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Archive for the ‘Superfund’ Category

The Lawyer Who Became DuPont’s Worst Nightmare

By NATHANIEL RICHJAN. 6, 2016

Just months before Rob Bilott made partner at Taft Stettinius & Hollister, he received a call on his direct line from a cattle farmer. The farmer, Wilbur Tennant of Parkersburg, W.Va., said that his cows were dying left and right. He believed that the DuPont chemical company, which until recently operated a site in Parkersburg that is more than 35 times the size of the Pentagon, was responsible. Tennant had tried to seek help locally, he said, but DuPont just about owned the entire town. He had been spurned not only by Parkersburg’s lawyers but also by its politicians, journalists, doctors and veterinarians. The farmer was angry and spoke in a heavy Appalachian accent. Bilott struggled to make sense of everything he was saying. He might have hung up had Tennant not blurted out the name of Bilott’s grandmother, Alma Holland White.

White had lived in Vienna, a northern suburb of Parkersburg, and as a child, Bilott often visited her in the summers. In 1973 she brought him to the cattle farm belonging to the Tennants’ neighbors, the Grahams, with whom White was friendly. Bilott spent the weekend riding horses, milking cows and watching Secretariat win the Triple Crown on TV. He was 7 years old. The visit to the Grahams’ farm was one of his happiest childhood memories.

When the Grahams heard in 1998 that Wilbur Tennant was looking for legal help, they remembered Bilott, White’s grandson, who had grown up to become an environmental lawyer. They did not understand, however, that Bilott was not the right kind of environmental lawyer. He did not represent plaintiffs or private citizens. Like the other 200 lawyers at Taft, a firm founded in 1885 and tied historically to the family of President William Howard Taft, Bilott worked almost exclusively for large corporate clients. His specialty was defending chemical companies. Several times, Bilott had even worked on cases with DuPont lawyers. Nevertheless, as a favor to his grandmother, he agreed to meet the farmer. ‘‘It just felt like the right thing to do,’’ he says today. ‘‘I felt a connection to those folks.’’

The connection was not obvious at their first meeting. About a week after his phone call, Tennant drove from Parkersburg with his wife to Taft’s headquarters in downtown Cincinnati. They hauled cardboard boxes containing videotapes, photographs and documents into the firm’s glassed-in reception area on the 18th floor, where they sat in gray midcentury-modern couches beneath an oil portrait of one of Taft’s founders. Tennant — burly and nearly six feet tall, wearing jeans, a plaid flannel shirt and a baseball cap — did not resemble a typical Taft client. ‘‘He didn’t show up at our offices looking like a bank vice president,’’ says Thomas Terp, a partner who was Bilott’s supervisor. ‘‘Let’s put it that way.’’

Terp joined Bilott for the meeting. Wilbur Tennant explained that he and his four siblings had run the cattle farm since their father abandoned them as children. They had seven cows then. Over the decades they steadily acquired land and cattle, until 200 cows roamed more than 600 hilly acres. The property would have been even larger had his brother Jim and Jim’s wife, Della, not sold 66 acres in the early ’80s to DuPont. The company wanted to use the plot for a landfill for waste from its factory near Parkersburg, called Washington Works, where Jim was employed as a laborer. Jim and Della did not want to sell, but Jim had been in poor health for years, mysterious ailments that doctors couldn’t diagnose, and they needed the money.

DuPont rechristened the plot Dry Run Landfill, named after the creek that ran through it. The same creek flowed down to a pasture where the Tennants grazed their cows. Not long after the sale, Wilbur told Bilott, the cattle began to act deranged. They had always been like pets to the Tennants. At the sight of a Tennant they would amble over, nuzzle and let themselves be milked. No longer. Now when they saw the farmers, they charged.

Wilbur fed a videotape into the VCR. The footage, shot on a camcorder, was grainy and intercut with static. Images jumped and repeated. The sound accelerated and slowed down. It had the quality of a horror movie. In the opening shot the camera pans across the creek. It takes in the surrounding forest, the white ash trees shedding their leaves and the rippling, shallow water, before pausing on what appears to be a snowbank at an elbow in the creek. The camera zooms in, revealing a mound of soapy froth.

‘‘I’ve taken two dead deer and two dead cattle off this ripple,’’ Tennant says in voice-over. ‘‘The blood run out of their noses and out their mouths. … They’re trying to cover this stuff up. But it’s not going to be covered up, because I’m going to bring it out in the open for people to see.’’

The video shows a large pipe running into the creek, discharging green water with bubbles on the surface. ‘‘This is what they expect a man’s cows to drink on his own property,’’ Wilbur says. ‘‘It’s about high time that someone in the state department of something-or-another got off their cans.’’

At one point, the video cuts to a skinny red cow standing in hay. Patches of its hair are missing, and its back is humped — a result, Wilbur speculates, of a kidney malfunction. Another blast of static is followed by a close-up of a dead black calf lying in the snow, its eye a brilliant, chemical blue. ‘‘One hundred fifty-three of these animals I’ve lost on this farm,’’ Wilbur says later in the video. ‘‘Every veterinarian that I’ve called in Parkersburg, they will not return my phone calls or they don’t want to get involved. Since they don’t want to get involved, I’ll have to dissect this thing myself. … I’m going to start at this head.’’

The video cuts to a calf’s bisected head. Close-ups follow of the calf’s blackened teeth (‘‘They say that’s due to high concentrations of fluoride in the water that they drink’’), its liver, heart, stomachs, kidneys and gall bladder. Each organ is sliced open, and Wilbur points out unusual discolorations — some dark, some green — and textures. ‘‘I don’t even like the looks of them,’’ he says. ‘‘It don’t look like anything I’ve been into before.’’

Bilott watched the video and looked at photographs for several hours. He saw cows with stringy tails, malformed hooves, giant lesions protruding from their hides and red, receded eyes; cows suffering constant diarrhea, slobbering white slime the consistency of toothpaste, staggering bowlegged like drunks. Tennant always zoomed in on his cows’ eyes. ‘‘This cow’s done a lot of suffering,’’ he would say, as a blinking eye filled the screen.

‘‘This is bad,’’ Bilott said to himself. ‘‘There’s something really bad going on here.’’

Bilott decided right away to take the Tennant case. It was, he says again, ‘‘the right thing to do.’’ Bilott might have had the practiced look of a corporate lawyer — soft-spoken, milk-complected, conservatively attired — but the job had not come naturally to him. He did not have a typical Taft résumé. He had not attended college or law school in the Ivy League. His father was a lieutenant colonel in the Air Force, and Bilott spent most of his childhood moving among air bases near Albany; Flint, Mich.; Newport Beach, Calif.; and Wiesbaden, West Germany. Bilott attended eight schools before graduating from Fairborn High, near Ohio’s Wright-Patterson Air Force Base. As a junior, he received a recruitment letter from a tiny liberal-arts school in Sarasota called the New College of Florida, which graded pass/fail and allowed students to design their own curriculums. Many of his friends there were idealistic, progressive — ideological misfits in Reagan’s America. He met with professors individually and came to value critical thinking. ‘‘I learned to question everything you read,’’ he said. ‘‘Don’t take anything at face value. Don’t care what other people say. I liked that philosophy.’’ Bilott studied political science and wrote his thesis about the rise and fall of Dayton. He hoped to become a city manager.

But his father, who late in life enrolled in law school, encouraged Bilott to do the same. Surprising his professors, he chose to attend law school at Ohio State, where his favorite course was environmental law. ‘‘It seemed like it would have real-world impact,’’ he said. ‘‘It was something you could do to make a difference.’’ When, after graduation, Taft made him an offer, his mentors and friends from New College were aghast. They didn’t understand how he could join a corporate firm. Bilott didn’t see it that way. He hadn’t really thought about the ethics of it, to be honest. ‘‘My family said that a big firm was where you’d get the most opportunities,’’ he said. ‘‘I knew nobody who had ever worked at a firm, nobody who knew anything about it. I just tried to get the best job I could. I don’t think I had any clue of what that involved.’’
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At Taft, he asked to join Thomas Terp’s environmental team. Ten years earlier, Congress passed the legislation known as Superfund, which financed the emergency cleanup of hazardous-waste dumps. Superfund was a lucrative development for firms like Taft, creating an entire subfield within environmental law, one that required a deep understanding of the new regulations in order to guide negotiations among municipal agencies and numerous private parties. Terp’s team at Taft was a leader in the field.

As an associate, Bilott was asked to determine which companies contributed which toxins and hazardous wastes in what quantities to which sites. He took depositions from plant employees, perused public records and organized huge amounts of historical data. He became an expert on the Environmental Protection Agency’s regulatory framework, the Safe Drinking Water Act, the Clean Air Act, the Toxic Substances Control Act. He mastered the chemistry of the pollutants, despite the fact that chemistry had been his worst subject in high school. ‘‘I learned how these companies work, how the laws work, how you defend these claims,’’ he said. He became the consummate insider.

Bilott was proud of the work he did. The main part of his job, as he understood it, was to help clients comply with the new regulations. Many of his clients, including Thiokol and Bee Chemical, disposed of hazardous waste long before the practice became so tightly regulated. He worked long hours and knew few people in Cincinnati. A colleague on Taft’s environmental team, observing that he had little time for a social life, introduced him to a childhood friend named Sarah Barlage. She was a lawyer, too, at another downtown Cincinnati firm, where she de­fended corporations against worker’s-compensation claims. Bilott joined the two friends for lunch. Sarah doesn’t remember him speaking. ‘‘My first impression was that he was not like other guys,’’ she says. ‘‘I’m pretty chatty. He’s much quieter. We complemented each other.’’

They married in 1996. The first of their three sons was born two years later. He felt secure enough at Taft for Barlage to quit her job and raise their children full-time. Terp, his supervisor, recalls him as ‘‘a real standout lawyer: incredibly bright, energetic, tenacious and very, very thorough.’’ He was a model Taft lawyer. Then Wilbur Tennant came along.

The Tennant case put Taft in a highly unusual position. The law firm was in the business of representing chemical corporations, not suing them. The prospect of taking on DuPont ‘‘did cause us pause,’’ Terp concedes. ‘‘But it was not a terribly difficult decision for us. I’m a firm believer that our work on the plaintiff’s side makes us better defense lawyers.’’

Bilott sought help with the Tennant case from a West Virginia lawyer named Larry Winter. For many years, Winter was a partner at Spilman, Thomas & Battle — one of the firms that represented DuPont in West Virginia — though he had left Spilman to start a practice specializing in personal-injury cases. He was amazed that Bilott would sue DuPont while remaining at Taft.

‘‘His taking on the Tennant case,’’ Winter says, ‘‘given the type of practice Taft had, I found to be inconceivable.’’

Bilott, for his part, is reluctant to discuss his motivations for taking the case. The closest he came to elaborating was after being asked whether, having set out ‘‘to make a difference’’ in the world, he had any misgivings about the path his career had taken.

‘‘There was a reason why I was interested in helping out the Tennants,’’ he said after a pause. ‘‘It was a great opportunity to use my background for people who really needed it.’’

Bilott filed a federal suit against DuPont in the summer of 1999 in the Southern District of West Virginia. In response, DuPont’s in-house lawyer, Bernard Reilly, informed him that DuPont and the E.P.A. would commission a study of the property, conducted by three veterinarians chosen by DuPont and three chosen by the E.P.A. Their report did not find DuPont responsible for the cattle’s health problems. The culprit, instead, was poor husbandry: ‘‘poor nutrition, inadequate veterinary care and lack of fly control.’’ In other words, the Tennants didn’t know how to raise cattle; if the cows were dying, it was their own fault.

This did not sit well with the Tennants, who began to suffer the consequences of antagonizing Parkersburg’s main employer. Lifelong friends ignored the Tennants on the streets of Parkersburg and walked out of restaurants when they entered. ‘‘I’m not allowed to talk to you,’’ they said, when confronted. Four different times, the Tennants changed churches.

Wilbur called the office nearly every day, but Bilott had little to tell him. He was doing for the Tennants what he would have done for any of his corporate clients — pulling permits, studying land deeds and requesting from DuPont all documentation related to Dry Run Landfill — but he could find no evidence that explained what was happening to the cattle. ‘‘We were getting frustrated,’’ Bilott said. ‘‘I couldn’t blame the Tennants for getting angry.’’

With the trial looming, Bilott stumbled upon a letter DuPont had sent to the E.P.A. that mentioned a substance at the landfill with a cryptic name: ‘‘PFOA.’’ In all his years working with chemical companies, Bilott had never heard of PFOA. It did not appear on any list of regulated materials, nor could he find it in Taft’s in-house library. The chemistry expert that he had retained for the case did, however, vaguely recall an article in a trade journal about a similar-sounding compound: PFOS, a soaplike agent used by the technology conglomerate 3M in the fabrication of Scotchgard.

Bilott hunted through his files for other references to PFOA, which he learned was short for perfluorooctanoic acid. But there was nothing. He asked DuPont to share all documentation related to the substance; DuPont refused. In the fall of 2000, Bilott requested a court order to force them. Against DuPont’s protests, the order was granted. Dozens of boxes containing thousands of unorganized documents began to arrive at Taft’s headquarters: private internal correspondence, medical and health reports and confidential studies conducted by DuPont scientists. There were more than 110,000 pages in all, some half a century old. Bilott spent the next few months on the floor of his office, poring over the documents and arranging them in chronological order. He stopped answering his office phone. When people called his secretary, she explained that he was in the office but had not been able to reach the phone in time, because he was trapped on all sides by boxes.

