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BAD CHEMISTRY
By Gay Daly
Natural Resources Defense Council
OnEarth
Winter 2006
http://www.nrdc.org/onearth/06win/chem1.asp
Hundreds of man-made chemicals -- in our air, our water, and our
food --
could be damaging the most basic building blocks of human
development.
Everyone knows that World War II left us, as a legacy, the
atomic bomb. Far
fewer people are aware that the war also left us a chemical
bomb, silently,
inexorably ticking away, that may threaten our health, our
intelligence, and
even our ability to reproduce. It may be exploding as you read.
Before the war, only a few synthetic chemicals --
laboratory-made compounds
that do not exist in nature -- had been invented. With the onset
of the war,
chemists eager to help their countries achieve victory began
inventing
plastics, pesticides, solvents, degreasers, insulators, and
other materials
that could be used to make more effective weapons, increase crop
yields, and
feed more soldiers. They were, understandably, more focused on
success than
on safety.
In peacetime, these same labs helped fuel the economic boom of
the second
half of the twentieth century, formulating new chemicals
manufacturers
needed to create cheaper, smarter products.
Federal regulation was fragmentary at best, and manufacturers
were allowed
to provide their own proofs of safety, a situation that remains
true today.
There are now more than 100,000 synthetic chemicals on the
market, and these
chemicals are everywhere. They enter our bodies and those of
other animals
through every possible route of transmission. They are in our
food supply,
so we eat them. They drift in the air, so we breathe them.
(Carried on
thermal currents, they have long since reached the Arctic, so
polar bears
breathe them too.) Present in landfills, they leach into the
water supply,
so we drink them. Released as effluent into lakes and rivers by
factories,
they affect the habitat of fish, frogs, and all aquatic life,
right down to
plankton. Ubiquitous in cosmetics, they are absorbed through our
skin.
Pregnant women pass them to their fetuses; mothers feed them to
their
newborns when they breastfeed. A large, uncontrolled scientific
experiment
has been in progress for the last 60 years, and the question now
is: Can we
figure out what the results are? And if those results show we
are in danger,
what we can do about it at this late date?
For almost two decades after the war, our great faith in the new
chemistry
went untested. It seemed as if one miracle after another emerged
from the
labs, providing abundant, cheap food, drugs to cure disease, and
technology
that made life easier and more pleasurable: televisions,
dependable cars,
inexpensive, reliable refrigerators to replace the icebox.
Rachel Carson pushed Americans to question these miracles when
she published
Silent Spring in 1962, and legislation was passed to address
concerns she
and others raised about environmental toxins. By the early
1970s, more
warning signs had showed up on the radar. DDT, the pesticide
that had saved
American soldiers who fought in the South Pacific from malaria
and been
sprayed on millions of acres of cropland, was fingered as a
killer of birds,
especially the beloved bald eagle. Eggshells thinned by exposure
to the
compound meant fewer hatchlings survived. DES, a drug believed
to prevent
miscarriage, was found to cause cancer in the young women whose
mothers took
it during pregnancy; emergency hysterectomies saved many of the
daughters'
lives, but at a terrible cost. PCBs, highly effective lubricants
and
insulators used in electrical capacitors, transistors, hydraulic
fluids,
plasticizers, inks, waxes and adhesives, were deforming and
killing birds
and fish; by 1971, Monsanto had voluntarily stopped making them.
Each of
these problems was seen as an isolated case: A few rogue
chemicals had
wreaked havoc, but havoc could be contained. Ban DDT, ban DES,
ban PCBs --
perhaps we couldn't undo the damage already done, but we thought
we could
stop it in its tracks and breathe a sigh of relief.
The average person still thinks about chemicals as single
entities, and our
system of federal regulation still decides on a case-by-case
basis whether
chemicals are safe enough to circulate in our world. But a
paradigm shift is
underway among some scientists, who have over the last 30 years
quietly
begun to wonder: By introducing so many substances that did not
evolve along
with living organisms over hundreds of millions of years, have
we
unwittingly initiated changes in our biology that may be
damaging it
profoundly?
