Excerpt (very long article)
A 6-month investigation finds that the revolving door between government and the chemical industry has led the EPA to rely on easily manipulated research. The result? Toxic substances remain in everyday products.
Scientists are trained to express themselves rationally. They avoid personal attacks when they disagree. But some scientific arguments become so polarized that tempers fray. There may even be shouting.
Such is the current state of affairs between two camps of scientists, health effects researchers and regulatory toxicologists. Both groups study the effects of chemical exposures in humans. Both groups have publicly used terms like “irrelevant,” “arbitrary,” “unfounded” and “contrary to all accumulated physiological understanding” to describe the other’s work. Privately, the language becomes even harsher, with phrases such as “a pseudoscience,” “a religion” and “rigged.”
The rift centers around the best way to measure the health effects of chemical exposures. The regulatory toxicologists typically rely on computer simulations called “physiologically based pharmacokinetic” (PBPK) modeling. The health effects researchers—endocrinologists, developmental biologists and epidemiologists, among others—draw their conclusions from direct observations of how chemicals actually affect living things.
The debate may sound arcane, but the outcome could directly affect your health. It will shape how government agencies regulate chemicals for decades to come; how toxic waste sites are cleaned up, how pesticides are regulated, how workers are protected from toxic exposure and what chemicals are permitted in household items. Those decisions will profoundly affect public health; the rates at which we suffer cancer, diabetes, obesity, infertility, and neurological problems like attention disorders and lowered IQ.
The link from certain chemicals to these health effects is real. In a paper published earlier this year, a group of leading endocrinologists concluded with 99 percent certainty that environmental exposure to hormone-disrupting chemicals causes health problems. They estimate that this costs the European Union healthcare system about $175 billion a year.
Closer to home, Americans are routinely sickened by toxic chemicals whose health effects have been long known. To cite one infamous example, people exposed to the known carcinogen formaldehyde in FEMA trailers after Hurricane Katrina suffered headaches, nosebleeds and difficulty breathing. Dozens of cancer cases were later reported. Then there are workplace exposures, which federal government estimates link to as many as 20,000 cancer deaths a year and hundreds of thousands of illnesses.
“We are drowning our world in untested and unsafe chemicals, and the price we are paying in terms of our reproductive health is of serious concern,” wrote the International Federation of Gynecology and Obstetrics in a statement released on October 1.
Yet chemical regulation in the United States has proceeded at a glacial pace. And corporate profit is at the heart of the story.
That the chemical industry exerts political influence is well documented. What our investigation reveals is that, 30 years ago, corporate interests began to control not just the political process but the science itself. Industry not only funds research to cast doubt on known environmental health hazards; it has also shaped an entire field of science—regulatory toxicology—to downplay the risk of toxic chemicals.
Our investigation traces this web of influence to a group of scientists working for the Department of Defense (DOD) in the 1970s and 1980s—the pioneers of PBPK modeling. It quickly became clear that this type of modeling could be manipulated to minimize the appearance of chemical risk. PBPK methodology has subsequently been advanced by at least two generations of researchers—including many from the original DOD group—who move between industry, government agencies and industry-backed research groups, often with little or no transparency.
The result is that chemicals known to be harmful to human health remain largely unregulated in the United States—often with deadly results. For chemicals whose hazards are just now being recognized, such as the common plastics ingredient bisphenol A (BPA) and other endocrine disruptors, this lack of regulation is likely to continue unless the federal chemical review process becomes more transparent and relies less heavily on PBPK modeling.
Here we lay out the players, the dueling paradigms and the high-stakes health consequences of getting it wrong.
The dawn of PBPK simulation
The 1970s and 1980s saw a blizzard of environmental regulation. The Clean Air Act, Clean Water Act and Toxic Substances Control Act, along with the laws that established Superfund and Community Right-to-Know Programs, for the first time required companies— and military bases—using and producing chemicals to account for their environmental and health impacts. This meant greater demand for chemical risk assessments as the Occupational Safety and Health Administration (OSHA) and the Environmental Protection Agency (EPA) began to establish safety standards for workplace exposures and environmental cleanups.
In the 1980s, the now-defunct Toxic Hazards Research Unit at the Wright-Patterson Air Force Base in Dayton, Ohio, was investigating the toxicity and health effects of chemicals used by the military. Of particular concern to the DOD were the many compounds used by the military to build, service and maintain aircraft, vehicles and other machinery; fuels and fuel additives, solvents, coatings and adhesives. The military is responsible for about 900 of the approximately 1,300 currently listed Superfund sites, many of which have been contaminated by these chemicals for decades.
In the mid-1980s, scientists at the Wright-Patterson Toxic Hazards Research Unit began using PBPK simulations to track how chemicals move through the body. Known as in silico (in computers) models, these are an alternative to testing chemicals in vivo (in live animals) or in vitro (in a test tube). They allow scientists to estimate what concentrations of a chemical (or its breakdown products) end up in a particular organ or type of tissue, and how long they take to exit the body. The information can then be correlated with experimental data to set exposure limits—or not.