‘‘I started seeing a story,’’ Bilott said. ‘‘I may have been the first one to actually go through them all. It became apparent what was going on: They had known for a long time that this stuff was bad.’’

Bilott is given to understatement. (‘‘To say that Rob Bilott is understated,’’ his colleague Edison Hill says, ‘‘is an understatement.’’) The story that Bilott began to see, cross-legged on his office floor, was astounding in its breadth, specificity and sheer brazenness. ‘‘I was shocked,’’ he said. That was another understatement. Bilott could not believe the scale of incriminating material that DuPont had sent him. The company appeared not to realize what it had handed over. ‘‘It was one of those things where you can’t believe you’re reading what you’re reading,’’ he said. ‘‘That it’s actually been put in writing. It was the kind of stuff you always heard about happening but you never thought you’d see written down.’’

The story began in 1951, when DuPont started purchasing PFOA (which the company refers to as C8) from 3M for use in the manufacturing of Teflon. 3M invented PFOA just four years earlier; it was used to keep coatings like Teflon from clumping during production. Though PFOA was not classified by the government as a hazardous substance, 3M sent DuPont recommendations on how to dispose of it. It was to be incinerated or sent to chemical-waste facilities. DuPont’s own instructions specified that it was not to be flushed into surface water or sewers. But over the decades that followed, DuPont pumped hundreds of thousands of pounds of PFOA powder through the outfall pipes of the Parkersburg facility into the Ohio River. The company dumped 7,100 tons of PFOA-laced sludge into ‘‘digestion ponds’’: open, unlined pits on the Washington Works property, from which the chemical could seep straight into the ground. PFOA entered the local water table, which supplied drinking water to the communities of Parkersburg, Vienna, Little Hocking and Lubeck — more than 100,000 people in all.

Bilott learned from the documents that 3M and DuPont had been conducting secret medical studies on PFOA for more than four decades. In 1961, DuPont researchers found that the chemical could increase the size of the liver in rats and rabbits. A year later, they replicated these results in studies with dogs. PFOA’s peculiar chemical structure made it uncannily resistant to degradation. It also bound to plasma proteins in the blood, circulating through each organ in the body. In the 1970s, DuPont discovered that there were high concentrations of PFOA in the blood of factory workers at Washington Works. They did not tell their workers this. In 1981, 3M — which continued to serve as the supplier of PFOA to DuPont and other corporations — found that ingestion of the substance caused birth defects in rats. After 3M shared this information, DuPont tested the children of pregnant employees in their Teflon division. Of seven births, two had eye defects. DuPont did not make this information public.

In 1984, DuPont became aware that dust vented from factory chimneys settled well beyond the property line and, more disturbing, that PFOA was present in the local water supply. DuPont declined to disclose this finding. In 1991, DuPont scientists determined an internal safety limit for PFOA concentration in drinking water: one part per billion. The same year, DuPont found that water in one local district contained PFOA levels at three times that figure. Despite internal debate, it declined to make the information public.

(In a statement, DuPont claimed that it did volunteer health information about PFOA to the E.P.A. during those decades. When asked for evidence, it forwarded two letters written to West Virginian government agencies from 1982 and 1992, both of which cited internal studies that called into question links between PFOA exposure and human health problems.)

By the ’90s, Bilott discovered, DuPont understood that PFOA caused cancerous testicular, pancreatic and liver tumors in lab animals. One laboratory study suggested possible DNA damage from PFOA exposure, and a study of workers linked exposure with prostate cancer. DuPont at last hastened to develop an alternative to PFOA. An interoffice memo sent in 1993 announced that ‘‘for the first time, we have a viable candidate’’ that appeared to be less toxic and stayed in the body for a much shorter duration of time. Discussions were held at DuPont’s corporate headquarters to discuss switching to the new compound. DuPont decided against it. The risk was too great: Products manufactured with PFOA were an important part of DuPont’s business, worth $1 billion in annual profit.

But the crucial discovery for the Tennant case was this: By the late 1980s, as DuPont became increasingly concerned about the health effects of PFOA waste, it decided it needed to find a landfill for the toxic sludge dumped on company property. Fortunately they had recently bought 66 acres from a low-level employee at the Washington Works facility that would do perfectly.

By 1990, DuPont had dumped 7,100 tons of PFOA sludge into Dry Run Landfill. DuPont’s scientists understood that the landfill drained into the Tennants’ remaining property, and they tested the water in Dry Run Creek. It contained an extraordinarily high concentration of PFOA. DuPont did not tell this to the Tennants at the time, nor did it disclose the fact in the cattle report that it commissioned for the Tennant case a decade later — the report that blamed poor husbandry for the deaths of their cows. Bilott had what he needed.

In August 2000, Bilott called DuPont’s lawyer, Bernard Reilly, and explained that he knew what was going on. It was a brief conversation.

The Tennants settled. The firm would receive its contingency fee. The whole business might have ended right there. But Bilott was not satisfied.

‘‘I was irritated,’’ he says.

DuPont was nothing like the corporations he had represented at Taft in the Superfund cases. ‘‘This was a completely different scenario. DuPont had for decades been actively trying to conceal their actions. They knew this stuff was harmful, and they put it in the water anyway. These were bad facts.’’ He had seen what the PFOA-tainted drinking water had done to cattle. What was it doing to the tens of thousands of people in the areas around Parkersburg who drank it daily from their taps? What did the insides of their heads look like? Were their internal organs green?

Bilott spent the following months drafting a public brief against DuPont. It was 972 pages long, including 136 attached exhibits. His colleagues call it ‘‘Rob’s Famous Letter.’’ ‘‘We have confirmed that the chemicals and pollutants released into the environment by DuPont at its Dry Run Landfill and other nearby DuPont-owned facilities may pose an imminent and substantial threat to health or the environment,’’ Bilott wrote. He demanded immediate action to regulate PFOA and provide clean water to those living near the factory. On March 6, 2001, he sent the letter to the director of every relevant regulatory authority, including Christie Whitman, administrator of the E.P.A., and the United States attorney general, John Ashcroft.

DuPont reacted quickly, requesting a gag order to block Bilott from providing the information he had discovered in the Tennant case to the government. A federal court denied it. Bilott sent his entire case file to the E.P.A.

‘‘DuPont freaked out when they realized that this guy was onto them,’’ says Ned McWilliams, a young trial lawyer who later joined Bilott’s legal team. ‘‘For a corporation to seek a gag order to prevent somebody from speaking to the E.P.A. is an extraordinary remedy. You could realize how bad that looks. They must have known that there was a small chance of winning. But they were so afraid that they were willing to roll the dice.’’

With the Famous Letter, Bilott crossed a line. Though nominally representing the Tennants — their settlement had yet to be concluded — Bilott spoke for the public, claiming extensive fraud and wrongdoing. He had become a threat not merely to DuPont but also to, in the words of one internal memo, ‘‘the entire fluoropolymers industry’’ — an industry responsible for the high-performance plastics used in many modern devices, including kitchen products, computer cables, implantable medical devices and bearings and seals used in cars and airplanes. PFOA was only one of more than 60,000 synthetic chemicals that companies produced and released into the world without regulatory oversight.

‘‘Rob’s letter lifted the curtain on a whole new theater,’’ says Harry Deitzler, a plaintiff’s lawyer in West Virginia who works with Bilott. ‘‘Before that letter, corporations could rely upon the public misperception that if a chemical was dangerous, it was regulated.’’ Under the 1976 Toxic Sub­stances Control Act, the E.P.A. can test chemicals only when it has been provided evidence of harm. This arrangement, which largely allows chemical companies to regulate themselves, is the reason that the E.P.A. has restricted only five chemicals, out of tens of thousands on the market, in the last 40 years.

It was especially damning to see these allegations against DuPont under the letterhead of one of the nation’s most prestigious corporate defense firms. ‘‘You can imagine what some of the other companies that Taft was representing — a Dow Chemical — might have thought of a Taft lawyer taking on DuPont,’’ Larry Winter says. ‘‘There was a threat that the firm would suffer financially.’’ When I asked Thomas Terp about Taft’s reaction to the Famous Letter, he replied, not quite convincingly, that he didn’t recall one. ‘‘Our partners,’’ he said, ‘‘are proud of the work that he has done.’’

Bilott, however, worried that corporations doing business with Taft might see things differently. ‘‘I’m not stupid, and the people around me aren’t stupid,’’ he said. ‘‘You can’t ignore the economic realities of the ways that business is run and the way clients think. I perceived that there were some ‘What the hell are you doing?’ responses.’’

The letter led, three years later, in 2006, to DuPont’s reaching a $16.5 million settlement with the E.P.A., which had accused the company of concealing its knowledge of PFOA’s toxicity and presence in the environment in violation of the Toxic Substances Control Act. (DuPont was not required to admit liability.) At the time, it was the largest civil administrative penalty the E.P.A. had obtained in its history, a statement that sounds more impressive than it is. The fine represented less than 2 percent of the profits earned by DuPont on PFOA that year.

Bilott never represented a corporate client again.

The obvious next step was to file a class-action lawsuit against DuPont on behalf of everyone whose water was tainted by PFOA. In all ways but one, Bilott himself was in the ideal position to file such a suit. He understood PFOA’s history as well as anyone inside DuPont did. He had the technical and regulatory expertise, as he had proved in the Tennant case. The only part that didn’t make sense was his firm: No Taft lawyer, to anyone’s recollection, had ever filed a class-action lawsuit.

It was one thing to pursue a sentimental case on behalf of a few West Virginia cattle farmers and even write a public letter to the E.P.A. But an industry-threatening class-action suit against one of the world’s largest chemical corporations was different. It might establish a precedent for suing corporations over unregulated sub­stances and imperil Taft’s bottom line. This point was made to Terp by Bernard Reilly, DuPont’s in-house lawyer, according to accounts from Bilott’s plaintiff’s-lawyer colleagues; they say Reilly called to demand that Bilott back off the case. (Terp confirms that Reilly called him but will not disclose the content of the call; Bilott and Reilly decline to speak about it, citing continuing litigation.) Given what Bilott had documented in his Famous Letter, Taft stood by its partner.

A lead plaintiff soon presented himself. Joseph Kiger, a night-school teacher in Parkersburg, called Bilott to ask for help. About nine months earlier, he received a peculiar note from the Little Hocking water district. It arrived on Halloween day, enclosed in the monthly water bill. The note explained that an unregulated chemical named PFOA had been detected in the drinking water in ‘‘low concentrations,’’ but that it was not a health risk. Kiger had underlined statements that he found particularly baffling, like: ‘‘DuPont reports that it has toxicological and epidemiological data to support confidence that exposure guidelines established by DuPont are protective of human health.’’ The term ‘‘support confidence’’ seemed bizarre, as did ‘‘protective of human health,’’ not to mention the claim that DuPont’s own data supported its confidence in its own guidelines.

Still, Kiger might have forgotten about it had his wife, Darlene, not already spent much of her adulthood thinking about PFOA. Darlene’s first husband had been a chemist in DuPont’s PFOA lab. (Darlene asked that he not be named so that he wouldn’t be involved in the local politics around the case.) ‘‘When you worked at DuPont in this town,’’ Darlene says today, ‘‘you could have everything you wanted.’’ DuPont paid for his education, it secured him a mortgage and it paid him a generous salary. DuPont even gave him a free supply of PFOA, which, Darlene says, she used as soap in the family’s dishwasher and to clean the car. Sometimes her husband came home from work sick — fever, nausea, diarrhea, vomiting — after working in one of the PFOA storage tanks. It was a common occurrence at Washington Works. Darlene says the men at the plant called it ‘‘Teflon flu.’’

In 1976, after Darlene gave birth to their second child, her husband told her that he was not allowed to bring his work clothes home anymore. DuPont, he said, had found out that PFOA was causing health problems for women and birth defects in children. Darlene would remember this six years later when, at 36, she had to have an emergency hysterectomy and again eight years later, when she had a second surgery. When the strange letter from the water district arrived, Darlene says, ‘‘I kept thinking back to his clothing, to my hysterectomy. I asked myself, what does DuPont have to do with our drinking water?’’

Joe called the West Virginia Department of Natural Resources (‘‘They treated me like I had the plague’’), the Parkersburg office of the state’s Department of Environmental Protection (‘‘nothing to worry about’’), the water division (‘‘I got shut down’’), the local health department (‘‘just plain rude’’), even DuPont (‘‘I was fed the biggest line of [expletive] anybody could have been fed’’), before a scientist in the regional E.P.A. office finally took his call.

‘‘Good God, Joe,’’ the scientist said. ‘‘What the hell is that stuff doing in your water?’’ He sent Kiger information about the Tennant lawsuit. On the court papers Kiger kept seeing the same name: Robert Bilott, of Taft Stettinius & Hollister, in Cincinnati.

Bilott had anticipated suing on behalf of the one or two water districts closest to Washington Works. But tests revealed that six districts, as well as dozens of private wells, were tainted with levels of PFOA higher than DuPont’s own internal safety standard. In Lubeck, the Kigers’ district, the water tested positive for PFOA at seven times the limit. All told, 70,000 people were drinking poisoned water. Some had been doing so for decades.