SHE WENT LOOKING
One of the researchers most responsible for raising this
question and
pressing to find answers is Theo Colborn, a woman whose career
path has been
anything but conventional. Colborn got her Ph.D. at 58, an age
at which most
people are beginning to think about retirement. By then, she had
raised four
children while working as a pharmacist, a job that required her
to know a
great deal about chemistry, biology, and health. In the 1970s
she began to
see disturbing patterns of illness in the six Colorado
communities where she
worked as a pharmacist. Eventually, she hypothesized that
everybody drank
from the local creek or river and each water source had its own
unique set
of toxins. She went to a number of conferences on water in the
Western
states and was shocked to find that all anybody talked about was
the
quantity of water -- and who owned it.
Divorced, without a mortgage, her children grown and gone,
Colborn decided
to go back to school to make herself an expert on the quality of
water. A
master's degree in freshwater ecology led to a doctorate in
zoology, then
two years as a Congressional Fellow in the Office of Technology
Assessment
in Washington.
Then, in 1987, she landed at the Conservation Foundation, where
her new boss
asked her to take on a survey of research on the impact of
pollution in the
Great Lakes, a study that determined the course of her life's
work. A
younger scientist would probably have wanted to make her own
mark rather
than reading over other people's work. There is little glory in
this kind of
analysis, no tenure. One of Colborn's gifts was that she enjoyed
looking for
patterns. She was, and is, one of those rare people who can hold
thousands
of details in her head, shuffling and reshuffling them, able to
tolerate the
uncertainty of not knowing where they will take her. For six
months, she
worked seven days a week, reading more than 2,000 research
papers and 500
government reports. She developed a primitive filing system: 43
boxes of
documents, one for each species that had been studied.
At first, Colborn went looking for increases in cancer, but she
found,
instead, other problems that disturbed her. Where hundreds of
bald eagles
had nested on the Great Lakes' shorelines, only 45 pairs
remained. Inland,
these birds had rebounded in the years since DDT had been
banned; near
cleaner lakes they also flourished. But on the shores of the
Great Lakes,
deformed birds were showing up across species with missing eyes,
crossed
bills, clubfeet. A startling number of gull and tern nests
sheltered twice
the number of eggs they should, which suggested that females
were sharing
nests, apparently for lack of a male companion. Many males were
not mating
or not parenting. Some birds were abandoning their nests
altogether. Chicks
seemingly born healthy quickly developed a wasting disease and
died. Creepy
stuff, but what did it mean? She sought out wildlife biologists
who told her
that they, too, sensed something was wrong, but none of them
could put a
finger on what it was. Tissue analyses of the animals kept
turning up the
same chemicals, including DDT, dieldrin, chlordane, lindane, and
PCBs.
Everyone knew that hundreds of chemicals had been discharged
into the lakes,
many of them persistent but impossible to measure with methods
available at
the time.
To tame the data, Colborn made an electronic spreadsheet for
species that
were most profoundly affected to figure out where the patterns
lay. Before
long, she realized that something fundamental had to be
happening to explain
such a wide range of symptoms: reproductive failures, genital
deformities,
thyroid malfunctions, behavioral abnormalities, and immune
suppression.
Eventually she decided the most likely probability was endocrine
damage.
Her knowledge of endocrinology was sketchy, so she set herself
the task of
mastering it. Endocrinology is the science of hormones, the
chemical signals
that, in myriad delicate and subtle ways, manage an organism's
most vital
functions. Hormones tell the ovaries and testes how to make eggs
and sperm,
tell the lungs how to breathe, the intestines how to digest, and
the heart
how to pump; they direct neurons in the brain. The way they do
their work is
an extraordinarily complicated dance that scientists are still
working to
comprehend. Estrogens, the female sex hormones, have been
accorded the most
attention so they are best understood; the male hormones,
androgens, run
second; and the thyroid, which controls brain development, is a
distant
third. If hormones cannot do their job properly, the
consequences are legion
-- some subtle, some disastrous. The wrong balance of estrogens
and
androgens, for instance, can lead to reproductive failure. If a
fetus
suffers even a small drop in thyroid hormone levels, learning
disabilities
may be the consequence, IQ points may be lost.
