Why the United States Leaves Deadly Chemicals on the Market
By Valerie Brown and Elizabeth Grossman
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 , 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.
Decades of deadly delay
PBPK
studies have stalled the regulation of numerous chemicals. In each
case, narrowly focused models developed by industry-supported research
concluded that risks were lower than previously estimated or were not of
concern at likely exposure levels.
Take, for example, methylene
chloride, the subject of the 1987 paper Wright-Patterson scientists
bragged had halted the EPA’s regulatory process. Despite the chemical
being identified as “probably carcinogenic to humans” by the U.N.
International Agency for Research on Cancer, a “reasonably anticipated”
human carcinogen by the U.S. National Toxicology Program, and an
“occupational carcinogen” by OSHA, the EPA has yet to limit its use.
EPA researchers noted this year that the 1987 PBPK model by the Wright-Patterson scientists remains the basis for the agency’s risk assessment.
Today,
methylene chloride remains in use—to produce electronics, pesticides,
plastics and synthetic fabrics, and in paint and varnish strippers. The
Consumer Product Safety Commission, OSHA and NIOSH have issued health
warnings, and the FDA bars methylene chloride from cosmetics— but no
U.S. agency has totally banned the chemical. The EPA estimates that some
230,000 workers are exposed directly each year.
According to OSHA,
between 2000 and 2012, at least 14 people died in the United States of
asphyxiation or heart failure after using methylene chloride-containing
products to refinish bathtubs. The Center for Public Integrity reports
that methylene chloride exposure prompted more than 2,700 calls to U.S.
poison control centers between 2008 and 2013.
Another telling
example of industry-funded PBPK studies’ influence is formaldehyde. This
chemical remains largely unrestricted in the United States, despite
being a well-recognized respiratory and neurological toxicant linked to
nasal cancer and leukemia, as well as to allergic reactions and skin
irritation. The
EPA’s toxicological review of formaldehyde,
begun in 1990, remains incomplete, in no small part because of delays
prompted by the introduction of studies—including PBPK models conducted
by CIIT/Hamner—questioning its link to leukemia.
If that link is
considered weak or uncertain, that means formaldehyde—or the companies
that employ the sickened workers—won’t be held responsible for the
disease. The chemical industry is well aware that “more people have
leukemia … than have nasal tumors,” says recently retired NIEHS
toxicologist James Huff.
Some of this CIIT/Hamner research was
conducted between 2000 and 2005 with funding from an $18,750,000 EPA
grant. In 2010, Hamner received $5 million from Dow, a
formaldehydeproduct manufacturer, for toxicity testing, including PBPK
modeling. The ACC, which opposes formaldehyde restriction, also
supported this research.
Consequently, apart from a few state
regulations and a pending EPA proposal to limit formaldehyde emissions
from composite wood products like plywood, companies can still use the
chemical—as in the FEMA trailers.
Cosmetics and personal-care
products can also be sources of formaldehyde exposure. This made
headlines in 2011 after hair salon workers using a smoothing product
called
Brazilian Blowout
reported nausea, sore throats, rashes, chronic sinus infections,
asthma-like symptoms, bloody noses, dizziness and other neurological
effects. “You can’t see it … but you feel it in your eyes and it gives
you a high,” salon owner and hair stylist Cortney Tanner tells
In These Times.
“They don’t teach this stuff in beauty school,” she says, and no one
warns stylists about these products or even suggests using a ventilator.
OSHA has issued a hazard alert
for these products and the FDA has issued multiple warnings, most
recently in September, but regulations prevent federal agencies from
pulling the products from store shelves. So, for formaldehyde, as in the
case of the paint strippers containing methylene chloride, exposures
continue.
BPA rings alarm bells
The chemical currently at
the center of the most heated debates about consumer exposure is BPA.
The building block of polycarbonate plastics,
BPA is used in countless products,
including the resins that line food cans and coat the thermal receipt
paper at cash registers and ATMs. While scientific evidence of adverse
health effects from environmentally typical levels of BPA mounts, and
many manufacturers and retailers have responded to public concern by
changing their products, federal regulatory authorities still resist
restricting the chemical’s use.
BPA does not produce immediate,
acute effects, like those experienced by salon workers exposed to
formaldehyde or machinists working with methylene chloride. But in
laboratory tests on animals, BPA is a known endocrine disruptor.
Structurally similar to natural hormones, endocrine disruptors can
interfere with normal cellular processes and trigger abnormal
biochemical responses.
These can prompt numerous health problems,
including cancer, infertility, and metabolic and neurological
disorders. BPA has also been linked to increased risk of cardiovascular
disease, diabetes and obesity.
To promote the idea that BPA is
safe, the chemical industry routinely lobbies policymakers and
“educates” consumers. What has not been widely discussed, however, is
how industry has backed PBPK studies that marginalized research showing
risks from environmentally typical levels of BPA. Many of these
doubt-inducing studies have been conducted by researchers whose careers
can be linked to the PBPK work done at Wright-Patterson. In published
critiques, health effects researchers—among them Gail Prins and Wade
Welshons—have detailed the many ways in which these PBPK models fail to
accurately reflect BPA exposure.
PBPK and endocrine disruption
Over
the past several decades, our evolving understanding of our bodies’
responses to chemicals has challenged previous toxicological
assumptions— including those that are fed into PBPK models. This is
particularly true of endocrine disruptors.