But Bilott faced a vexing legal problem. PFOA was not a regulated substance. It appeared on no federal or state list of contaminants. How could Bilott claim that 70,000 people had been poisoned if the government didn’t recognize PFOA as a toxin — if PFOA, legally speaking, was no different than water itself? In 2001, it could not even be proved that exposure to PFOA in public drinking water caused health problems. There was scant information available about its impact on large populations. How could the class prove it had been harmed by PFOA when the health effects were largely unknown?

The best metric Bilott had to judge a safe exposure level was DuPont’s own internal limit of one part per billion. But when DuPont learned that Bilott was preparing a new lawsuit, it announced that it would re-evaluate that figure. As in the Tennant case, DuPont formed a team composed of its own scientists and scientists from the West Virginia Department of Environmental Protection. It announced a new threshold: 150 parts per billion.

Bilott found the figure ‘‘mind-blowing.’’ The toxicologists he hired had settled upon a safety limit of 0.2 parts per billion. But West Virginia endorsed the new standard. Within two years, three lawyers regularly used by DuPont were hired by the state D.E.P. in leadership positions. One of them was placed in charge of the entire agency. ‘‘The way that transpired was just amazing to me,’’ Bilott says. ‘‘I suppose it wasn’t so amazing to my fellow counsel in West Virginia who know the system there. But it was to me.’’ The same DuPont lawyers tasked with writing the safety limit, Bilott said, had become the government regulators responsible for enforcing that limit.

Bilott devised a new legal strategy. A year earlier, West Virginia had become one of the first states to recognize what is called, in tort law, a medical-monitoring claim. A plaintiff needs to prove only that he or she has been exposed to a toxin. If the plaintiff wins, the defendant is required to fund regular medical tests. In these cases, should a plaintiff later become ill, he or she can sue retroactively for damages. For this reason, Bilott filed the class-action suit in August 2001 in state court, even though four of the six affected water districts lay across the Ohio border.

Meanwhile the E.P.A., drawing from Bilott’s research, began its own investigation into the toxicity of PFOA. In 2002, the agency released its initial findings: PFOA might pose human health risks not only to those drinking tainted water, but also to the general public — anyone, for instance, who cooked with Teflon pans. The E.P.A. was particularly alarmed to learn that PFOA had been detected in American blood banks, something 3M and DuPont had known as early as 1976. By 2003 the average concentration of PFOA in the blood of an adult American was four to five parts per billion. In 2000, 3M ceased production of PFOA. DuPont, rather than use an alternative compound, built a new factory in Fayetteville, N.C., to manufacture the substance for its own use.

Bilott’s strategy appeared to have worked. In September 2004, DuPont decided to settle the class-action suit. It agreed to install filtration plants in the six affected water districts if they wanted them and pay a cash award of $70 million. It would fund a scientific study to determine whether there was a ‘‘probable link’’ — a term that delicately avoided any declaration of causation — between PFOA and any diseases. If such links existed, DuPont would pay for medical monitoring of the affected group in perpetuity. Until the scientific study came back with its results, class members were forbidden from filing personal-injury suits against DuPont.

A reasonable expectation, at this point, was that the lawyers would move on. ‘‘In any other class action you’ve ever read about,’’ Deitzler says, ‘‘you get your 10 bucks in the mail, the lawyers get paid and the lawsuit goes away. That’s what we were supposed to do.’’ For three years, Bilott had worked for nothing, costing his firm a fortune. But now Taft received a windfall: Bilott and his team of West Virginian plaintiff lawyers received $21.7 million in fees from the settlement. ‘‘I think they were thinking, This guy did O.K.,’’ Deitzler says. ‘‘I wouldn’t be surprised if he got a raise.’’

Not only had Taft recouped its losses, but DuPont was providing clean water to the communities named in the suit. Bilott had every reason to walk away.

He didn’t.

‘‘There was a gap in the data,’’ Bilott says. The company’s internal health studies, as damning as they were, were limited to factory employees. DuPont could argue — and had argued — that even if PFOA caused medical problems, it was only because factory workers had been exposed at exponentially higher levels than neighbors who drank tainted water. The gap allowed DuPont to claim that it had done nothing wrong.

Bilott represented 70,000 people who had been drinking PFOA-laced drinking water for decades. What if the settlement money could be used to test them? ‘‘Class members were concerned about three things,’’ Winter says. ‘‘One: Do I have C8 in my blood? Two: If I do, is it harmful? Three: If it’s harmful, what are the effects?’’ Bilott and his colleagues realized they could answer all three questions, if only they could test their clients. Now, they realized, there was a way to do so. After the settlement, the legal team pushed to make receipt of the cash award contingent on a full medical examination. The class voted in favor of this approach, and within months, nearly 70,000 West Virginians were trading their blood for a $400 check.

The team of epidemiologists was flooded with medical data, and there was nothing DuPont could do to stop it. In fact, it was another term of the settlement that DuPont would fund the research without limitation. The scientists, freed from the restraints of academic budgets and grants, had hit the epidemiological jackpot: an entire population’s personal data and infinite resources available to study them. The scientists designed 12 studies, including one that, using sophisticated environmental modeling technology, determined exactly how much PFOA each individual class member had ingested.

It was assured that the panel would return convincing results. But Bilott could not predict what those results would be. If no correlation was found between PFOA and illness, Bilott’s clients would be barred under the terms of the agreement from filing any personal-injury cases. Because of the sheer quantity of data provided by the community health study and the un­limited budget — it ultimately cost DuPont $33 million — the panel took longer than ex­pected to perform its analysis. Two years passed without any findings. Bilott waited. A third year passed. Then a fourth, a fifth, a sixth. Still the panel was quiet. Bilott waited.

It was not a peaceful wait. The pressure on Bilott at Taft had built since he initiated the class-action suit in 2001. The legal fees had granted him a reprieve, but as the years passed without resolution, and Bilott continued to spend the firm’s money and was unable to attract new clients, he found himself in an awkward position.

‘‘This case,’’ Winter says, ‘‘regardless of how hugely successful it ends up, will never in the Taft firm’s mind replace what they’ve lost in the way of legal business over the years.’’

The longer it took for the science panel to conduct its research, the more expensive the case became. Taft continued to pay consultants to interpret the new findings and relay them to the epidemiologists. Bilott counseled class members in West Virginia and Ohio and traveled frequently to Washington to attend meetings at the E.P.A., which was deciding whether to issue advisories about PFOA. ‘‘We were incurring a lot of expenses,’’ Bilott says. ‘‘If the scientific panel found no link with diseases, we’d have to eat it all.’’

Clients called Bilott to say that they had received diagnoses of cancer or that a family member had died. They wanted to know why it was taking so long. When would they get relief? Among those who called was Jim Tennant. Wilbur, who had cancer, had died of a heart attack. Two years later, Wilbur’s wife died of cancer. Bilott was tormented by ‘‘the thought that we still hadn’t been able to hold this company responsible for what they did in time for those people to see it.’’

Taft did not waver in its support of the case, but the strain began to show. ‘‘It was stressful,’’ Sarah Barlage, Bilott’s wife, says. ‘‘He was exasperated that it was lasting a long time. But his heels were so dug in. He’s extremely stubborn. Every day that went by with no movement gave him more drive to see it through. But in the back of our minds, we knew that there are cases that go on forever.’’

His colleagues on the case detected a change in Bilott. ‘‘I had the impression that it was extremely tough on him,’’ Winter says. ‘‘Rob had a young family, kids growing up, and he was under pressure from his firm. Rob is a private person. He didn’t complain. But he showed signs of being under enormous stress.’’

In 2010, Bilott began suffering strange attacks: His vision would blur, he couldn’t put on his socks, his arms felt numb. His doctors didn’t know what was happening. The attacks recurred periodically, bringing blurry vision, slurred speech and difficulty moving one side of his body. They struck suddenly, without warning, and their effects lasted days. The doctors asked whether he was under heightened stress at work. ‘‘Nothing different than normal,’’ Bilott told them. ‘‘Nothing it hadn’t been for years.’’

The doctors ultimately hit upon an effective medication. The episodes ceased and their symptoms, apart from an occasional tic, are under control, but he still doesn’t have a diagnosis.

‘‘It was stressful,’’ Bilott says, ‘‘not to know what the heck was going on.’’

In December 2011, after seven years, the scientists began to release their findings: there was a ‘‘probable link’’ between PFOA and kidney cancer, testicular cancer, thyroid disease, high cholesterol, pre-eclampsia and ulcerative colitis.

‘‘There was relief,’’ Bilott says, understated nearly to the point of self-effacement. ‘‘We were able to deliver what we had promised to these folks seven years earlier. Especially since, for all those years, DuPont had been saying that we were lying, trying to scare and mislead people. Now we had a scientific answer.’’

As of October, 3,535 plaintiffs have filed personal-injury lawsuits against DuPont. The first member of this group to go to trial was a kidney-cancer survivor named Carla Bartlett. In October, Bartlett was awarded $1.6 million. DuPont plans to appeal. This may have ramifications well beyond Bartlett’s case: Hers is one of five ‘‘bellwether’’ cases that will be tried over the course of this year. After that, DuPont may choose to settle with every afflicted class member, using the outcome of the bellwether cases to determine settlement awards. Or DuPont can fight each suit individually, a tactic that tobacco companies have used to fight personal-injury lawsuits. At the rate of four trials a year, DuPont would continue to fight PFOA cases until the year 2890.

DuPont’s continuing refusal to accept responsibility is maddening to Bilott. ‘‘To think that you’ve negotiated in good faith a deal that everybody has abided by and worked on for seven years, you reach a point where certain things were to be resolved but then remain contested,’’ he says. ‘‘I think about the clients who have been waiting for this, many of whom are sick or have died while waiting. It’s infuriating.’’

As part of its agreement with the E.P.A., DuPont ceased production and use of PFOA in 2013. The five other companies in the world that produce PFOA are also phasing out production. DuPont, which is currently negotiating a merger with Dow Chemical, last year severed its chemical businesses: They have been spun off into a new corporation called Chemours. The new company has replaced PFOA with similar fluorine-based compounds designed to biodegrade more quickly — the alternative considered and then discarded by DuPont more than 20 years ago. Like PFOA, these new substances have not come under any regulation from the E.P.A. When asked about the safety of the new chemicals, Chemours replied in a statement: ‘‘A significant body of data demonstrates that these alternative chemistries can be used safely.’’

Last May, 200 scientists from a variety of disciplines signed the Madrid Statement, which expresses concern about the production of all fluorochemicals, or PFASs, including those that have replaced PFOA. PFOA and its replacements are suspected to belong to a large class of artificial compounds called endocrine-disrupting chemicals; these compounds, which include chemicals used in the production of pesticides, plastics and gasoline, interfere with human reproduction and metabolism and cause cancer, thyroid problems and nervous-system disorders. In the last five years, however, a new wave of endocrinology research has found that even extremely low doses of such chemicals can create significant health problems. Among the Madrid scientists’ recommendations: ‘‘Enact legislation to require only essential uses of PFASs’’ and ‘‘Whenever possible, avoid products containing, or manufactured using, PFASs. These include many products that are stain-resistant, waterproof or nonstick.’’

When asked about the Madrid Statement, Dan Turner, DuPont’s head of global media relations, wrote in an email: ‘‘DuPont does not believe the Madrid Statement reflects a true consideration of the available data on alternatives to long-chain perfluorochemicals, such as PFOA. DuPont worked for more than a decade, with oversight from regulators, to introduce its alternatives. Extensive data has been developed, demonstrating that these alternatives are much more rapidly eliminated from the body than PFOA, and have improved health safety profiles. We are confident that these alternative chemistries can be used safely — they are well characterized, and the data has been used to register them with environmental agencies around the world.’’

Every year Rob Bilott writes a letter to the E.P.A. and the West Virginia D.E.P., urging the regulation of PFOA in drinking water. In 2009, the E.P.A. set a ‘‘provisional’’ limit of 0.4 parts per billion for short-term exposure, but has never finalized that figure. This means that local water districts are under no obligation to tell customers whether PFOA is in their water. In response to Bilott’s most recent letter, the E.P.A. claimed that it would announce a ‘‘lifetime health advisory level for PFOA’’ by ‘‘early 2016.’’

This advisory level, if indeed announced, might be a source of comfort to future generations. But if you are a sentient being reading this article in 2016, you already have PFOA in your blood. It is in your parents’ blood, your children’s blood, your lover’s blood. How did it get there? Through the air, through your diet, through your use of nonstick cookware, through your umbilical cord. Or you might have drunk tainted water. The Environmental Working Group has found manufactured fluoro­chemicals present in 94 water districts across 27 states (see sidebar beginning on Page 38). Residents of Seattle; Wilmington, Del.; Colorado Springs; and Nassau County on Long Island are among those whose water has a higher concentration of fluorochemicals than that in some of the districts included in Rob Bilott’s class-action suit. The drinking water in Parkersburg itself, whose water district was not included in the original class-action suit and has failed to compel DuPont to pay for a filtration system, is currently tainted with high levels of PFOA. Most residents appear not to know this.

Where scientists have tested for the presence of PFOA in the world, they have found it. PFOA is in the blood or vital organs of Atlantic salmon, swordfish, striped mullet, gray seals, common cormorants, Alaskan polar bears, brown pelicans, sea turtles, sea eagles, Midwestern bald eagles, California sea lions and Laysan albatrosses on Sand Island, a wildlife refuge on Midway Atoll, in the middle of the North Pacific Ocean, about halfway between North America and Asia.