Colborn drew up a list of world-class scientists from different
fields
-- endocrinology, biology, immunology, toxicology, psychiatry,
ecology,
anthropology -- whose work gave them, collectively, the
expertise to test
her suspicions, and invited them to the Wingspread Conference
Center in
Racine, Wisconsin, in the summer of 1991. "I was scared to
death! There I
was, a brand-new Ph.D. who knew only a handful of wildlife
biologists." She
did her best to set up conditions in which this wary bunch could
find common
ground. "I kept them working from morning till night so they had
to get to
know each other," she says. "Thank God there were no cell phones
back then."
Right away, people began to see surprising connections between
their work.
They stayed up talking into the small hours.
The term endocrine disruption was coined at the meeting. As the
fruit of
their work, the group issued a consensus statement that has
stood up well to
the test of subsequent research. The participants agreed that
many man-made
chemicals had the potential to disrupt the endocrine system of
animals,
including humans, by mimicking the activity of a hormone, by
blocking it, or
through other mechanisms, and that many wildlife populations had
already
been affected. Even more disturbing, they emphasized that the
fetus and
newborn are at greatest risk, and that the effects might not be
manifested
until the animal was mature. Perhaps the greatest bombshell was
the
statement that "the concentrations of a number of synthetic sex
hormone
[disruptors] measured in the U.S. human population today are
well within the
range and dosages at which effects are seen in wildlife
populations."
Suddenly, this was not about cleaning up a few lakes; the health
of all the
creatures in our care was at stake -- including the health of
our unborn
children.
MOUNTAINS OF DATA
In the years since that conference, research on endocrine
disruption has
picked up speed; Colborn and her staff have built a database of
33,000
articles to make that research accessible. Chemical
manufacturers have
funded many studies that have almost uniformly concluded that
endocrine
disruption does not occur or, if it does, is not harmful. This
is hardly
surprising because a great deal of money is at stake. (To offer
just one
example: In 2002 U.S. companies produced 2.8 million tons of
bisphenol A
[BPA], a synthetic estrogen used to make baby bottles, plastic
water
bottles, dental sealants, and resin liners for metal food cans.
At 94 cents
a pound, this translates to sales of more than $5.3 billion in
that year
alone.) By contrast, federally funded academic researchers, who
have no
financial stake in the outcome of their work, have found much
compelling
evidence that synthetic chemicals, including BPA, do cause
endocrine
disruption and that the damage can be serious.
One discovery in particular changed the ground of all endocrine
disruption
research. Frederick vom Saal, a reproductive endocrinologist at
the
University of Missouri, established in 1997 that significant
effects can be
seen at extremely low levels of exposure, parts per billion and
even per
trillion. These levels are present in the blood of humans as
well as
animals.
The next logical step would be to expose human subjects to these
chemicals,
but it is considered unethical to subject humans to substances
that might
damage their endocrine function. So rats and mice have had to
stand in for
humans, just as they do in cancer research.
Over the last 10 years, vom Saal has studied the effects of BPA
on mice, and
others have followed his lead. Collaborating with Wade Welshons,
a
veterinary medical researcher also at the University of
Missouri, he
established in 1997 that male mice whose mothers were exposed to
BPA during
gestation routinely developed enlarged prostates. Further
research found
that BPA has many other impacts. In male offspring, exposure of
the mother
results in decreased sperm counts, decreased motility of sperm,
an increase
in malformed sperm, and smaller testes. In females, researchers
have
observed early onset of puberty, larger uteri, polycystic
ovaries, deformed
and incomplete vaginal structures and tissues, enlargement of
mammary ducts
and milk glands in the breast, and an increase in miscarriages.
Damage by
BPA, vom Saal notes, is not limited to reproductive effects.
Structural
changes in the brain; immune-system damage; learning problems;
hyperaggression; and changes in sexual behavior, social
interactions, and
play behavior have also been documented.
