”
Philippe Grandjean, who has been a physician and environmental health researcher for more than 40 years, has also been affected by the realization of just how long he and others were kept in the dark about the harms of the chemicals. “I lost my confidence in the scientific literature,” said Grandjean. As he sees it, his whole profession has been stained by the experience. “We in my field have failed.”
oxFAQs™ for Perfluoroalkyls
This fact sheet answers the most frequently asked health questions (FAQs) about perfluoroalkyls. It is one in a series of summaries about hazardous substances and their health effects. It is important you understand this information because these substances may harm you. The effects of exposure to any hazardous substance depend on the dose, the duration, how you are exposed, personal traits and habits, and whether other chemicals are present. For more information, call the ATSDR Information Center at 1-800-232-4636.
What are perfluoroalkyls (PFAs)?
Perfluoroalkyls (PFAs) are a group of man-made chemicals that are not found naturally in the environment. Some chemicals that are in this group PFAs include:
- perfluorooctanoic acid (PFOA)
- perfluorooctane sulfonic acid (PFOS)
- perfluorononanoic acid (PFNA)
- perfluorohexane sulfonic acid (PFHxS)
- perfluordecanoic acid (PFDeA)
These PFAs were used to protect products like carpet and fabric, and as a coating for paper and cardboard packaging. They can also be found in some fire-fighting foams.
- The two PFAs made in the largest amounts in the United States were PFOA and PFOS. However, most companies have stopped making these two chemicals.
Where are PFAs found in the environment?
- PFAs can be found in air, soil, and water.
- They break down very slowly in air within days or weeks, but then fall to the ground where they can enter water or soil.
- PFAs do not break down in water or soil and may be carried over great distances by wind or rain.
How can I be exposed to PFAs?
- You may be exposed to PFAs in the air; in indoor dust, food, and water; and in some home products. However, the main sources of exposure to PFAs, such as PFOA and PFOS, are usually from eating food and drinking water that has these chemicals.
- Breast feeding infants may be exposed to PFAs since these chemicals have been found in breast milk. The benefits of breastfeeding are well known and almost always outweigh any potential risk, but you can talk with your doctor about concerns.
- Children can be exposed to PFAs in carpet since they are closer to the ground and play on the floor.
- Workers in facilities that make or use PFAs can be exposed to higher amounts of these chemicals and have higher levels in their blood.
- Some communities near factories that made or used PFOA and PFOS or in areas that used certain types of firefighting foam that spread into the environment may have been exposed to high levels of these substances in their drinking water.
How can PFAs affect my health?
A large number of studies have examined possible relationships between levels of PFAs in blood and harmful health effects in people. However, most of these studies analyzed only a small number of chemicals, and not all PFAs have the same health effects. Research suggests that high levels of certain PFAs may:
- increase cholesterol levels;
- decrease how well the body responds to vaccines;
- increase the risk of thyroid disease;
- decrease fertility in women;
- increase the risk of serious conditions like high blood pressure or pre-eclampsia in pregnant women;
- lower infant birth weights; however, the decrease in birth weight is small and may not affect the infant’s health.
At this time, scientists are still learning about the health effects of exposures to mixtures of PFAs.
One way to learn about whether PFAs will harm people is to conduct studies in lab animals. Most of these studies have tested doses of PFOA and PFOS that are higher than levels found in the environment.
- These animal studies have found that PFOA and PFOS can cause damage to the liver and the immune system.
- PFOA and PFOS have also caused birth defects, delayed development, and newborn deaths in lab animals.
Humans and animals react differently to PFAs, and not all effects observed in animals may occur in humans.
- Scientists have ways to estimate how the exposure and effects in animals compare to what they would be in humans.
- What they learn from this process helps them decide how to protect people from harm caused by chemical exposure.
Can PFAs cause cancer?
Studies do not clearly show whether PFAs cause cancer in people. People exposed to high levels may have increased risk of kidney cancer or testicular cancer. However, these studies are not consistent and may not have looked at other factors like smoking.
Studies in animals have shown that PFOA and PFOS can cause cancer in the liver, testes, pancreas, and thyroid. However, some scientists believe that humans may not develop the same cancers as animals.
The International Agency for Research on Cancer has classified PFOA as possibly carcinogenic (causing cancer) to humans, but it has not evaluated whether other PFAs may also cause cancer. The Department of Health and Human Services has not yet evaluated whether PFOA and other PFAs can cause cancer. The Environmental Protection (EPA) suggest that there is evidence that PFAs may have the potential to cause cancer.
How can I protect my family from exposure to PFAs?
- If you do not know about PFAs levels in your water, ask your local health department.
- If your drinking water contains PFAs above the EPA Lifetime Health Advisory, consider using an alternative or treated water source for any activity in which you might swallow water. Check for fish advisories for water bodies where you fish. Follow fish advisories that tell people to stop or limit eating fish from waters contaminated with PFAs or other compounds.
Can a medical test show whether I’ve been exposed to PFAs?
A blood test can measure individual PFAs compounds in your blood, but this is not a test routinely done in a doctor’s office.
If you have PFAs in your blood, you have been exposed to these chemicals and absorbed them into your body at some time. However, having PFAs in your blood does not necessarily mean that you will become ill from PFAs.
Has the federal government made recommendations to protect human health?
The EPA has set drinking water levels for PFOA and PFOS of 70 parts per trillion. You can learn more by visiting: https://www.epa.gov/ground-water-and-drinking-water/drinking-water-health-advisories-pfoa-and-pfos.
Where can I get more information?
For more information, call CDC-INFO at 1-800-232-4636.
You can also get information on ATSDR’s PFAS website: https://www.atsdr.cdc.gov/pfas/index.html.
You can also contact your community or state health or environmental quality department if you have any more questions or concerns.
Where can I get more information?
If you have questions or concerns, please contact your community or state health or environmental quality department or:
For more information, contact:
Agency for Toxic Substances and Disease Registry
Division of Toxicology and Human Health Sciences
1600 Clifton Road NE, Mailstop F-57
Atlanta, GA 30333
Phone: 1-800-CDC-INFO · 888-232-6348 (TTY)
Email: Contact CDC-INFO
ATSDR can also tell you the location of occupational and environmental health clinics. These clinics specialize in recognizing, evaluating,