‘‘We see a situation,’’ Joe Kiger says, ‘‘that has gone from Washington Works, to statewide, to the United States, and now it’s everywhere, it’s global. We’ve taken the cap off something here. But it’s just not DuPont. Good God. There are 60,000 unregulated chemicals out there right now. We have no idea what we’re taking.’’

Bilott doesn’t regret fighting DuPont for the last 16 years, nor for letting PFOA consume his career. But he is still angry. ‘‘The thought that DuPont could get away with this for this long,’’ Bilott says, his tone landing halfway between wonder and rage, ‘‘that they could keep making a profit off it, then get the agreement of the governmental agencies to slowly phase it out, only to replace it with an alternative with unknown human effects — we told the agencies about this in 2001, and they’ve essentially done nothing. That’s 14 years of this stuff continuing to be used, continuing to be in the drinking water all over the country. DuPont just quietly switches over to the next substance. And in the meantime, they fight everyone who has been injured by it.’’

Bilott is currently prosecuting Wolf v. DuPont, the second of the personal-injury cases filed by the members of his class. The plaintiff, John M. Wolf of Parkersburg, claims that PFOA in his drinking water caused him to develop ulcerative colitis. That trial begins in March. When it concludes, there will be 3,533 cases left to try.

Further Reading

For more about DuPont’s FPOA pollution, see ‘‘The Teflon Toxin’’ by Sharon Lerner (The Intercept, Aug. 17, 2015) and ‘‘Welcome to Beautiful Parkersburg, West Virginia’’ by Mariah Blake (The Huffington Post, Aug. 27, 2015).

Nathaniel Rich is a contributing writer for the magazine and the author of ‘‘Odds Against Tomorrow.’’ He lives in New Orleans and is a frequent contributor to The New York Review of Books and The Atlantic.

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The Lake Effect by Nancy Nichols

By the time the PCB problem was isolated in January 1976, the Illinois Environmental Protection Agency believed that Outboard Marine was delivering approximately nine to ten tons of PCBs to the harbor each day. The PCB content of the sludge at the bottom of the harbor ranged from 240,000 to 500,000 parts per million depending on when and where the sample was taken. That means that either one in two or one in four grains of sand or silt at the bottom of the harbor was not actually sand or silt, but was a PCB instead. page 43

Waukegan would take its turn on the national stage two years later, in 1984,when a U.S. Environmental Protection official, Rita Lavelle, was accused of secretly meeting with lakefront polluters in an effort to strike a cleanup deal that heavily favored industry… In the aftermath of the scandal, the full extent of Waukegan’s chemical contamination was revealed… Eventually, three separate Superfund sites, named after the 1980 federal legislation that allocated funds to clean them up, were designated in Waukegan. Two of the sites are adjacent to the lake… In addition, more than a dozen other sites form what federal and state regulators call an expanded study area, which stretches along the lakefront from one end of town to the other. These smaller sites contain the waste products from a tannery, a steel company, a paint factory, a pharmaceutical company, and a scrap yard. Together these sites contain not just PCBs, but an alphabet soup of pollutants. “Just about every chemical we know to be dangerous to human health is in one of those sites,” Says Margaret Quinn, a professor at the University of Massachusetts, Lowell, who specializes in human exposure assessment. In addition to PCBs, these chemicals include benzene and other volatile organic compounds, arsenic. lead, asbestos, polycyclic aromatic hydrocarbons (PAHs), dioxins, vinyl chloride, and ammonia. Various chemicals among these have been associated with reproductive diseases, learning and attention deficits in children, birth defects, immune system deficiencies, and some forms of cancer.

Was there a relationship between my sister’s cancer and the toxins of our childhood? My sister certainly thought so. And many other people have suspected, often correctly, that elements in their environment have had an effect on their health. Yet because of the long time it takes for a cancer to develop and because of relative mobility of our lives today, it can be challenging to establish a casual link between a disease and its origin.

pages 5 -6

“Ovaries are approximately three centimeters long by one and one-half centimeters wide by one centimeter thick,” writes Ethel Sloan in, “The Biology of Women.”… Whichever edition you consult will tell you that the ovary is about the size of an almond and that it produces the female hormone estrogen. During the monthly menstrual cycle, each ovary forces an egg through a wall of tissue and afterward repairs that rupture in a process called ovulation. “The ovary is no beauty,” writes Natalie Angier in “Woman: An Intimate Geography, “It is scarred and pitted, for each cycle of ovulation leaves behind a blemish where an egg follicle has been emptied of its contents. The older the woman, the more scarred her ovaries will be. It is this continual bursting and repairing–part and parcel of the ovarian life cycle–that makes the ovary vulnerable to cancer.

Scientists have long theorized that as cells multiply each month to repair the breach in the ovarian wall, more opportunities are created for mistakes in the DNA copying process, which in turn increases the chances of a malignant mutation. More ovulations, in other words, mean more chances for mistakes.

Risk factors for the disease therefore include never giving your ovaries a break by being pregnant or having a child. The other risk factor is having a close relative with the disease. That would be my sister, of course, and that would bring our story back home….

Doctors at this hospital and elsewhere have long speculated that there were significant environmental factors associated with ovarian cancer. The vagina provides a runway to the ovaries not simply for sperm but for many other substances as well. Significantly, women who have their tubes tied experience a lower rate of ovarian cancer than those who do not. Some have theorized that this may be because the pathways to the ovaries has been blocked, keeping outside agents at bay.

For example, some researchers have found a link between talcum powder and ovarian cancer–though several other studies have produced conflicting results. Some early forms of talcum may have contained asbestos and thus given researchers their positive findings. Indeed, at least one retrospective study found a much higher disease rate among women who used talc prior to 1960 than those who used is after–giving at least some credence to the idea that the use of asbestos-laden talc increases a woman’s risk of ovarian cancer.

My sister speculated that asbestos had contributed to her illness. A group of naturally occurring fibrous materials that are fire-resistant, asbestos has been thought to cause adverse health effects since the first century. Yet, as writer Paul Brodeur tells us in his book on asbestos, Outrageous Misconduct, its role in causing the disease asbestosis, a noncancerous condition in which the lungs scar so badly that they won’t expand and contract properly, was not well established in medical literature until the 1970s.

In the years before my sister died, when I was an editor for the Harvard Business Review, I worked on a piece written by Bill Sells, the man who had run the Johns-Manville plants in Waukegan in the early 1970s–a time when deaths from asbestosis and other asbestos-related diseases were beginning to occur in the workforce at an alarming rate. After noting that his job included the unenviable task of visiting his sick and dying employees at the local hospital, he offered this description of his first visit to the factory: “The plant lay at the back of a sprawling complex built in the 1920s. Its view of Lake Michigan was obscured by a landfill several stories high. A road wound through this mountain of asbestos-laden scrap, and as I drove through it for the first time I stopped to watch a bulldozer crush a 36-inch sewer pipe. A cloud of dust swirled around my car.” Inside the plant, he said, he found “asbestos-laden dust coating almost every visible surface.”

An EPA official charged with overseeing the cleanup of the Johns-Manville plant, Brad Bradley, has a similar recollection. Standing at the edge of the 350-acre Superfund site that overlooks Lake Michigan, Bradley recalled his first visit there in 1982. He remembers asking an asbestos expert where he thought they would find the fibers. “I think they are everywhere,” said the expert. Indeed, virtually anywhere on the site that Bradley scuffed the ground with his boot, he found the telltale fibers.

People are more likely to connect the fiber with asbestosis than with ovarian cancer. However, a thirty-year study of nearly two thousand women who worked with asbestos while manufacturing gas masks during World War II showed these women to be seven times more likely to die from ovarian cancer than a control group. My sister’s medical history seems to tell a different story, though, and the link between asbestos and ovarian cancer in general does not appear to be a strong one. The ovarian cancer specialist I saw at the clinic was quick to point out that my sister’s record indicated that her cancer was preceded by endometriosis.

The phrase “painful periods” does not begin to describe the torture that my mother and sister endured during menstruation. White and sweating, doubled over with pain, they retreated to the bed or the couch until the pain and the bleeding passed. When I recounted my mother’s experience, the ovarian cancer specialist suggests that my mother also likely suffered from endometriosis.

Endometriosis is a once rare disease that is now common. When the disease was first named and discovered in 1921 by a New York physician, there were only twenty reports of the illness in the medical literature. Today, the National Institutes of Health estimates that roughly 5.5 million women suffer from the disease in the United States, and as many as 89 million women may have it worldwide. An exact number is hard to come by, since the disease can only properly be diagnosed during surgery. Still, about one-third of women of childbearing age suffer some symptoms–including pelvic pain and infertility–and in the United States at least, the average age of onset has been declining…

Endometriosis is a complex condition, and no one is certain what causes it. Some scientists believe it is an immune system disorder. Others believe that women with endometriosis lack the ability to shed cells that have migrated and are growing where they should not be. Other scientists have focused on a genetic component of the disease since it can run in families. A woman with a sister or mother with endometriosis, for example, is three to seven times more likely to get the disease.

The mechanisms of endometriosis are not that different from those that create cancer: they involve cell proliferation, the migration of cells, and a change in their cellular nature. Endometriosis grows unchecked and invades surrounding tissues, and the body’s immune system fails to rid itself of the misplaced lesions. In the same way, the body fails to rid itself of cancerous lesions.

It is often but not always the case that the kind of cancer my sister suffered from, ovarian clear-cell adenocarcinoma, is preceded by endometriosis, and many believe that there is a relationship between the two diseases. Some scientists believe that endometriosis–in certain cases–is a kind of precancerous condition, and others believe that the two diseases spring forth in unison. Other experts theorize that the endometrial cells themselves drive the proliferation of cancer once it has started by producing their own estrogen. Each lesion is capable of increasing the local production of estrogen, so that once the disease takes hold it is capable of feeding itself.

In my sister’s case, cancerous growths arose within her endometrial lesions. Whatever the exact mechanism of disease development, women with the type of ovarian cancer that my sister suffered from have higher rates of endometriosis that the general female population. In one study, about 70 percent of the women with clear-cell ovarian cancer also had endometriosis.

Scientists have long suspected that chemicals of the type found in Waukegan–dioxins, PCBs, and polycyclic aromatic hydrocarbons (PAHs)–play a role in human endometriosis.

pages 75 – 81

Carson died in 1964, but her work and her life serve as a warning to everyone who struggles with cancer. “As we pour millions into research and invest all our hopes in vast programs to find cures for established cases of cancer,” she wrote, “we are neglecting the golden opportunity to prevent, even while we seek to cure.”

Carson’s favorite quote, from Abraham Lincoln, can be found snuggled into her almost daily letters to Freeman, where she explains what keeps her going through her treatments and on to finish her groundbreaking book. It reads: “To sin by silence when they should protest, makes cowards of men.”

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Songbirds Dying From DDT in Michigan Yards

Superfund site blamed

by Brian Bienkowski

ST. LOUIS, Mich. – Jim Hall was mowing the town’s baseball diamond when he felt a little bump underneath him. “And there it was, a dead robin,” he said.

Just last week, he found another one. “Something is going on here,” said Hall, who has lived in this mid-Michigan town of 7,000 for 50 years.

Two dead birds may not seem like much. But for this town, it’s a worrisome legacy left behind by a chemical plant-turned-Superfund site.

After residents complained for years about dead birds in their yards, 22 American robins, six European starlings and one bluebird were collected for testing.

The results, revealed last week: The neighborhood’s songbirds are being poisoned by DDT, a pesticide that was banned in the United States more than 40 years ago. Lethal concentrations were found in the birds’ brains, as well as in the worms they eat.

“I’ve never seen anything like it. When people told me about it I didn’t believe it. And then we ran these tests. These are some of the highest-ever recorded levels in wild birds,” said Matt Zwiernik, a Michigan State University assistant professor of environmental toxicology who led the testing.

The birds’ brains contained concentrations of DDE, a breakdown product of DDT, from 155 to 1,043 parts per million, with an average of 552. “Thirty in the brain is the threshold for acute death,” Zwiernik said. “All the birds exceeded that by at least two- or three-fold, and many by much more than that.” Twelve of the 29 birds had brain lesions or liver abnormalities.

The culprit is a toxic mess left behind by Velsicol Chemical Corp., formerly Michigan Chemical, which manufactured pesticides until 1963, a year after Rachel Carson’s book Silent Spring exposed the hazards of DDT, especially for birds. Populations of bald eagles and other birds crashed when DDT thinned their eggs, killing their embryos. The pesticide, known for accumulating in food webs and persisting for decades in soil and river sediment, was banned in the United States in 1972.

The nine-block neighborhood has become a real-life example of Carson’s “Fable for Tomorrow” in Silent Spring. “It was a spring without voices. On the mornings that had once throbbed with the dawn chorus of robins, catbirds, doves, jays, wrens, and scores of other bird voices there was now no sound; only silence lay over the fields and woods and marsh,” Carson wrote.

Velsicol is infamous for one of the worst chemical disasters in U.S. history: In 1973 a flame retardant compound they manufactured – polybrominated biphenyls, or PBBs – was mixed up with a cattle feed supplement, which led to widespread contamination in Michigan. Thousands of cattle and other livestock were poisoned, about 500 farms were quarantined and people across Michigan were exposed to a chemical linked to cancer, reproduction problems and endocrine disruption.