Chemical manufacturers have worked hard to counter this academic
research,
hiring chemists to study and discredit the results. Vom Saal and
others have
had to spend enormous amounts of time and money defending their
work,
resources better devoted to moving forward onto new ground.
Researchers
funded by industry, curiously, tend to find that every chemical
is safe. In
2004, vom Saal tallied up results of all the studies he could
find on BPA.
He discovered that of 104 studies done by independent
researchers, 94 found
adverse effects and 10 found no effects. Of the 11 studies
conducted by
industry-supported researchers, zero identified adverse effects.
Marian
Stanley, a spokesperson for the American Chemical Council, which
represents
the interests of chemical manufacturers, says, "We are unaware
of any big
discrepancies between the experimental research supported by
industry and by
others. Animal studies -- that is, credible experimental
research -- from
all sectors show basically the same results across the board."
In fact, Colborn observes, academic researchers have been able
to
demonstrate the effects of chemicals at very low doses, but
industry labs
have not been able to replicate their work, and use their lack
of results to
claim that the chemicals are safe. Colborn says that independent
researchers
have identified possible causes of these discrepancies. Diet is
key; animal
chow that has more soy, which itself is mildly estrogenic, may
skew results.
Housing rats in plastic cages or stainless steel may throw
things off since
some plastics disrupt endocrine levels but metal does not.
Intrauterine
position can affect results: For instance, a male rat that grew
in utero
between two female rats will be born with higher levels of
estrogen in its
blood than one that grew between two male rats. Controlling for
all these
variables is hard and expensive. The most contentious variable
has been
breed of rat. Early in the process, researchers determined that
the Charles
River Sprague Dawley rat was so tough that it barely responded
to estrogenic
compounds. Many scientists whose work is funded by chemical
manufacturers
have continued to use this strain, a practice deplored by
Colborn and other
independent researchers.
Pat Hunt, a geneticist at Washington State University, was
shocked when she
discovered how great a difference a worn-out plastic cage could
make.
Suddenly, 40 percent of the healthy control mice in an
experiment began to
make eggs with grossly abnormal chromosome behavior where she
expected to
see a rate of 1 to 2 percent. She traced the problem back to BPA
they were
exposed to when it leached out of their cages and water bottles.
She spent
five years on the problem, making certain of her results before
publishing
"because I was going to say exposure to this chemical used in
plastics can
cause miscarriages." Today, at conferences, Hunt urges fellow
scientists to
take endocrine disruption seriously. "The mouse is an incredibly
robust
breeder while we humans are, comparatively, so fragile." She is
concerned
about delay. "If we wait till we see an increase in
chromosomally abnormal
[human] miscarriages or a sharp drop in sperm count, by the time
that big an
effect comes up on the radar screen, we need to ask ourselves if
we are
going to be reproducing as a species or not."
Research on male sex hormones, or androgens, has shot forward in
the past
decade, and the man most responsible for this progress is Earl
Gray, a
toxicologist who works for the Environmental Protection Agency
in Research
Triangle Park, North Carolina. In 1995, he started by
administering very low
doses of the fungicide vinclozolin to pregnant rats.
Vinclozolin was widely used until 2002, when the EPA began to
restrict it
because of its potential health effects. Gray found that the
rats' male
offspring were born with nipples, malformed scrota and testes,
vaginal
pouches, and cleft phalluses with hypospadias (urethral openings
in the
wrong place, along the shaft of the penis or in the scrotum).
This finding
is particularly resonant for human health, since the rate of
hypospadias in
human infants doubled for no known reason between 1968 and 1993.
The animals
in this experiment also displayed delayed puberty, lower sperm
counts, and
reduced fertility.
Gray went on to examine trenbolone acetate, a synthetic steroid
used as a
growth promoter in beef cattle in the United States and as a
performance-enhancer by athletes who purchase it illegally over
the
Internet. Trenbolone, excreted in animal waste, shows up in
rivers and
streams where, Gray believes, it may affect aquatic animals.
