FERTILITY

Colborn, Dumanosky and Meyers, Our Stolen Future, Penguin, 1997. 




FIFTY WAYS TO LOSE YOUR FERTILITY



DESPITE THE PROBLEMS IT WOULD LATER CAUSE, DES LIVED UP TO THE
promise in one regard-it mimicked natural estrogen.  This fact
alone is an intriguing puzzle, for this man-made chemical bears
surprisingly little structural resemblance to natural estrogen. 
How could it act like a hormone?
         This question lies at the heart of the deepening mystery of
how foreign chemicals trick the body and disrupt its own chemical
messengers.  In the past half century since DES appeared,
scientists have learned that DES is not unique in its hormone
effects.  One by one, they have stumbled upon many other
chemicals-both man-made and natural compounds-that act like
hormones, and gradually the realization has dawned that the world
is full of hormone disruptors.  Unlike DES, however, most don't
come in little pills.
         By an interesting coincidence, in the very same year that
Edward Dodds announced the synthesis of DES, a Swiss chemist,
Paul Meu,ller, discovered a powerful new pesticide, and both
synthetic chemicals made their debut amid great acclaim in 1938.
just as DES was heralded as a "wonder drug," DDT was hailed as a
"miraculous pesticide."
Dodds received a knighthood for his efforts in synthesizing sex
hormones, and Meuller won the Nobel Prize in 1948. 
         Twelve years after the advent of these compounds, researchers
at Syracuse University learned the two chemicals shared a deeper
kinship.  Although DDT had been developed to kill insects and not
for use as a drug or synthetic hormone, it, too, seemed to have
the effect of estrogen when it was given to young roosters: it
feminized them.  The males treated with DDT had severely
underdeveloped testes and failed to grow the ample combs and
wattles that roosters display.  In considering these results,
Verlus Frank Lindeman and his graduate student Howard Burlington
noted that the chemical structure of DDT bears a similarity to
that of DES.
         However much these two synthetic chemicals resemble each
other, these impostors do not look much like estrogen or the
other steroid hormones made by the body itself.  The steroid
hormone family is one of three hormone groups, which are
generally classified according to their chemical structure or
function.  The steroid hormones that help carry on the body's
never-ending internal conversation all share a common
architecture based on four rings.  The male and female hormones,
testosterone and estrogen, may have powerfully different effects,
but in diagrams of their chemical structure, they are remarkably
similar.  The divergent destinies of male and female hinge on an
atom here and there.  By contrast, DDT and DES .have a two-ringed
configuration.  The difference between this arrangement and that
of estrogen is immediately apparent even to someone who has never
taken chemistry.  Based on their structure, it would be
impossible to mistake these synthetic chemicals for members of
the steroid hormone family.
         Yet for reasons that still aren't fully understood, the body
does mistake them for the real thing.

         The plastic model John McLachlan holds in his hand looks like
a mass of colored bubble-gum balls.  It is the size and general
shape of a small loaf of Italian bread.
         More than two decades after he first embarked on his
exploration of DES, McLachlan is sitting on the edge of a table
in his office at the National Institute of Environmental Health
Sciences, giving a lesson in Chemical Messengers 101-the basics
on how the body communicates through hormones.  Like many natural
teachers, he has a theatrical flair and a penchant for metaphor. 
He reaches automatically for a prop to demonstrate his point. 
This isn't simply science, it is a fascinating story-the tale of
the estrogen receptor, which consorts so readily with foreigners
that it has earned a reputation.  Some scientists call it
"promiscuous."
         The plastic model is a gargantuan representation of estradiol,
one of the three principal types of estrogen manufactured by the
ovaries and dispersed into the bloodstream.
         McLachlan, a fifty-year-old man with a head of curly gray
locks and merry dark eyes that gleam like onyx, then cups his
free hand.  This is an estrogen receptor, a special protein found
inside cells in many parts of the body, including the uterus, the
breasts, the brain, and the liver.  The receptor receives the
chemical message, in this case estrogen, sent from the ovaries,
picking up signals from the bloodstream in the same way a
cellular phone picks up radio signals flying about, Like a
cellular phone, it is supposed to receive only those intended for
it.
         The body has hundreds of different kinds of receptors, each one
designed for a particular kind of chemical signal.  Some receive
messages from the thyroid gland, which may cue cells to consume
more oxygen and generate more heat.  Others are tuned to the
adrenal glands, which send messages that regulate blood pressure
and the body's response to stress.  The hypothalamus in the brain
has all kinds of receptors to monitor hormone levels in the blood
so the brain can signal the hormone-producing glands when
adjustments are needed.  And there is a whole class of mystery
receptors, known as "orphan" receptors, that are tuned to
messages that scientists have not yet identified.