The U.S. Environmental Protection Agency took control of the site in 1982 and the plant was demolished in the mid-1990s, leaving behind three Superfund sites in the 3.5-square mile town.

EPA officials did not respond to repeated requests for comment on the poisoned birds and the Superfund cleanup.

Of most concern is the 54-acre site that once contained Velsicol’s main plant, which backs up to the neighborhood where residents have found dead birds on their lawns.

“When he [Zwiernik] tells people about what we have going on here, people say ‘Really? That’s a 1960s problem,’ ” said Ed Lorenz, a professor at nearby Alma College and vice chair of the Pine River Superfund Citizen Task Force, which represents the community. Hall is the chair of the task force.

While there is a long-term health study for residents who had been exposed to PBBs, no one is monitoring their exposure to DDT or looking for possible human health effects. Elsewhere, traces of the pesticide have been linked in some human studies to reproductive problems, including reduced fertility and altered sperm counts.

“There’s definitely concern about the plant, the plant site, health and the environment,” said St. Louis City Manager Robert McConkie. “But we’ve learned to live with it.”

The town’s median household income is 43 percent lower than the state’s. About 22 percent of its families live below the poverty line.

The birds apparently have been poisoned by eating worms living in contaminated soil near the old chemical plant. No studies have been conducted to see whether the DDT has contaminated any vegetables or fruits grown in yards.

Jane Keon, secretary of the task force, said the Michigan Department of Environmental Quality ignored their complaints about dead birds for years.

But Dan Rockafellow, the state agency’s project manager for the site, said it took time to collect enough bird samples to test.

“People would tell us they found dead birds all the time, but birds disappear quickly. Cats, raccoons, other animals get to them,” Rockafellow said. “They weren’t just lying around everywhere.”

Keon said that for two decades the EPA stayed only on the plant site, “as if the chain link fence would hold in the chemicals or something.”

State officials didn’t start testing people’s yards until 2006, when they found several yards highly contaminated with DDT and PBBs.

EPA contractors now are cleaning up 59 yards. (One homeowner refused the cleanup.) Next year the agency plans on adding another 37 yards outside of the nine-block area.

Most of the contamination is in the top six inches of the soil, probably from the chemicals drifting over from the plant, Rockafellow said. However, some yards have DDT and PBBs deeper in the soil, which could be due to Velsicol’s offer of free fill dirt to their neighbors decades ago.

The cleanup is driven by ecological risk, not risk to the homeowners, Rockafellow said. “This is because of the dead robins.”

When asked why it took so long to address the contaminated yards, Rockafellow said it came down to “knowing where the chemicals were. Once we did we fenced those areas off.” Those areas were cleaned up in the fall of 2012, he said, and that spurred “aggressive sampling in the neighborhood.”

Now the neighborhood is buzzing with trucks and workers. Clad in construction helmets and orange vests, workers contracted by the EPA tear up yards, remove dirt, fill it back in and lay new sod.

It isn’t the first time St. Louis wildlife has been contaminated. The Pine River’s contaminated sediment has resulted in a no-consumption advisory for all species of its fish. From 1998 to 2006, most of the Superfund site’s cleanup money – about $100 million – went toward cleaning up the river. After polluted mud was dredged up, preliminary testing has shown that DDT levels are declining in bass and carp downstream of the site, Rockafellow said.

However, DDT and PBBs remain in the river’s sediment and soil, he said. In addition, traces of a chemical that is a byproduct of DDT manufacturing, pCBSA, have been found in the city’s water system, so new water mains will tap into a nearby town’s water supply.

“Our first priority was water and the second priority is now getting the lawns cleaned up,” Rockafellow said.

The bird testing by the Michigan State researcher was largely unfunded, except for a small amount from the community task force. Zwiernik said the EPA and state need to determine if the cleanup actually stops birds from dropping dead.

“They have to have some kind of future monitoring program to test the remediation effort’s success. We’ve had a difficult time to get regulators to listen to that,” he said.

While birds in the rest of the region aren’t at risk, “the robins’ population in the nine-block area is decimated year over year,” he said.

Residents of the neighborhood go about their business of watering flowers and walking their dogs. “It’s sad because a lot of people here are losing some beautiful trees,” Keon said. She pointed to a large Victorian home with new, patchy sod. “The owner of that home said this was going to be his retirement home,” Keon said.

For Hall, leaving St. Louis is not an option. Pollution or not, this is home.

“It’s a nice place to raise your family, great community, people love and take care of each other,” Hall said. “If I ran away, I’d be running away from my responsibility to leave this place better for the next generation.”

By Brian Bienkowski
Staff Writer
Environmental Health News

August 6, 2014

Health experts are questioning the Environmental Protection Agency and Michigan state officials for their decades-long delays in cleanup of a Superfund site that is killing songbirds in yards, possibly leaving people at risk, too.

After years of complaints from residents, researchers recently reported that robins and other birds are dropping dead from DDT poisoning in the mid-Michigan town of St. Louis, which was contaminated by an old chemical plant.

“The more we know about DDT the more dangerous we find out it is for wildlife, yes, but humans, too,” said Dr. David Carpenter, director of the University at Albany – State University of New York’s School of Public Health and an expert in Superfund cleanups.

Velsicol Chemical Corp., formerly Michigan Chemical, manufactured pesticides at the plant until 1963. DDT, known for accumulating in food webs and persisting for decades in soil and river sediment, was banned in the United States in 1972.

The dead robins and other songbirds tested last month at Michigan State University had some of the highest levels of DDT ever recorded in wild birds. They were contaminated by eating worms in the neighborhood’s soil.

The EPA has been in control of the Superfund site since 1982, and the residents and songbirds have been living with the highly-tainted soil in their yards for decades. This summer, EPA contractors are excavating contaminated soil from 59 yards in the town of 7,000 people. Another 37 yards will be cleaned up next year.

EPA and state officials are not conducting any testing to determine how highly exposed the residents are, or whether they are experiencing any health effects.

Carpenter said research elsewhere has linked DDT exposure to effects on fertility, immunity, hormones and brain development. Fetuses are particularly at risk. It also may induce asthma.

“Let’s say your backyard has DDT in it. If wind blows, and kicks up dust, you might [be exposed to] DDT. The sun shines, water evaporates, you might get a little DDT,” Carpenter said. “And who knows what other chemical exposure they’re getting from the site.”

Michele Marcus, an Emory University epidemiologist, said she and her team of health experts heard “shocking stories” when they visited the neighborhood near the dismantled chemical plant last December.

“We heard from several people in the neighborhood that back in the day [decades ago] on several occasions alarms would go off and the neighborhood would be covered in white powder,” Marcus said. “It would take the paint off of people’s cars. Imagine what it was doing to people.”

When asked why it took three decades to address contamination in people’s yards next to the plant, Thomas Alcamo, remedial project manager for the Superfund site, said “hindsight is 20-20.” He said there were some “obvious problems” with the initial cleanup but he maintained it was “not an oversight.”

“This was just a natural progression of the Superfund. It’s just a continual investigation of the plant site itself,” Alcamo said. “Then we looked at the [Pine] river and focused efforts there. Then the state looked at residential areas.”

The Michigan Department of Environmental Quality started sampling some yards in a nine-block area near the plant in 2006, after complaints from residents. Orange fences were installed around heavily contaminated areas. The EPA cleaned up those yards in 2012, Alcamo said. Further sampling, however, found that nearly the entire neighborhood needs cleanup so more excavations began this summer.

Jonathan Chevrier, an epidemiologist at McGill University, said research suggests that fetuses and young children are most vulnerable to DDT. The major worry is brain development in the womb, he said. “Research shows those with prenatal exposure scored lower on neurodevelopmental scales,” which can indicate lower IQs, he said.

There also is evidence that DDT is linked to low birth weights. In addition, a study last month found female mice exposed as a fetus were more likely to have diabetes and obesity later in life.

“The way it kills insects is by affecting the nervous system. It induces a rapid firing of neurons, exhausts them, and then the insect is killed,” Chevrier said. “It’s very plausible that it would attack humans’ nervous systems in the same way.” DDT also may disrupt thyroid hormones, which are critical for brain development, he said.

Nevertheless, EPA officials said St. Louis residents are not in danger. Alcamo said the levels in the soil are not high enough to pose an immediate risk to people.

“This [cleanup] is all for long-term risk so there’s no one that needs to leave during cleanup activities,” he said.

The EPA has not issued recommendations on gardening or other activities while the yards are cleaned up, other than keeping people away from the removed dirt. The agency is monitoring air and controlling dust, Alcamo said. “As long as they wash vegetables,” they should be fine because DDT doesn’t uptake into plants, he said.

However studies have found that some plants can take up DDT, including pumpkin and zucchini and some corn.

Health experts disputed Alcamo’s contention that the DDT levels are not high enough to pose a risk to people. There is no such thing as a level of DDT that “we don’t need to worry about,” Carpenter said.

“It doesn’t seem like there’s a clear health threshold,” Chevrier added. “That doesn’t mean there isn’t one, but, if there is, scientists haven’t found it.”

Velsicol is infamous for one of the worst chemical disasters in U.S. history: In 1973 its flame retardant compound – polybrominated biphenyls, or PBBs – was mixed up with a cattle feed supplement, which led to widespread contamination in Michigan.

Marcus and her colleagues are studying people exposed during the PBB mix-up. They also have launched a new study to examine the levels of PBB, DDT and other chemicals in former Velsicol workers and their families.

Some of the chemical workers in Marcus’ study live adjacent to the plant, but the study does not cover the entire contaminated neighborhood.

Alcamo said community health studies are “outside the scope” of what the EPA does.

Most of the contamination is in the top six inches of the soil, probably from the chemicals drifting over from the plant, but some yards have DDT as deep as four feet, according to an EPA report from April.

All 59 houses tested had at least one soil sample that contained more than 4.1 parts per million of DDT that the EPA set as a cleanup standard. Two-thirds of the yards had at least one sample with more than double the 4.1 parts per million guideline.

The EPA uses a DDT cleanup standard of 5 parts per million based on studies to protect wildlife health, Alcamo said.

“We are using an excavation level of 4.1 ppm DDT to ensure that we are 95 percent confident that we are meeting the 5 ppm number,” he said.

Michigan’s cleanup criteria, based on protecting people from exposure, is 57 ppm for DDT. One home had levels more than twice that amount –140 parts per million in the top six inches of soil.

Alcamo said the EPA is now over-excavating many yards to be certain of cleanup. Contractors will remove about 30,000 tons of contaminated soil this summer.

Alcamo said the EPA has made “great progress,” including a Pine River cleanup. There’s been a “98 percent reduction in fish tissue concentrations of DDT,” he said.

In addition, the EPA is providing 90 percent of the funding to overhaul St. Louis’ drinking water supply because low levels of a DDT byproduct, pCBSA, have been found in the city’s water system.

But Gary Smith, a lifelong resident of St. Louis, said the EPA failed St. Louis on the first round of cleanup, and it cannot happen again.

“We just want the doggone neighborhood cleaned up so we can put an end to this,” said Smith, 63, who is treasurer of the Pine River Superfund Citizen Task Force. “We don’t want to be called a toxic town. We want people to say ‘hey, they cleaned it up.’

“Let’s go the extra mile and not have this be an embarrassment for the EPA again,” he said. “’We have no money’ may be true, but it’s a poor excuse.”

Carpenter said it’s unfortunate that people were probably exposed to DDT for many years.

“The EPA is simply overwhelmed with hazardous sites,” Carpenter said.

EHN welcomes republication of our stories, but we require that publications include the author’s name and Environmental Health News at the top of the piece, along with a link back to EHN’s version.

For questions or feedback about this piece, contact Editor in Chief Marla Cone at mcone@ehn.org.

Follow Brian Bienkowski on Twitter.

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Camp Lejeune and the U.S. Military’s Polluted Legacy
By Alexander Nazaryan / July 16, 2014 5:36 AM EDT

The old railroad track, now a bike and jogging path, winds through the forest that separates Camp Lejeune from Highway 24, which caters to the thousands of Marines stationed here with cheap barbershops that will trim your high-and-tight for $5, furniture stores for the many young families on base, a couple of gun shops, a few bars and the requisite jiggle joint. None of this familiarly shabby Americana is even remotely visible from the verdant path. Trees crowd the sylvan trail like overeager children at a Fourth of July parade, their branches poking through the base’s barbed wire fence. You hear far more woodpeckers and thrushes than Osprey helicopters. Spend enough time on this lush greenway or on the dunes of nearby Onslow Beach and you might forget that Camp Lejeune may be, as Dan Rather once said, “the worst example of water contamination this country has ever seen.”

Camp Lejeune, in Jacksonville, North Carolina, is a toxic paradox, a place where young men and women were poisoned while in the service of their nation. They swore to defend this land, and the land made them sick. And there are hundreds of Camp Lejeunes across the country, military sites contaminated with all manner of pollutants, from chemical weapon graveyards to vast groundwater deposits of gasoline. Soldiers know they might be felled by a sniper’s bullet in Baghdad or a roadside bomb in the gullies of Afghanistan. They might even expect it. But waterborne carcinogens are not an enemy whose ambush they prepare for.

That toxic enemy is far more prevalent than most American suspect, not to mention far more intractable. That the Department of Defense is the world’s worst polluter is a refrain one often hears from environmentalists, who have long-standing, unsurprising gripes with the military-industrial complex. But politics aside, the greenies have a convincing point. Dive into the numbers, as I did, and the Pentagon starts to make Koch Industries look like an organic farm.