PBPK simulations made testing faster and cheaper, something attractive to both industry and regulators. But the PBPK model has drawbacks. “It tells you nothing about effects,” says Linda Birnbaum, director of both the National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP). Observational studies and laboratory experiments, on the other hand, are designed to discover how a chemical affects biological processes.
Even regulatory toxicologists who support PBPK acknowledge its limitations: “[PBPK models] are always going to be limited by the quality of the data that go into them,” says toxicologist James Lamb, who worked for the NTP and EPA in the 1980s and is now principal scientist at the consulting firm Exponent.
The late health effects researcher Louis Guillette, a professor at the Medical University of South Carolina famous for studies on DDT’s hormonedisrupting effects in Florida alligators, put it more bluntly: “PBPK? My immediate response; Junk in, junk out. The take-home is that most of the models [are] only as good as your understanding of the complexity of the system.”
Many biologists say PBPK-based risk assessments begin with assumptions that are too narrow, and thus often fail to fully capture how a chemical exposure can affect health. For example, a series of PBPK studies and reviews by toxicologist Justin Teeguarden of the Pacific Northwest National Laboratory in Richland, Wash., and his colleagues suggested that BPA breaks down into less harmful compounds and exits the body so rapidly that it is essentially harmless. Their research began with certain assumptions; that BPA only mimics estrogen weakly, that it affects only the body’s estrogen system, and that 90 percent of BPA exposure is through digestion of food and beverages. However, health effects research has shown that BPA mimics estrogen closely, can affect the body’s androgen and thyroid hormone systems, and can enter the body via pathways like the skin and the tissues of the mouth. When PBPK models fail to include this evidence, they tend to underestimate risk.
Because of its reliance on whatever data are included, PBPK modeling can be deliberately manipulated to produce desired outcomes. Or, as University of Notre Dame biologist Kristin Shrader-Frechette, who specializes in human health risk assessment, says: “Models can offer a means of avoiding the conclusions derived from actual experiments.” In other words, PBPK models can be customized to provide results that work to industry’s advantage.
That’s not to say PBPK itself is to blame. “Let’s not throw the baby out completely with the bathwater,” says New York University associate professor of environmental medicine and health policy Leo Trasande. “However, when you have biology telling you there are basic flaws in the model, that’s a compelling reason that it’s time for a paradigm shift.”
A handy tool for industry
That PBPK studies could be used to make chemicals appear safer was as clear in the 1980s as it is now. In a 1988 paper touting the new technique, Wright-Patterson scientists explained how their modeling had prompted the EPA to stop its regulation process for a chemical of great concern to the military, methylene chloride.
Methylene chloride is widely used as a solvent and as an ingredient in making plastics, pharmaceuticals, pesticides and other industrial products. By the 1990s, the U.S. military would be the country’s second greatest user. Methylene chloride was—and remains—regulated under the Clean Air Act as a hazardous air pollutant because of its carcinogenic and neurotoxic effects.
Between 1985 and 1986, the National Institute for Occupational Safety and Health estimated that about 1 million workers a year were exposed to methylene chloride, and the EPA classified the compound as a “probable human carcinogen.” A number of unions, including United Auto Workers and United Steelworkers, also petitioned OSHA to limit on-the-job exposure to methylene chloride.
In 1986, OSHA began the process of setting occupational exposure limits. Stakeholders were invited to submit public comments.
Among the materials submitted was a PBPK study by Melvin Andersen, Harvey Clewell—both then working at Wright-Patterson—and several other scientists, including two employed by methylene chloride product manufacturer Dow Chemical. Published in 1987, this study concluded, “Conventional risk analyses greatly overestimate the risk in humans exposed to low concentrations [of methylene chloride].”
Later that year, the EPA revised its previous health assessment of methylene chloride, citing the Wright-Patterson study to conclude that the chemical was nine times less risky than previously estimated. The EPA “has halted its rulemaking on methylene chloride [based on our studies],” wrote Wright-Patterson scientists in 1988.
OSHA, too, considered the Wright-Patterson study in its methylene chloride assessment—and its rulemaking dragged on another 10 years before the agency finally limited exposure to the chemical.
The usefulness of PBPK modeling to industry did not escape the Wright-Patterson researchers. “The potential impact,” wrote Andersen, Clewell and their colleagues in 1988, “is far reaching and not limited to methylene chloride.” Using PBPK models to set exposure limits could help avoid setting “excessively conservative”—i.e., protective— limits that could lead to “unnecessary expensive controls” and place “constraints on important industrial processes.” In other words, PBPK models could be used to set less-stringent environmental and health standards, and save industry money.
So far, they’ve been proven right. The work done at Wright-Patterson set the stage for the next 30-plus years. Results obtained using PBPK modeling—especially in industry-funded research, often conducted by former Wright-Patterson scientists—have downplayed the risk and delayed the regulation of numerous widely used and commercially lucrative chemicals. These include formaldehyde, styrene, tricholorethylene, BPA and the pesticide chlorpyrifos. For many such chemicals, PBPK studies contradict what actual biological experiments conclude. Regulators often defer to the PBPK studies anyway.