         Each hormone and its particular receptor have a "made for each
other" attraction, which scientists describe as a "high
affinity." When they encounter one another, they grab hold,
engaging in a molecular embrace known as "binding."
         McLachlan demonstrates by moving the plastic model through the
air toward the receptor, showing how the estradiol docks in the
pocket of the receptor like a Star Trek vehicle returning to the
much larger mother ship.  Hormone molecules are tiny compared to
the sprawling receptors.
         They fit together, he notes, like a lock and key, and once
joined, they move into the cell's nucleus to "turn on" the
biological activity associated with the hormone.  This union of
hormone and receptor targets genes that trigger the production of
particular proteins.  In the case of estrogen, these proteins
accelerate cell division.  So when estrogen joins with receptors
in the uterus, it will cause the lining of that organ to thicken. 
Estrogen produces such a response in the first half of the
menstrual cycle to prepare the uterus in the event an egg is
fertilized when ovulation occurs at midcycle.
         This lock-and-key notion has dominated the theory of how the
body communicates through hormones.  In endocrinology textbooks,
one still finds flat assertions that receptors are highly
discriminating about chemical structure and will bind only to
their intended hormone or a very closely related compound. 
Although theory holds true in a general way, realitv is proving
considerably messier and unpredictable, not only in the case of
the estrogen receptor but with other hormone receptors as well.
         When Dodds and his colleagues announced they had developed a
synthetic estrogen, they did not understand how DES was able to
mimic the hormone in the body.  They just knew empirically that
it worked.  A quarter century passed before other researchers
discovered the receptors that receive the chemical messages and
finally came to understand what made DES effective.  It somehow
insinuates itself into this estrogen receptor.
         As he explains this, McLachlan maneuvers a model of a DES
molecule into the pocket of his imaginary receptor, which readily
accepts it as the real thing.  Surprisingly, this chemical con
artist triggers the system more effectively than estradiol, the
body's own estrogen.
         Perhaps even more important, research has discovered that this
synthetic chemical manages to circumvent a mechanism that pro-
tects a developing fetus from excessive estrogen exposure, which
can disrupt its development.  The blood of the mother and the
developing fetus contain special proteins that soak up almost all
the estrogen circulating in the blood and make it unavailable to
receptors.  But these proteins-called sex steroid binding
globulin--do not recognize DES and thus do not bind with it.  As
a consequence, only a tiny fraction of the natural estrogen in
the bloodstream will be free, but all the DES will be
biologically active.  Whether these protective substances
recognize and soak up other man-made hormone mimics is a major
unanswered question, but evidence suggests that these, too, can
make an end run around them-an unfortunate fact if true, for that
leaves the unborn all the more vulnerable to disruption.  Without
this defense mechanism to prevent overexposure to estrogenic
chemicals, even seemingly low concentrations of hormone mimics
may still pose a hazard.
         The relative strength of hormone impostors is another consid-
eration.  Most hormone impostors are considerably less potent
than DES or estradiol because they do not bind as firmly to the
estrogen receptor.  Some scientists have therefore suggested that
these "weak" estrogens are probably not powerful enough to cause
problems.  Howard Bern, a distinguished researcher who has
explored the effects of weak estrogens, is not so sanguine.  Bern
is a comparative endocrinologist at the University of California
at Berkeley and a major figure in experimental DES research.
         "The real issue is the special sensitivity of the developing
organism," Bern says.  It may be particularly vulnerable not only
because it is undergoing rapid development but also because its
hormone receptors aren't as discriminating as those of an adult. 
"It may not see the difference between weak and strong
estrogens."
         In experiments with mice, Bern found that so-called weak es-
trogens seem to have a far more potent effect on the unborn than
on exposed adults.  What happens in adults, he stresses, is no
basis for predicting what these chemicals can do to the unborn.
         It is also important to keep in mind that natural estrogens
operate at extremely low concentrations, measured in parts per
trillion.  In contrast, these so-called weak estrogens are
present in human blood and body fat in concentrations of parts
per billion or parts per million-levels sometimes thousands to
millions of times greater than natural estrogens.  So even though
the contaminant levels may seem miniscule, they are not
necessarily inconsequential.
         The understanding of hormone receptors, which has grown
rapidly since they were first identified in the mid-1960s, also
sheds light on why DES and other hormone disruptors have such
similar effects across an astonishing range of species.  Classic
accounts of evolution tend to emphasize innovation and change in
the story of life on Earth, but there has been a strong
conservative streak in evolution as well.  A good deal has
persisted through eons largely unaltered, especially elements of
basic design, such as the endocrine system.