In size alone, the Department of Defense dwarfs the footprint of any corporation: 4,127 installations spread across 19 million acres of American soil. Maureen Sullivan, who heads the Pentagon’s environmental programs, told me her office must contend with 39,000 contaminated sites (to be fair, a single base can have several, some as small as a single building).

Camp Lejeune is one of the Department of Defense’s 141 Superfund sites; that’s about 10 percent of all Superfund sites, easily topping any other polluter. And if the definition is broadened out beyond proprietary Pentagon installations, then about 900 of the 1,200 or so Superfund sites in the United States are “abandoned military facilities or facilities that produced materials and products for or otherwise supported military needs,” according to a presidential panel on cancer.

“Almost every military site in this country is seriously contaminated,” said John D. Dingell, a soon-to-retire Michigan congressman who served in World War II. “Lejeune is one of many.”

These military sites form a sort of toxic archipelago across the land: Kelly Air Force Base in Texas, where the Air Force allegedly dumped trichloroethylene (TCE) into the soil, part of what some residents call a “toxic triangle” in south-central Texas; McClellan Air Force Base near Sacramento, California, which includes not only fuel plumes and industrial solvents but also radioactive waste; Umatilla Chemical Depot in the plains of northern Oregon, where mustard gas and VX nerve gas were stored; Rocky Mountain Arsenal, a onetime sarin stockpile just north of Denver; the Massachusetts Military Reservation on Cape Cod, poisoned by explosives and perchlorate, a rocket fuel component that is emerging as a major Pentagon pollutant. But because Camp Lejeune’s abuses and betrayals are more flagrant, it has become a test case for whether the military can defend our soil without ruining it.

To those who suffered at Camp Lejeune, an ugly truth about the American military has revealed itself, a truth no amount of compensation or self-flagellation can vanquish. “I would never recommend to anyone that they go into the Marine Corps,” said former Marine corporal Peter Devereaux, who has good reason to believe that his breast cancer is the result of drinking Camp Lejeune’s tainted water. The Marines, he said, “are like a mafia.”

As I was finishing this article, one of the Camp Lejeune activists I’d been speaking to sent me a short, sad email. “So much for our environment,” the brief note said, linking to a Supreme Court ruling that was published that morning, June 9. The case, CTS Corporation v. Waldburger, called into question how long defendants in North Carolina had to sue industry for sickness or death caused by pollution. By ruling for CTS, the polluter, the Supremes indirectly but incontrovertibly complicated the efforts of those seeking compensation at Camp Lejeune. The fight, always hard, suddenly got harder.

Methyl-Ethyl Death

Among those who could never again be charmed again by Camp Lejeune’s bucolic seaside surroundings is Jerry Ensminger, who today lives in nearby White Lake, North Carolina. Ensminger joined the Marines during the Vietnam War, in which his brother had been wounded. After a stint in Okinawa, he was assigned to Camp Lejeune in 1973. He and his wife lived in a housing complex on the base’s northern edge. Their second daughter, Janey, was born in 1976. Photographs show a pretty girl with bangs and cheeks like apples. In one picture, she clenches her teeth and proudly shows off invisible biceps, in what looks like an imitation of her ball-busting drill sergeant of a father.

But then, no more happy pictures. At the age of 6, Janey was diagnosed with leukemia. In the photographs that follow, her hair is cut short. Deposits of fat, from treatments, pad her body. You can see that she knows things no child should have to know. On September 24, 1985, Janey Ensminger died. She was 9.

There were many Janeys at Lejeune, and some didn’t even make it through their first year of life. As Mike Magner writes in A Trust Betrayed, his masterfully thorough book on Camp Lejeune, the base hosted a grim dance of miscarriages, stillbirths and inexplicable postnatal deaths, especially during the 1960s and ’70s: Christopher Townsend, dead at 3½ months from a legion of ailments; Michelle McLaughlin, dead at birth; Eileen Marie Stasiak, dead in the womb. Ricky Gagnoni, alive but a single month, started to bleed from his mouth as his mother fed him and died the next day. So many infants perished at Camp Lejeune that a nearby cemetery had a section mourning parents named “Baby Heaven[1] [2] .”

Finding no other answers, grieving parents turned the loaded gun of guilt upon themselves. “I blamed myself for years,” a mother named Mary Freshwater would later testify. “I hated myself, I hated my body, ’cause I thought I had failed my children.” Standing at a podium, unable or unwilling to hide her tears, she held up the pajamas her infant son was wearing when he died. She had never washed the vomit he’d left on them. She said that after his death, base officials urged her and her husband to try again. They did. And their next son died, too.

“I have two graves out in Onslow Memorial Park,” Freshwater said.

Those with plots at Baby Heaven now know that, as early as 1981, officials at the base were told that the millions of gallons of drinking water consumed by the base’s 100,000 or so residents each day were full of what toxicologists call “methyl-ethyl death,” informal shorthand for a variety of known and suspected carcinogens. But the first batch of groundwater wells was not shut down until the fall of 1984 and the winter of 1985. The base became a Superfund site in 1989, but even today, the full extent of the camp’s contamination is not known. Blame that on poor record-keeping, stonewalling, arrogance or just plain ignorance. The U.S. Environmental Protection Agency (EPA) isn’t even sure how many people have been poisoned by Camp Lejeune’s bad water, though estimates suggest that it was consumed by as many as a million people.

How much the likes of Ensminger deserve in financial compensation for their grief is the most complex question of all: Suffering at once yearns for a dollar amount and resists such crass calculation. Ensminger is one of about 3,500 people involved in litigation against the Department of Defense. They thought the Marine Corps, which proudly professes to leave no man behind, would own up to its mistakes. As they pushed the Marines to reveal what they knew about Lejeune’s drinking water, and when, they figured that the motto Semper Fidelis (“Always Faithful”) was more than just a sales pitch.

Now, they know better.

Kevin Shipp knows better, too. As an agent of the Central Intelligence Agency, he was stationed at Camp Stanley, an Army site right near San Antonio’s heavily polluted Kelly Air Force Base. (During our conversation, Shipp would not reveal exactly where he was stationed or his job there, though other outlets had previously identified both.) Shipp and his family lived at the base, which is believed to be a secret weapons storage facility, for two years starting in June 1999.

Unlike the largely unsuspecting residents of Camp Lejeune, the Shipps realized quickly that something was amiss. One of his sons told The New York Times that “the house that our family was moved into was planted on top of a lot of buried ammunition. One time, me and my little brother dug up a mustard gas shell.” Their house was also teeming with mold, which made them ill. “My children were bleeding from their noses, vomiting, had severe headaches and strange rashes on the exposed areas of their skin,” Shipp later wrote. “My wife became bedridden with headaches so severe, she had to be placed on morphine. … I began to have burning in my lungs…and was losing my short-term memory.”

In 2002, Shipp left the CIA and sued his employer for placing him in a mold-ridden house. The case was eventually dismissed on the basis of the State Secrets Privilege.

When we spoke, Shipp, who now lives in Jacksonville, Florida, described Camp Stanley as a “toxic mess.” Not only is it littered with aging munitions, but its water has been poisoned in a fashion strikingly similar to Camp Lejeune’s.

“Frankly,” Shipp told me, “they don’t care.”

Men With Mastectomy Scars

Camp Lejeune, built in 1941, is 240 square miles in area, making it the largest Marine base east of the Mississippi River, and the second largest in the nation after Camp Pendleton, near San Diego. Situated at the swampy mouth of the New River, it is an ideal training ground for the sorts of amphibious assaults that are the Marines’ favored means of arriving at the war dance. From here, leathernecks shipped out to the Pacific theater of World War II, Korea and Vietnam. The Marines killed in the 1983 terrorist bombings of a barracks in Beirut had also come from Lejeune; a memorial to them sits in a wooded glade at the camp’s edge.

In the decade before Camp Lejeune was built, the chemical industry saw the advent of the “safety solvents” TCE and tetrachloroethylene (PCE). These were chemical cleaning agents of the organochlorine group: TCE was a degreaser for machine parts; PCE was used in dry cleaning.

A military base is rife with machines. This sounds obvious, but it’s quite striking when you see all those tanks and airplanes and amphibious vehicles that seem perfectly poised for battle, even on a humid North Carolina afternoon when overseas wars might as well be waged in another galaxy. Part of that readiness is cleanliness, which your average military mechanic would have achieved, until very recently, by washing grease-covered parts in TCE.

In 2004, a former Marine named Joseph Paliotti decided to clear his conscience. He was on the verge of perishing from cancer, and he suspected that Camp Lejeune had something to do with it. He had spent 16 years working on the base. “We’d come down there, we used to dump it: DDT, cleaning fluid, batteries, transformers, vehicles,” he told his local television station. “I knew sooner or later something was gonna happen.” Several days later, Paliotti died.

The cleaning of clothes might seem like a more innocuous matter, but that’s only because most people don’t have much of a notion of how a dry cleaning enterprise works. You surrender your clothes; they return immaculate. Magic! As it happens, the chemicals that cleanse a shirt are about as carcinogenic as those that cleanse an airplane engine.

One of the places at Camp Lejeune that could care for your uniform was ABC One Hour Cleaners, which sits just a few yards from the edge of the base. The dry cleaners, which started operation in 1964 and ended on-site cleaning service in 2005, did nothing different from what thousands of other dry cleaners did around the United States: It used PCE as a cleaning solvent. Some of the PCE sludge was used to fill potholes, while much of the liquid waste ended up in the ground, just like the TCE used to clean machines across the road, behind the barbed wire.

The TCE and PCE percolated through the sandy soil of Camp Lejeune and into the shallow Castle Hayne aquifer, from which the base drew its water. Also flowing into the soil was benzene from the Hadnot Point fuel farm. A component of gasoline, benzene is an aromatic hydrocarbon. Its name does not mean that it is pleasantly pungent. Instead, the deceptively alluring adjective refers to the strong carbon-hydrogen latticework of the compound. Like other aromatic hydrocarbons, benzene is a carcinogen that readily enters the body.

An Associated Press report found that as “late as spring 1988, the underground tanks at Hadnot Point were leaking about 1,500 gallons of fuel a month—a total of more than 1.1 million gallons, by some estimates.” Eventually, the leaked fuel would form an underground layer 15 feet deep, a carcinogenic band essentially covering the aquifer from which the drinking water was drawn.

Among those who drank that water was Mike Partain, who was born on base. His father was a Marine, as was his grandfather. He lived in the same housing complex where the Ensmingers conceived their daughter Janey. He joined the Navy but was discharged because of a debilitating rash that would overtake his body without explanation. Eventually, Partain ended up in Tallahassee, Florida, where he was a teacher and, later, an insurance adjuster.

Then married with four children, Partain was in good health until the age of 39. (He has since divorced; “my marriage didn’t survive Lejeune,” he told me.) Toxins, like terrorist sleeper cells, are patient. As he would later write for the website of Semper Fi, a documentary about Camp Lejeune, in April 2007 “my wife gave me a hug before bed one night. As she did, her hand came across a curious bump situated above my right nipple. There was no pain, but it felt very odd.” Partain went for tests, which revealed an almost incredible diagnosis: breast cancer.

Male breast cancer is rare enough in the general population, especially for someone like Partain who has no history of the disease in his family. According to the Agency for Toxic Substances and Disease Registry, only about 7 breast cancer victims out of 1,000 are men. Yet it turned out that many other men who’d lived on Camp Lejeune had developed breast cancer: Partain told me that he knows of 85 victims. Several of these aging men, showing mastectomy scars, posed for a 2011 calendar.

Coincidences do happen, even in cancer epidemiology. What looks like obvious causation to some may be just cruel fate, but the overall infrequency of the disease, combined with its relatively high frequency among the men of Camp Lejeune, as well as the other ailments plaguing those who lived on the base, made clear that there was a connection. “This has all the characteristics of a male breast cancer cluster,” the noted epidemiologist Richard Clapp said at the time. Camp Lejeune is, in fact, now widely believed to be the largest known cluster of the male variant of the disease.

“So Much Audacity”

The Superfund law, passed in 1980, did not apply to federal facilities until 1986. Once it was exposed to litigation, the Department of Defense could no longer dismiss the environmental movement as a mere leftist nuisance. The EPA did better under self-described “environmental president” George H.W. Bush than it had under Ronald Reagan. The Clinton presidency appeared to embolden the regulators, even as the centrist Democrat allowed the Superfund tax on industry to expire in 1995. The presidency of George W. Bush, however, proved a long-sought reprieve for polluters, as the wannabe Texan quickly stocked the EPA with friends of industry.

The attacks of 9/11 proved an especially ripe opportunity for the Pentagon to push back against the oversight implemented in 1986. With the EPA already weakened by the White House and the wounded country in a bellicose mood, the Pentagon asked, in 2003, for a pass on pollution. The Department of Defense figured that Americans were far more afraid of terrorists than polluters. “The manner in which certain environmental laws are being applied is seriously hampering our military training opportunities,” Defense Secretary Donald Rumsfeld wrote in an April 2003 letter to EPA head Christine Todd Whitman.

Military officials did not anticipate the resistance they would encounter on Capitol Hill. Perhaps the most vociferous critic of the exemptions was Dingell. “Nowhere has a single set of legislative proposals had so much audacity and so little merit,” thundered the aging legislator during one hearing. “I would note that the Defense Department is supposed to defend the nation, not to defile it.”