A web of influence
At the time that PBPK modelling was being developed, the chemical industry was struggling with its public image. The Bhopal, India, disaster—the methyl isocyanate release that killed and injured thousands—happened in 1984. The following year, a toxic gas release at a West Virginia Union Carbide plant sent about 135 people to hospitals.
In response to these incidents, new federal regulations required companies to account for the storage, use and release of hazardous chemicals. The minutes from a May 1988 Chemical Manufacturers Association (CMA) meeting show industry was feeling the pressure. Noting the federal scrutiny and the growing testing requirements, the CMA recommended that industry help “develop exposure data” and “explore innovative ways to limit required testing to that which is needed.”
Industry had already begun to do this by founding a number of research institutes such as the Chemical Industry Institute of Toxicology (CIIT), a nonprofit toxicology research institute (renamed the Hamner Institutes in an act of linguistic detoxification in 2007). This period also saw the rise of for-profit consulting firms like Environ (1982), Gradient (1985), ChemRisk (1985) and K.S. Crump and Company (1986), with which industry would collaborate advantageously in the following decades.
“Our goal was to do the science that would help the EPA and other regulatory bodies make the policies,” explained William Greenlee, Hamner president and CEO, in an interview for a business website. Indeed, over the past 30 years, Hamner and these consultancies have produced hundreds of PBPK studies, often with the support of chemical companies or trade groups. Overwhelmingly, these studies downplay or cast doubt on chemicals’ health effects—and delay regulation.
“I have seen how scientists from the Hamner Institutes can present information in a way that carefully shapes or controls a narrative,” says Laura Vandenberg, an assistant professor of environmental health sciences at University of Massachusetts Amherst. She explains that Hamner scientists often use narrow time windows or present data in a limited context, rejecting information that does not conform to their models. “These are the kinds of tactics used to manufacture doubt,” she says.
A close look at the authors of studies produced by these industry-linked research groups reveals a web of influence traceable to Wright-Patterson (see chart on following page). At least 10 researchers employed at or contracted by Wright-Patterson in the 1980s went on to careers in toxicology at CIIT/Hamner, for-profit consulting firms or the EPA. About half have held senior positions at Hamner, including the co-authors of many of the early Wright-Patterson PBPK studies: Melvin Anderson, now a chief scientific officer at Hamner, and Harvey Clewell, now a senior investigator at Hamner and principal scientist at the consulting firm ENVIRON. “I’m probably given credit as the person who brought PBPK into toxicology and risk assessment,” Andersen told In These Times.
A revolving door between these industry-affiliated groups and federal regulators was also set in motion. More than a dozen researchers have moved from the EPA to these for-profit consultancies; a similar number have gone in the other direction, ending up at the EPA or other federal agencies.
Further blurring the public-private line, CIIT/Hamner has received millions of dollars in both industry and taxpayer money. The group stated on its website in 2007 that $18 million of its $21.5 million annual operating budget came from the “chemical and pharmaceutical industry.” Information about its corporate funders is no longer detailed there, but Hamner has previously listed as clients and supporters the American Chemistry Council (formerly the CMA, and one of the most powerful lobbyists against chemical regulation), American Petroleum Institute, BASF, Bayer CropScience, Dow, ExxonMobil, Chevron and the Formaldehyde Council. At the same time, over the past 30 years, CIIT/Hamner has received nearly $160 million in grants and contracts from the EPA, DOD and Department of Health and Human Services. In sum, since the 1980s, these federal agencies have awarded hundreds of millions of dollars to industry-affiliated research institutes like Hamner.
But the federal reliance on industry-linked researchers extends further. Since 2000, the EPA has signed a number of cooperative research agreements with the ACC and CIIT/ Hamner. All involve chemical toxicity research that includes PBPK modeling. And in 2014, Hamner outlined additional research it will be conducting for the EPA’s next generation of chemical testing—the ToxCast and Tox21 programs. Over the past five years, Hamner has received funding for this same research from the ACC and Dow.
Meanwhile, the EPA regularly contracts with for-profit consultancies to perform risk assessments, assemble peer review panels and select the scientific literature used in chemical evaluations. This gives these private organizations considerable sway in the decision-making process, often with little transparency about ties to chemical manufacturers. The upshot: Experts selected to oversee chemical regulation often overrepresent the industry perspective.
These cozy relationships have not gone unnoticed; the EPA has been called to task by both its own Office of Inspector General and by the U.S. Government Accountability Office. “These arrangements have raised concerns that ACC or its members could potentially influence, or appear to influence, the scientific results that may be used to make future regulatory decisions,” wrote the GAO in a 2005 report.
Asked for comment by In These Times, the EPA said these arrangements do not present conflicts of interest.
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