After
experiments on the fathead minnow, Gray concluded that
trenbolone was a
powerful androgen: Female offspring of mothers exposed to the
compound grew
tubercles, part of the reproductive system usually seen only in
males, and
had fewer babies. Observers of wildlife are beginning to report
similar
effects around the world. Effluents from pulp and paper mills
are
sufficiently androgenic to sex-reverse female fish in Florida,
the Baltic
Sea, and New Zealand.
Gray is an extraordinarily productive researcher, at the top of
his field.
One can only wonder how much more he might discover if he had
more
resources. Because of a hiring freeze at EPA, Gray's staff of
technicians
has shrunk from three to one, limiting the number of experiments
he can do.
THREATS TO OUR HEALTH
It is extremely difficult to obtain direct evidence that
endocrine-disrupting chemicals cause reproductive damage in
humans, for
reasons beyond the ethical one. For instance, determining the
effect of any
particular chemical on an individual is nearly impossible
because it is so
difficult to figure out which chemicals the individual's mother
was exposed
to during pregnancy. However, Shanna Swan, director of the
Center for
Reproductive Epidemiology at the University of Rochester School
of Medicine
and a researcher who is at the forefront of this effort,
published last May
the first study to link prenatal exposure to phthalates to
outcomes in
offspring.
She had recruited a group of pregnant women and measured nine
phthalate
metabolites in their urine. This chemical group had already been
shown to
disrupt the endocrine system in rodents and is ubiquitous in our
world -- in
plastics, nail polish, perfumes, toothbrushes, pesticides,
paint, and the
coating on time-release pills. Then Swan asked pediatricians who
knew
nothing about the maternal exposure levels to measure the
distance between
the genitals and the anus in the male babies. Then this distance
was divided
by the infant's weight to establish an anogenital index (AGI), a
biomarker
animal researchers have long used because it is predictive of
the healthy
development of the genitals in rodents. Short AGI correlates
with smaller
penises, smaller, ill-defined scrota, and incomplete testicular
descent.
Swan found that a boy born to a mother with a high exposure to
dibutyl
phthalate (DBP), for example, was 10 times more likely to have a
short AGI
than a child of a mother with a low exposure to DBP. Swan points
out that
this was a small study of 85 infants; she has proposed a larger
study of 600
families to investigate these effects further. She believes the
research is
necessary because the mothers of babies with short AGIs had been
exposed to
levels of phthalates that, according to estimates from the
Centers for
Disease Control and Prevention, are present in the bodies of
one-quarter of
all American women.
It is already clear that synthetic chemicals can also powerfully
affect the
thyroid gland, which is critical to brain development and
function,
according to Thomas Zoeller, an endocrinologist at the
University of
Massachusetts Amherst. But work is still in an early stage; much
remains to
be understood about how the thyroid functions and how that
functioning can
be disrupted. Zoeller's lab works with PCBs even though they
were banned in
1979, largely because the behavior of these chemicals is well
understood,
which makes it easier both to predict their behavior in the lab
and to
interpret it. Moreover, although PCB levels dropped at first
after the ban,
these chemicals have such a long half-life that the rate of
decline leveled
off in the mid-1990s, which means they will belong to our
bodies' burden of
toxins for a long time to come.
Zoeller has determined that exposing a fetus to PCBs leads to
profound
changes in the brain. "The corpus callosum is a big bridge of
white matter
that connects the two hemispheres, and in our experimental
animals, the PCBs
cause a reduction in the size of the corpus callosum," he says.
This may
prove to be a very important finding, he explains, because "a
number of
neuropsychological diseases in humans have been linked to the
development of
the corpus callosum -- for example, autism and Tourette's."
However, he
emphasizes that we don't know yet if the link is causative.
Zoeller also
suspects that disruption of the thyroid may be contributing to
the sharp
spike in learning disabilities observed over the past two
decades, a spike
that cannot, he says, be explained away by improvements in
diagnosis.