Despite an industry-friendly White House on its side, the Pentagon failed to earn the exemptions from environmental laws. Just as important, its overreach brought national attention to the then little-known problem of military pollution, with Camp Lejeune coming to serve as an example of what happened when the Department of Defense was left to police itself.

Sullivan, the Pentagon’s chief environmental officer, said that to clean up all of the Pentagon’s pollution would cost American taxpayers $27 billion. Nevertheless, she is upbeat about the challenges before her, noting that the Department of Defense has done all it could to meet new regulations. Its shortcomings, she said, resulted from a widespread ignorance about the danger of certain chemicals, which was hardly restricted to the Pentagon. “We all grew,” she told me, “at the same time.”

Others are skeptical of the Pentagon’s efforts to come clean. One report by the religiously nonpartisan U.S. Government Accountability Office deemed “daunting” the Pentagon’s “task of cleaning up thousands of military bases and other installations across the country.” It concluded that “identifying and investigating these hazards will take decades, and cleanup will cost many billions of dollars.” The GAO has also found that regulators lack the muscle to make the Pentagon clean up its many messes.

“A World Trade Center in Slow Motion”

Today, Camp Lejeune is a tidy base of red-brick buildings and thick groves of pine. Occasionally, one sees vistas of the New River, which opens into a bright blue bowl of a bay. Marines can rent cabins on a beach that recalls untrammeled stretches of Cape Cod. The base is home to a rare variety of woodpecker, as well as the Venus flytrap. The place looks ordinary, even pretty in places, if you can get past the punishing Southern heat. It is like a body whose wounds have healed, though the scars are still visible if you know where to look: the yellow poles of observation wells, empty lots behind barbed wire, groves in which dump sites hide. But most people aren’t looking.

We pass an unexceptional building on the side of the road. Here, the base once stored the toxic pesticide DDT, made infamous by Rachel Carson’s Silent Spring. Later, the same building became a day care center, with kids playing in ground soaked with an incontrovertible poison. I told the environmental officials who led me around the base that I was reminded of something that Ernest Hemingway once wrote: “All things truly wicked start from an innocence.” I don’t think they knew if this was supposed to be condemnation or exculpation. I don’t know, either.

The ignorance argument falls loud and flat when it comes to TCE, which could have been classified as a known carcinogen much earlier than 2011, which was when the EPA finally released its long-awaited determination of the solvent’s manifold dangers. According to a two-part Los Angeles Times series on trichloroethylene, the EPA realized in the 1990s that TCE was “as much as 40 times more likely to cause cancer than [the agency] had previously believed.” Its efforts to classify TCE as a carcinogen were largely hindered by the Pentagon, which produced experts confidently assuring that TCE’s danger was overblown. Those attempts at assuaging concerns failed, but the delay was costly, while the contamination remains vast and the cleanup has been slow. David Ozonoff, an epidemiologist at Boston University, called the nation’s TCE problem “a World Trade Center in slow motion.”

The public affairs and environmental officials who took me around Camp Lejeune were young, informed and sunny in disposition, not quite the clenched-anus Dick Cheney minions one expects of the nefarious military-industrial complex. They told me, proudly, that the water at the base was now probably the cleanest in the nation. One hears a similar refrain about both Woburn, Massachusetts, and Toms River, New Jersey, the infamous cancer clusters where water was also tainted with TCE. What they don’t say is that today’s pristine water has been paid for by past generations, many times over.

Yet several dozen sites remain, each benzene plume, munitions dump and TCE-laden lot its own private battlefield. It will be decades before the base is fully clean, though past neglect appears to have been replaced by penitent diligence. Solar thermal panels have already been installed on 2,000 homes, improbably making Camp Lejeune one of the largest residential communities in the nation to use solar energy. Even more improbable, earlier this year Camp Lejeune won an environmental restoration award from the Pentagon, beating out bases across the various services. Of course, that’s partly because there was so much here to restore.

“They’re Slick”

In 2012, advocates like Jerry Ensminger and Mike Partain won a victory when President Barack Obama signed the Honoring America’s Veterans and Caring for Camp Lejeune Families Act, which is supposed to ensure that those sickened by Lejeune water get medical treatment from the Department of Veteran Affairs. The law is also known as the Janey Ensminger Act, a nod to the father who turned his howling grief into righteous anger. In the Oval Office, Ensminger stood next to the president and looked over his shoulder, as if to make sure the bill was properly signed.

Ensminger said working on Camp Lejeune has been like “pulling teeth.” He wasn’t exaggerating all that much. Earlier this spring, Obama’s Department of Justice filed an amicus curiae brief to the Supreme Court in CTS Corporation v. Waldburger, in which 25 Asheville, North Carolina, residents were suing an electronic firm for contaminating their well water. The brief was in favor the polluter, not the alleged victims. That seemed to put the administration at odds with its position on the treatment of victims of toxic exposure.

When the Supreme Court ruled in favor of CTS in June, it essentially said that North Carolina’s 10-year statute of repose trumps the Superfund law’s statute of limitations. A statute of repose is much friendlier to business, while a statute of limitations favors those, like Ensminger, who might want to sue a potential polluter, since it gives them much more time to discover the result of their illness (which could take far more than a single decade to manifest). Some observers noted that the Supreme Court ruling could make it difficult for the Camp Lejeune lawsuits to proceed.

“It doesn’t matter,” Ensminger said a couple of days before the Supreme Court decision. “I’m not quitting.” In the hours after the ruling, he and his lawyers quickly identified a seeming loophole in the majority opinion that they were eager to exploit, while North Carolina legislators rushed to pass legislation that would preserve the legal claims of both CTS and Camp Lejeune victims. (North Carolina Governor Pat McCrory signed the bill in late June.)

“You gotta watch these people like a hawk, man,” Ensminger told me of the Marines. “They’re slick.” The armed forces took his daughter. They took so many other lives, too, without firing a single shot.

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“Our Stolen Future,” by Theo Colborn, Dianne Dumanoski, and John Peterson Myers.
Hand-Me-Down Poisons Excerpt

Gilbertson had given Colborn complete access to his meticulously organized collection of material on each animal species that breeds in the Great Lakes basin–data that he had gathered over the years and arranged in chronological order in three-ring binders. Colborn was awed by the elegance of the effort and by the years of dedication and scholarly consideration that it reflected. With a sense of history, Gilbertson had gone to great lengths to collect papers and studies dating back a half century or more–literature documenting that the problems seen today in the birds and wildlife along the lakes had not been reported before World War II. In the bald eagle file, she found evidence of parallel declines in the postwar period in the bald eagle in North America and in its European cousin, the white-tailed sea eagle, along with a collection of reports detailing the concentrations of synthetic chemical contaminants found in both species. Photocopies from Gilbertson’s archive had greatly enriched Colborn’s files, but their conversations, during which Gilbertson generously shared his broad experience, had proven even more valuable.

Over lunch in the Canadian Wildlife Service cafeteria, Colborn, Gilbertson, and Fox had discussed the wildlife evidence contradicting the frequent claims that the lakes had been cleaned up. The two Canadians shared the conviction the wildlife work had likely implications for human health and constituted a warning humans ought to heed. In her survey of the scientific literature, Colborn had been fascinated by some of Fox’s work, which reported evidence of behavioral changes in wildlife as well as signs of physical damage.

In herring gull colonies, particularly in highly polluted areas of Lakes Ontario and Michigan, Fox and his colleagues had found nests with twice the normal number of eggs–a sign that the birds occupying the nests were two females instead of the expected male-female pair. The phenomenon, which persisted in some areas, had been particularly prevalent in the mid to late 1970s. During this period, Fox had collected and preserved seventeen near-term embryos and newly hatched chicks from the affected colonies in hopes that he might eventually discover what was causing this unusual behavior and other reproduction problems.

A few years later, Fox encountered a scientist who might help him find the answer. Michael Fry, a wildlife toxicologist at the University of California at Davis, had investigated how the pesticide DDT and other synthetic chemicals disrupt the sexual development of birds after hearing reports of nests with female pairs in western gull colonies in southern California. While some looked for an evolutionary explanation for the phenomenon, Fry had suspected contamination. Reports in scientific literature indicated that a number of synthetic chemicals, including the pesticide DDT, could somehow act like the female hormone estrogen.

To test his theory, Fry had injected eggs taken from western gull and California gull colonies in relatively uncontaminated areas with four substances–two forms of DDT; DDE, the breakdown product of DDT; and methoxychlor, another synthetic pesticide that had also been reported to act like the hormone estrogen. The experiment showed that the levels of DDT reported in contaminated areas would disrupt the sexual development of male birds. Fry noted a feminization of the males’ reproductive tracts, evident by the presence of typically female cell types in the testicles or, in cases of higher doses, by the presence of an oviduct, the egg-laying canal normally found in females. Despite all this internal disruption, the chicks had no visible defects and looked completely normal.

As soon as he could make arrangements, Fox shipped the preserved embryos and chicks off to Fry in California. In his examination of the birds’ reproductive tracts, Fry found that five of the seven males were significantly feminized and two had visibly abnormal sex organs. Five of the nine females showed significant signs of disrupted development as well, including the presence of two egg-laying canals instead of the one that is normal in gulls. Such disruption, Fry noted, could indicate that the birds had been exposed to chemicals that acted like the female hormone estrogen.

Earlier experiments by other researchers had shown that exposing male birds to estrogen during development affects the brain as well as the reproductive tract and permanently suppresses sexual behavior. When chicken and Japanese quail eggs received estrogen injections, the males that hatched never crowed, strutted, or exhibited mating behavior as adults.

Taken together, the evidence in the Great Lakes suggested that the females were nesting together because of a shortage of males, which might be absent because they were disinterested in mating or incapable of reproducing. Though most eggs in these same sex nests were infertile, these females sometimes managed to mate with an already paired male and hatch a chick. The female pairs appeared to be an effort to make the best of a bad situation.

Fox and others had noticed other behavioral abnormalities as well, particularly in birds that had high levels of chemical contamination. In Lake Ontario colonies, the birds showed aberrant parental behavior, including less inclination to defend their nests or sit on their eggs. In unsuccessful nests, the incubating eggs were unattended for three times as long as in the nests where birds successfully produced offspring. A study comparing reproduction in Forster’s terns nesting in clean and contaminated areas reported that nest abandonment and egg disappearance, often due to theft by predators, was substantial in the contaminated area on Lake Michigan but virtually nonexistent in the clean colony on a smaller lake in Wisconsin. Parental inattentiveness clearly diminished the chances that the eggs would hatch and the chicks would survive.

What Colborn remembered afterward about the conversation was how cautious they had all been. Despite the shared view that wildlife findings had implications for humans, no one wanted to acknowledge the unspoken question hanging in the air. No one dared ask whether synthetic chemicals might be having similar disrupting effects on human behavior. Those were treacherous waters they all preferred to avoid.

pages 20 – 22

For additional information – http://www.ourstolenfuture.org/

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EPA’s Blind Spot: Hexavalent Chromium in Coal Ash
Coal ash may be the secret source of cancer-causing chromium in your drinking water

EPA’s Blind Spot: Hexavalent Chromium in Coal Ash

Author: Lisa Evans, Earthjustice Contributing Authors: Barb Gottlieb, Physicians for Social Responsibility; Lisa Widawsky, Jeff Stant, Abel Russ, John Dawes, Environmental Integrity Project Environmental Consultant: J. Russell Boulding
February 1, 2011

Introduction

Hexavalent chromium is again in the headlines. In the 1990s, Erin Brockovich achieved fame by uncovering the presence of extraordinarily high levels of industrial hexavalent chromium contamination in the drinking water of a small desert town ravaged by cancer. Today, attention to the deadly chemical is fueled by new data and extensive scientific research. In December 2010, the Environmental Working Group released a report documenting the cancer-causing chemical in tap water in 31 of 35 cities tested in the United States.1 Days later, on December 31, 2010, the California Office of Environmental Health Hazard Assessment (OEHHA) completed a multi-year, peer- reviewed examination of the oral toxicity of the chemical, involving scientists in both the public and private sectors, and released a ground breaking proposal to establish a public health goal for hexavalent chromium in drinking water of just 0.02 parts per billion (or ug/L), 5,000 times lower than the current federal drinking water standard for total chromium.2

On January 11, 2011, on the heels of these announcements, the U.S. Environmental Protection Agency (EPA) issued new guidelines recommending that public water utilities nationwide test drinking water for hexavalent chromium (Cr(VI)).3 EPA’s swift reaction to the widespread presence of hexavalent chromium in American tap water is laudable. However, EPA’s well-placed concern for protection of public health has a dangerous blind spot. While government regulators express concern for small quantities of the cancer-causing substance in our water, they are ignoring one of the largest sources of the hazardous chemical—coal combustion waste (or coal ash)4 from the nation’s coal burning power plants.

This report documents the connection between coal ash and hexavalent chromium. It reviews the sources, toxicity, and known coal ash dump sites where chromium has been found in groundwater. The report identifies studies of numerous power plants where testing of coal ash leachate found extremely high levels of hexavalent chromium. The report also identifies 28 coal ash disposal sites in 17 states where groundwater was documented to exceed existing federal or state standards for chromium and to exceed by many orders of magnitude the proposed California drinking water goal for hexavalent chromium. These contaminated coal ash dump sites are likely the tip of the iceberg. The threat of drinking water contamination by hexavalent chromium is present in hundreds of communities near unlined coal ash disposal sites across the United States. While the EPA doesn’t need another reason to define coal ash as a hazardous waste, it certainly has one now.