Cause-and-effect
relationships between endocrine disruptors and health problems can be
hard to pinpoint. We now know that early—even prenatal— exposure to
endocrine disruptors can set the stage for adult disease. In addition, a
pregnant woman’s exposures may affect not only her children but also
her grandchildren. These
transgenerational effects
have been documented in animal experiments. The classic human evidence
came from victims of DES, a drug prescribed in the 1940s, 1950s and
1960s to prevent miscarriages. Daughters of women who took the endocrine
disruptor developed reproductive cancers, and preliminary research
suggests
their daughters may be at greater risk for cancer and other reproductive problems.
“The
transgenerational work raises an incredible specter,” says Andrea Gore,
who holds the Vacek Chair in Pharmacology at the University of Texas at
Austin and edits the influential journal
Endocrinology. “It’s not just what you’re exposed to now, it’s what your ancestors were exposed to.”
Complicating
PBPK modeling further, hormone-mimicking chemicals, just like hormones,
can have biological effects at concentrations as low as parts per
trillion.
In addition, environmental exposures most often occur as mixtures,
rather than in isolation. And each individual may respond differently.
“PBPK
doesn’t come close” to capturing the reality of endocrine disruption,
the late developmental biologist Louis Guillette told
In These Times,
in part because modelers are “still asking questions about one chemical
exposure with one route of exposure.” Even for health effects
researchers, understanding of mixtures’ effects is in its infancy.
The
debate over how endocrine disruption can be represented in PBPK models
has intensified the unease between regulatory toxicologists and health
effects researchers. That tension is particularly well-illustrated by a
recent series of events that also reveal how some journal editors
privilege the industry’s point of view.
A life-and-death debate
In February 2012 the World Health Organization (WHO) and the U.N. Environment Programme (UNEP) published
a report
intended to inform regulation worldwide. The authors were an
international group of health effects researchers with long experience
studying endocrine disruption.
“There is an increasing burden of
disease across the globe in which [endocrine disruptors] are likely
playing an important role, and future generations may also be affected,”
said the report. These diseases, it continued, are being seen in humans
and wildlife, and include male and female reproductive disorders,
changes in the numbers of male and female babies born, thyroid and
adrenal gland disorders, hormone-related cancers and neurodevelopmental
diseases.
The backlash from toxicologists was immediate. Over the
next few months—as the EU prepared to begin its regulatory
decision-making on endocrine disruptors—the editors of 14 toxicology
journals each published an
identical commentary harshly criticizing the WHO/UNEP conclusions.
The
commentary included a letter from more than 70 toxicologists urging the
EU not to adopt the endocrine disruption framework. The letter said
that the WHO/UNEP report could not be allowed to inform policy because
its science is “contrary to all accumulated physiological
understanding.”
This commentary was followed by further attacks. One critique, published in the journal
Critical Reviews in Toxicology, was funded and vetted by the ACC.
These
commentaries infuriated health effects researchers. Twenty endocrine
journal editors, 28 associate editors and 56 other scientists—including
several WHO/UNEP report authors—signed a
statement in Endocrinology, saying in part:
The
dismissive approach to endocrine disruption science put forth … is
unfounded, as it is [not] based on the fundamental principles of how the
endocrine system works and how chemicals can interfere with its normal
function.
Endocrinology editor Andrea Gore tells
In These Times
that she and other health effects researchers don’t think the
scientifically demonstrated dangers of endocrine disruptors are subject
to debate. “There are fundamental differences between regulatory
toxicologists and what I refer to as ‘people who understand the
endocrine science.’ ”
The outcome of this debate and the structure
of future regulatory toxicity testing in the United States and Europe
is not yet clear. The EPA appears to be attempting to incorporate
endocrine disruption into PBPK models, but many scientists are skeptical
the process will produce reliable results, given the models’
limitations and the complexity of endocrine effects.
From science to activism
Although
couched in complex language, these arguments are not academic, but have
profound implications for public health. Disorders and diseases,
increasingly linked to exposure to endocrine disruptors— including
metabolic, reproductive, developmental and neurological problems—are
widespread and increasing. About
20 percent of U.S. adults
show at least three of the five indicators of metabolic syndrome:
obesity, diabetes, high blood pressure, high cholesterol and heart
disease.
Neurological problems, including behavioral and learning disabilities in children as well as Parkinson’s disease, are increasing rapidly.
Fertility rates in both men and women are declining. Globally, the average sperm count has dropped 50 percent in the last 50 years.
Scientists
typically shy away from activism, but many now believe it’s what’s
needed to punch through the machinations and inertia regarding chemical
regulation. Shanna Swan, Mount Sinai professor of preventive medicine,
obstetrics, gynecology and reproductive medicine, notes that some of the
biggest reductions in chemical exposures have happened in response to
consumer pressure on both industry and policymakers. Or, as the
University of California’s Bruce Blumberg says, “I think we need to take
the fight to the people.”
The Endocrine Society stressed the urgency of addressing these public health impacts in a
statement released September 28. Not surprisingly, industry disagreed, calling this science “unsupported” and “still-unproven.”
Meanwhile,
PBPK studies continue to succeed in sowing doubt about adverse health
effects of endocrine disorders. Their extremely narrow focus leads to
narrow conclusions that often result in calls for more research before
regulation. In regulatory decisions, “the assumption is that if we don’t
know something, it won’t hurt us,” says University of Massachusetts,
Amherst professor of biology R. Thomas Zoeller. In other words, the
burden of proof remains on health effects researchers to prove harm, not
on industry to prove safety—and proving harm is difficult, especially
when other scientists are seeding doubt.
But the clock is ticking. As Washington State University geneticist Pat Hunt told
In These Times,
“If we wait [to make regulatory decisions] for ‘proof’ in the form of
compelling human data, it may be too late for us as a species.”
This investigation was supported by the Leonard C. Goodman Institute for Investigative Reporting and published originally in
In These Times.