A careful study published in 1996 by Joseph and Sandra Jacobson
suggests
Zoeller is right to be concerned. Testing children of mothers
who ate Great
Lakes fish contaminated by PCBs, they found that children whose
mother's
blood and breast milk, along with umbilical cord blood, showed
the highest
concentrations of PCBs had lower IQs -- on average six points
lower -- than
children of mothers with the lowest concentration. Joe Jacobson
points out
that what he and his wife documented was a correlation between
exposure and
a drop in IQs rather than proof that PCBs caused the drop. The
children with
greatest exposure also exhibited memory and attention deficits
and were
twice as likely to be at least two years behind kids in the
lowest exposure
group in reading comprehension. None of these impacts sounds
catastrophic,
but they could mean more kids who can't sit still in class and
are miserable
in school. The Jacobsons followed these children only until they
were 11 so
they do not know how those exposures affected them later in
life. But
children who have difficulty in school may well grow up less
able to read,
write, or think clearly.
Two brooding questions have hung over endocrine-disruption
research. One:
Are the effects of endocrine-disrupting chemicals additive -- if
you are
exposed to many of them, will their effects add up to produce
greater
changes in hormonal activity? And two: Are the effects handed
down from one
generation to the next? The first attempts to study these
questions suggest
that the answers are likely to be: yes and yes.
In 2005 Kevin Crofton, a neurotoxicologist who works for the EPA
at Research
Triangle Park in North Carolina, published a finding that helped
to confirm
many researchers' worst fears. Crofton gave rats different doses
of mixtures
of three classes of chemicals -- dioxins, PCBs, and
dibenzofurans -- at
concentrations ranging from approximately those that would be
found in
humans to levels 100 times higher. The chemicals in the mixture
were chosen
because they are found in foods people eat, from fish to breast
milk. The
highest dose he used for each chemical was still so low that he
had seen no
endocrine-disrupting effects for that chemical at that level. At
the lower
doses, Crofton found that the effect of the mixture was additive
and that it
significantly reduced the animals' level of thyroxine, the most
common
thyroid hormone. At higher doses, he observed that the mixtures
reduced
thyroxine synergistically so that the sum of their effect was
slightly
greater than simple addition. A fetus must have enough thyroxine
for the
brain to develop properly; adults need thyroxine to regulate
metabolism and
heart rate.
This and many other recent studies of mixtures up the ante
considerably.
They cut right through the endless debates about whether the
levels of
exposure to a chemical in any given experiment accurately
reflect the levels
at which humans or animals are actually exposed to that compound
in the
environment. These studies suggest that we can't solve the
problem by taking
a handful of the most dangerous chemicals off the market;
instead, we will
have to consider whether all endocrine disruptors need to go.
The European
Union has already begun to move in this direction.
The second question, whether effects are handed down from one
generation to
the next, got an answer almost by accident. Michael Skinner, a
molecular and
cellular biologist who focuses on reproductive biology at
Washington State
University, wanted to look at how cells communicate during the
development
of ovaries and testes. He dosed a group of pregnant rats at
mid-gestation
with vinclozolin, an anti-androgen (a substance that blocks
androgenic
hormonal activity), and another group with the pesticide
methoxychlor, which
is estrogenic, to see if either would alter the development of
their
offspring. A research fellow in his lab bred that first
generation of
babies, which was not part of the plan. She apologized, but
Skinner told her
not to worry, to seize it instead as an opportunity to examine
the impact on
a second generation. Everyone in his lab was stunned when they
found that
both chemicals wreaked significant damage. According to Skinner,
of those
exposed to vinclozolin, "greater than 90 percent of the males
developed
subfertility with a dramatic increase in developing sperm
undergoing cell
death" for not one but four generations. Further analysis
established that
the rats in both experiments had suffered germ-cell defects, the
result of a
chemical modification of their DNA. Both males and females
developed various
diseases as they aged. For example, female offspring of the
first generation
developed a condition equivalent to pre-eclampsia in human
mothers, which
can result in severe complications for the baby and death for
the mother. In
humans, incidence of pre-eclampsia has risen sharply over the
last 20 years,
and no one knows why. Skinner points out that he used a level of
toxins
higher than what people would be exposed to in ordinary
circumstances, but
he believes that "women in their mid-gestation pregnancies
should be very
cautious about their environmental exposures."