Hexavalent Chromium and Coal Ash: The Deadly Connection

It has long been known that chromium readily leaches from coal ash.5 Chromium, however, occurs primarily in two forms: trivalent chromium, which is an essential nutrient in small amounts, and hexavalent chromium, Cr(IV), which is highly toxic even in small doses. In EPA’s latest report on the hazardous contaminants in coal ash, the agency made two important findings:

 Coal ash leaches chromium in amounts that can greatly exceed EPA’s threshold for hazardous waste at 5000 parts per billion (ppb),6 and

 The chromium that leaches from coal ash is “nearly 100 percent [hexavalent] Cr(VI).”7

Remarkably, the U.S. Department of Energy (DOE) and the energy industry have also known for years about the aggressive leaching of hexavalent chromium from coal ash. In a 2006 report co-sponsored by DOE, the Electric Power Research Institute (EPRI) found definitively that the chromium that leaches from coal ash (including FGD sludge) is 97– 100 percent hexavalent chromium.8

These findings, buried in government reports, need to see the light of day. Hundreds – maybe thousands – of leaking and unlined coal ash dumps are situated near water supplies. EPA and DOE have demonstrated that the contaminated leachate (the liquid leaking from coal ash landfills and ponds) is often rich in this cancer-causing chemical. Therefore it is imperative that EPA Administrator Lisa Jackson act decisively to protect U.S. communities from this significant source of hexavalent chromium.

Hexavalent Chromium’s Deadly Link to Cancer

In 2008, a two-year study by the U.S. Department of Health and Human Services’ National Toxicology Program (NTP)9 demonstrated that hexavalent chromium in drinking water causes cancer in laboratory animals.10 While it has long been known that hexavalent chromium causes lung cancer when inhaled, the NTP undertook a study of Cr(VI) ingestion following a request from California’s Office of Environmental Health Hazard Assessment (OEHHA). Based on a variety of cancerous oral and intestinal tumors, the NTP study definitively concluded “hexavalent chromium can also cause cancer in animals when administered orally.”11

Furthermore, scientists believe chronic ingestion of minute amounts of Cr(VI) can be harmful. In fact, after an extensive peer-reviewed study, the California Office of Environmental Health Hazard Assessment lowered its original hexavalent chromium draft goal by 66 percent this year to account for the special sensitivity of infants and children to carcinogens. California’s proposed public health goal, 0.02 parts per billion, is a mere 0.02% of the present federal drinking water standard for total chromium. If the current federal drinking water standard (100 parts per billion) is compared to a 100-yard football field, California’s proposed goal for Cr(VI)would be a distance of three-quarters of an inch.

According to EPA’s 2010 draft toxicological review of hexavalent chromium, EPA agrees with the estimate of cancer potency used by California’s Office of Environmental Health Hazard Assessment. California’s Draft Public Health Goal12 and the U.S. EPA Draft Toxicological Review of Hexavalent Chromium13 both use the same cancer potency value for ingested hexavalent chromium of 0.5 (mg/kg-d)-1. Using EPA’s default assumptions for body weight and drinking water ingestion rate, it is possible to estimate the lifetime cancer risk associated with drinking water at the current federal drinking water standard for total chromium of 100 ppb (established in 1991) – the risk is 1.4 in 1,000 people.14 This risk is 140 – 1400 times greater than EPA’s range of acceptable cancer risk (between1 in 100,000 and 1 in 1,000,000 people).15 Clearly, in view of this elevated risk recognized by both EPA and OEHHA, the 1991 federal drinking water standard of 100 ppb for total chromium is not sufficiently protective of human health from ingestion of hexavalent chromium. While a new federal drinking water standard for hexavalent chromium may be higher than California’s proposed goal of 0.02 ppb, this health-protective level, as well as the current federal standard, are used as a comparison to coal ash-contaminated waters in this report.

Ingestion of Hexavalent Chromium Is Missing from EPA’s Coal Ash Risk Assessment

Although the cancer risk associated with Cr(VI) in groundwater is substantial, EPA completely ignored this risk in its proposed coal ash rulemaking. While Cr(VI) was discussed in the preamble to the proposed rule, it was treated as a carcinogen by inhalation only. For purposes of calculating the human health risk by ingestion, Cr(VI) was treated as a non-carcinogen.16 Despite the clear findings of NTP’s 2008 studies, the cancer risk of ingested Cr(VI) was not mentioned once in EPA’s 400-page “Health and Ecological Risk Assessment for Coal Combustion Wastes.”

Coal Ash Dump Sites Are Significant Sources of Hexavalent Chromium

Coal ash can leach deadly quantities of Cr(VI) to drinking water.17 For example, in the 2006 study18 by the Electric Power Research Institute, an organization that vehemently opposes a hazardous designation for coal ash, EPRI tested leachate—liquid collected from wells, ponds or seeps at coal ash dumps—at 29 coal ash landfills and ponds and found hexavalent chromium at hundreds of times the proposed California drinking water goal at 15 coal ash disposal sites. Their findings included three landfills where leachate exceeded the proposed drinking water goal by 5,000 times, with two landfills exceeding that goal by 100,000 and 250,000 times. The location of these potentially deadly dumps is not known, but the high levels of hexavalent chromium at the sites may pose a danger to those living near the landfills. Table A lists the coal ash dump sites where leachate was found containing hexavalent chromium over 5,000 times the proposed California health goal.

Table A

Coal Ash Dump Sites Identified by the Electric Power Research Institute with Leachate containing Hexavalent Chromium (Cr(VI))

The access/view the table go to page 5 – http://www.psr.org/assets/pdfs/epas-blind-spot.pdf

In addition, data from known coal ash disposal sites obtained from EPA reports19 and recent studies by Earthjustice, the Environmental Integrity Project (EIP) and the Sierra Club20 make it eminently clear that the threat is widespread and serious. For example, chromium in groundwater contaminated by a coal ash landfill in Ohio reached 1.68 parts per million – a level 84,000 times California’s proposed drinking water goal (if nearly all the chromium measured was hexavalent, as predicted in both EPA’s and EPRI’s reports). Table B lists 28 coal ash dump sites in 17 states where coal ash contaminated groundwater was found to contain chromium at levels exceeding the current federal drinking water standard (100 ppb) or an applicable state standard (50 ppb for groundwater in North Carolina). Often EPA did not provide a specific value for the chromium found in groundwater wells, but simply indicated that it was greater than the federal standard of 100 ppb. These chromium concentrations, if 100 percent hexavalent chromium, represent a level 5,000 times higher than the proposed California goal. In Table B, all chromium is assumed to be hexavalent chromium, a premise supported by the studies conducted by EPA, DOE and EPRI. In addition, most of the coal ash ponds, landfills and fill sites listed below are unlined – a factor that greatly increases the danger to neighboring communities. Lastly, while many of the sites below have undergone some form of remediation under Superfund or state authorities, in most cases the contamination has been left in place, and there may be little attempt to monitor its migration offsite to protect well users from harmful exposure to hexavalent chromium or other toxic metals commonly found in coal ash leachate.

Uniontown, Ohio: A Coal Ash Site Where Health May be Endangered

The Industrial Excess Landfill, near Uniontown, Ohio is an example of the kind of site that may be posing a threat to the surrounding community from contamination of drinking water with hexavalent chromium. The landfill is a Superfund site surrounded on three sides by residential neighborhoods. Roughly one million tons of coal ash were dumped at the landfill in the 1960s. The landfill was closed in 1980, and EPA listed it as a Superfund site in 1986. Groundwater monitoring since then has shown chromium concentrations to be increasing to very dangerous levels. Systematic groundwater monitoring began in 1987, and chromium was detected at concentrations up to 180 ppb in off-site wells. Sampling in the early 1990s found concentrations of chromium over 100 ppb in eight monitoring wells, with concentrations up to 739 ppb. Monitoring through 2001 detected chromium at up to 1,680 ppb in off-site wells located in or near residential areas- over 15 times the federal drinking water standard. Residents report many incidences of cancer in the affected neighborhoods.

Despite alarming evidence of off-site groundwater contamination with heavy metals, including chromium, metals monitoring was phased out around 2001, and remedial actions stopped in 2005. And yet the potential for human exposure to this contamination is very high—there are almost 4,000 private drinking water wells within two miles of the site, and about 90 wells within 1,500 feet. Some homes have been provided with alternative water supplies, but many have not. The cancer risk associated with drinking water having chromium concentrations over 100 ppb is greater than 1 in 1,000. The risk associated with the highest known concentration, 1,680 ppb, would be greater than 1 in 50. Furthermore, this cancer risk would be amplified by the presence of arsenic and other carcinogens in the coal ash contaminant plume.

EPA Laboratory Testing of Coal Ash Reveals Dramatic Chromium Leaching

EPA also found that leachate produced in the laboratory from coal ash at a variety of plants contained sky-high chromium. In a 2009 report, EPA tested coal ash leachate by obtaining waste from numerous operating power plants.21 EPA found that many ashes and sludges produce leachate extremely rich in chromium. The table below provides EPA’s results from five plants. These results represent the highest level of chromium in leachate determined by EPA lab tests. Unlike the EPRI data in Table A and the groundwater and surface water data in Table B, the results below were not field samples. However, EPA used a leach test that mimics field conditions in order to determine the range of chromium that would leach from coal ash disposed under real-world conditions. If this leachate were seeping or leaking into groundwater from a landfill or pond, it could threaten drinking water wells and human health. While the public is not likely to be exposed to coal ash leachate at full strength, leachate this rich in chromium, even if it is diluted as it flows through groundwater, can still pose a significant hazard when it reaches drinking water wells.

How much chromium is released by U.S. Coal-Fired Power Plants each year?

The amount of chromium released by our nation’s coal-burning power plants dwarfs all other industrial sources. According to EPA’s Toxic Release Inventory, the electric power industry dumps over ten million pounds of chromium and chromium compounds in on-and off-site disposal sites each year. Between 2000 and 2009, over 116 million pounds of chromium and chromium compounds were released from coal-fired power plants. The overwhelming majority of this chromium ends up in unlined or inadequately lined coal ash landfills, ponds, and mines. See Table D.

In 2009, the electric power industry reported 10.6 million pounds of chromium and chromium compounds were released to the environment (10.1 million of which was dumped in disposal sites). These 10.6 million pounds represent 24 percent of the total chromium and chromium compounds released by all industries in 2009. See Chart, below. In fact, the top ten chromium-releasing coal-fired power plants alone released almost 1.8 million pounds of chromium and chromium compounds in 2009, and each of these has at least one – if not, more than one – unlined coal ash disposal unit. Despite the obvious significance of this source of chromium, coal-fired power plants are rarely tagged as a source of hexavalent chromium.

As the Air Gets Cleaner, the Threat to Drinking Water Increases

EPA has found that as power plants reduce their emissions of nitrogen oxides (NOX) by employing pollution controls at the power plant stacks, more hexavalent chromium is found in the flue gas desulfurization (FGD) sludge.22 According to EPA, over half of the U.S. coal-fired capacity is projected to be equipped with SCR and/or FGD technology by 2020.23 In fact, EPA anticipates an increase of approximately 16% in scrubbed units by 2015.24 Thus as the Clean Air Act requires more and more plants to install pollution controls, we may experience a much greater threat to our drinking water from hexavalent chromium if disposal of the increased volume of FGD sludge is not properly controlled.

EPA Must Determine that Coal Ash is Hazardous

Although coal ash readily leaches hexavalent chromium, the waste is currently not federally regulated and is routinely dumped in unlined ponds and pits and used as construction fill without restriction. EPA must keep this dangerous chemical out of our water – by regulating coal ash as a hazardous waste, thereby requiring its disposal in safe, secure landfills.

In addition, EPA should immediately investigate the ponds, landfills and fill sites identified in this report to determine if public health is being threatened by exposure to hexavalent chromium, including:

 The three landfills identified in the DOE/EPRI report where Cr(VI) levels in leachate exceed proposed drinking water goals by thousands to hundreds of thousands of times (Table A);

 The 28 landfills, ponds and fill sites where groundwater has been contaminated with chromium over the current federal drinking water standard (Table B) and thousands of times over the proposed drinking water goal (Table B); and

 The disposal sites at the five plants where EPA’s laboratory tests document the potential for dangerous levels of Cr(VI) to leach from ash and sludge (Table C).

EPA must conduct these investigations to ensure that highly contaminated leachate from these coal ash disposal sites is not leaking into drinking water and threatening human health. However, it is important to understand that these sites do not represent the universe of coal ash sites that have contaminated groundwater with chromium. Most coal ash disposal sites in the U.S. is are not monitored sufficiently to determine whether they are contaminating groundwater, and certainly very few coal ash sites are monitored for hexavalent chromium at all. Ultimately only the regulation of coal ash under subtitle C of the Resource Conservation and Recovery Act will ensure that these disposal sites, as well as every coal ash dump in the nation, are constructed securely and monitored sufficiently to keep hexavalent chromium out of our drinking water.

To access the tables, sources, and additional information click below.

EPA’s Blind Spot: Hexavalent Chromium in Coal Ash

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