WE ARE UNPROTECTED
Fewer than a thousand of the 100,000 synthetic chemicals have
been tested
for endocrine disruption by anybody, but even the little we know
is
alarming. Sadly, the government's effort to mount a response has
been
checked continually by insufficient funding for research and
regulation, by
the complexity of the science that must be done, and by
industry's
well-funded efforts to delay the EPA's plans to test chemicals.
After the Wingspread conference, Colborn worked to raise
awareness of
endocrine disruption in citizens and legislators. With two
gifted
collaborators, John Peterson Myers and the science writer Dianne
Dumanoski,
Colborn wrote Our Stolen Future, a book for the lay reader. In
1996, the
year it was published, Congress passed ambitious legislation
mandating the
testing of all synthetic chemicals to determine whether they
cause endocrine
disruption. The Endocrine Disruptor Screening and Testing
Advisory Committee
(EDSTAC) was charged to recommend a testing protocol within two
years.
From the start, EDSTAC faced considerable obstacles. One was its
size: 39
members, including chemical company representatives and
environmental
activists, but only five bench scientists. Gina Solomon, a
Harvard-trained
physician who had just started work at the Natural Resources
Defense Council
(NRDC), where she is now a senior scientist, remembers, "It was
often hard
to get a word in edgewise, let alone talk through anything." She
adds,
"These were public meetings with audiences of up to 100, held in
anonymous
airport hotels around the country so there could be local
participation and
comment, which is a good thing, but it created a disconnect. The
committee
was charged to do a very technical scientific task."
Discussions were contentious. Representatives of some chemical
manufacturers
were accompanied by teams of lawyers who had to consult on every
issue. At
one point, the committee reached a seemingly hopeless impasse on
how to
define an endocrine disruptor. A compromise was finally achieved
when
Colborn suggested that they "describe" rather than "define" the
term. How to
define an adverse effect of an endocrine disruptor also ate up
oceans of
time. The law required an investigation of estrogenic effects of
synthetic
chemicals but did not limit the investigation to estrogen alone.
Industry
wanted to look only at estrogens, while Colborn and others
believed all
hormones should be studied. Eventually androgens were included,
and later
thyroid hormones were added as well, but it took months to reach
these
agreements. (Other hormonal systems that are not yet part of the
testing
include the pancreas, where malfunction can lead to diabetes or
obesity; the
pituitary gland; the pineal gland, which controls sleep; and the
thymus,
critical to the immune system.)
The committee was also divided about whether the goal was to
protect human
health or the health of wildlife. Colborn considered this a
false dichotomy
because she does not see animals and humans as two groups with
separate
fates. If wildlife suffers, so do humans. Yet, while evidence of
harm to
wildlife was mounting, how to pin down causal connections to
human health
remained a vexed question. Representatives of industry were
quick to exploit
the dilemma inherent in the research: They argued that anything
less than
the gold standard of experiments conducted with human control
groups would
be "unsound science," experiments that everyone agreed could
never be
conducted for ethical reasons.
Despite these difficulties, EDSTAC met its deadline: In August
1998, its
final report recommended 14 assays, or tests, and a plan for
making
decisions about how many of these tests a chemical had to pass
before it
could be deemed safe.
Not even one assay has been approved as we go to press. Before
testing can
begin, protocols have to be agreed upon for conducting each
assay and then
each assay has to be validated by running trials in multiple
labs to prove
that results are reproducible from one lab to the next.
Establishing
protocols and validating them has proved to be extraordinarily
difficult and
time-consuming.
But the work is all the more important because the chemical
companies
themselves will be responsible for conducting these tests.
Still, the
process of validating the government's battery of assays has
eaten up seven
years. Colborn says that lack of resources has been the biggest
deterrent to
progress: "With the lack of funding and the limited staff
provided to the
EPA, we could not have expected much more." Solomon of the NRDC
is
cautiously optimistic but warns that validation has seemed
within reach
several times before, only to be disrupted by unforeseen
difficulties.
Colborn fears that money and time will be thrown away testing
high doses
instead of low doses, on adult rats rather than embryos, on
Charles River
Sprague Dawley rats that won't react.
Gray is, like Colborn, keenly impatient with the delays, but he
believes the
proposed assays will tell us what we need to know. "We have
reliable
screening assays for identifying estrogens and anti-estrogens
and androgens
and anti-androgens that have been used in the scientific
community for
decades," Gray says. "These assays are reproducible, and they're
diagnostic
of endocrine effect. They produce valid, interpretable results."
SHOW US THE MONEY
Given the strength of the science and the risks in play, it
would seem that
it is time to spend the money to do the testing and move the
regulatory
process forward. Unfortunately, the reverse seems to be
happening. In 2003,
2004, and 2005, the Bush administration tried to cut all EPA
funding for
independent scientists who do endocrine-disruptor research.
While these
efforts failed, the total budget for those three years was still
less than
$15 million. (By contrast, Japan recently spent $135 million on
a research
program and has identified some 70 chemicals as endocrine
disruptors.)
Spokespeople for chemical companies maintain that the levels at
which humans
are exposed to endocrine disruptors are not dangerous. Marian
Stanley at the
American Chemical Council states: "The consensus of the research
is clear
that there is no evidence that humans have been adversely
affected by
environmental exposures to endocrine active substancesŠand there
is not
convincing evidence of a growing human health issue." Still,
there are signs
that manufacturers have read the handwriting on the wall and are
making
changes to avoid liability suits down the line. Procter & Gamble
has removed
dibutyl phthalate (DBP) from all products that it sells around
the world.
Unilever, Revlon and L'Oréal have pledged to take chemicals
banned in Europe
out of any products they sell here. Baxter International is
developing an
alternative to phthalates for its medical bags and tubes. And
methoxychlor,
one of the pesticides Michael Skinner tested that showed
endocrine damage
through four generations, quietly disappeared from the U.S.
market last year
when Drexel Chemical failed to re-register it with the EPA.
Colborn is encouraged by these developments, but she is still
extremely
worried because these few withdrawals "don't begin to clean up
the womb
environment." Solomon worries, too, particularly with regard to
food
production and supply. "Every time a pesticide is re-registered
by the EPA,
the registration contains a boilerplate statement that there is
no evidence
that this chemical causes endocrine disruption, but that after
tests are
approved there may need to be additional testing. In the
meantime, that
chemical may be affecting the health of hundreds of thousands of
farm
workers or millions of people who eat the crops that are sprayed
with that
chemical."
In addition to the chemicals already released into the
environment, 2,000
new chemicals go to market every year, and each may have the
potential to be
another DDT, a DES, a PCB, all of which turned out to be
powerful endocrine
disruptors. The biggest hurdle to solving the problem is
funding. Colborn
and others have proposed that those who profit from these
chemicals be made
financially responsible for determining the environmental safety
of their
products. Money could be paid by manufacturers into a trust, or
directly to
the government, so that manufacturers could not influence the
outcome of the
testing.
Instead of drifting along for years, nibbling away at the
problem of how to
remove endocrine disruptors from the environment, Colborn hopes
we will
throw our collective will and enough resources into finishing
the job as
quickly as possible. "Think of how many billions we've spent on
cancer
research. If these chemicals threaten our ability to reproduce,
then we
ought to be spending at least as much money on understanding how
they work
and whether we need to get them out of our environment," she
says. "If we
can't reproduce, whether we get cancer or not will be a moot
point."
...........
RELATED LINKS:
BODY BURDEN: THE POLLUTION IN PEOPLE:
http://www.bodyburden.org
ENVIRONMENTAL WORKING GROUP REPORT:
http://www.ewg.org/reports/skindeep/report/executive_summary.php
SEARCHABLE PRODUCT GUIDE:
http://www.ewg.org/reports/skindeep/browse_products.php
------------
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Published by David Sunfellow
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