         As scientists have explored hormone receptors in different
animals, they have marveled at the lack of change over millions
of years of evolution.  Whether in a turtle, or mouse, or a
human, the endocrine system produces a chemically identical
estradiol that binds to an estrogen receptor.  The discovery of
similar estrogen receptors in animals as distinct as turtles and
humans suggests that the internal communication system based on
hormones and receptors is an ancient adaptation that arose early
in the evolution of vertebratesthe evolutionary branch of animals
with backbones that includes humans.  Scientists believe that
turtles have undergone little change since they arose from a
reptilian ancestor over 200 million years ago, long before modern
mammals appeared on the scene.
         Although receptor research demonstrated,that impostor chem-
icals such as DDT and DES do bind with the estrogen receptor, it
has not really illuminated why the receptor readily accepts them.
The similarity between DDT and DES led scientists to expect that
they might find a common structural feature to explain the
phenomenon, but the mystery of hormone mimics would not yield to
such a simple explanation.  To their bewilderment, they found
that the estrogen receptor binds to chemicals with a variety of
strikingly different structures.  It is a lock that can be opened
with devices that bear as little resemblance to natural estrogen
as a hammer does to a key.  Even more puzzling, a wrench might
work as well as a hammer.
         DDT was, moreover,  just the first surprise.  At roughly the
same time that researchers in the United States were giving the
pesticide to chickens, other scientists from a distant continent
and an entirely different field would stumble upon another
estrogen mimic in the most bizarre place.
         The early 1940s seemed like a particularly promising time for
the sheep ranchers in the gently rolling hills south of Perth in
western Australia.  Three unusually good seasons had followed one
after another, and with the favorable weather, the pastures
exploded into lush, green growth, allowing the sheep to graze for
an exceptionally long time.  According to the ranchers in the
region, the sheep-handsome, burly merinos that produce fine,
luxurious wool-had never looked so good.
         But just when things had never been better, a strange epidemic
began hitting the flocks-an epidemic of infertility.  The first
sign was a striking increase in stillborn lambs.  Then the ewes
carrying lambs failed to go into labor; the lambs died and often
the mothers as well.  Each year the problem worsened until
finally, even after repeated breeding to fertile rams, most of
the ewes simply did not conceive at all.  In a matter of five
years, the breeding programs stopped cold, and ranchers in the
area faced financial disaster.  Without the irrepressible
exuberance of the gamboling lambs, spring did not really seem
like spring.
         After extensive detective work that involved not only the
state agricultural specialists but federal scientists as well,
researchers finally determined that the cause of the sterility
epidemic wasn't to be found in poison or disease or a genetic
defect.  The cause was clover.
         Fifteen years earlier, ranchers had started to work on improv-
ing their natural pastures by sowing a species of clover native
to the Mediterranean region in Europe.  The early strain of
subterranean clover seemed equally well suited to the local
climate and in a short time it brought great increases in the
productivity on these ranches.  For reasons the researchers could
not pinpoint at first, it also caused this strange reproductive
malady, which they named "clover disease."
         The first scientific paper on this phenomenon appeared in the
Australian Veterinary Journal in 1946, but it took several more
years to isolate three chemicals suspected of causing the
sterility.  In the end, however, researchers determined that only
one of these chemicals, formononetin, was the culprit.  This
natural compound, which escapes breakdown in the sheep's stomach,
can, like DES and DDT, mimic the biological effects of estrogen.
         Surprisingly, plant evolution had produced chemicals that mimic
estrogen long before Dodds synthesized DES in the laboratory, and
not just one or two, but many-twenty of which are now known to
science.  To date, researchers have found these estrogenic
substances in at least three hundred plants from more than
sixteen different plant families.  The list includes many foods
that feed the world as well as some of our favorite herbs and
seasonings.  Hormone mimics lurk in parsley, sage, and garlic; in
wheat, oats, rye, barley, rice, and soybeans; in potatoes,
carrots, peas, beans, and alfalfa sprouts; in apples, cherries,
plums, and pomegranates; and even in coffee and bourbon whiskey. 
Like DES and DDT, these plant compounds can fool the estrogen
receptor.
         If the clover in Australia were the only case of a natural hor-
mone mimic in the annals of science, it might be shrugged off as
an evolutionary fluke, but the presence of an estrogenic
substance in so many diverse plant species suggests this is no
accident.
         So why are plants making estrogens?"Plants are making oral
contraceptives to defend themselves," says Claude Hughes, a
researcher exploring the effects of hormonelike compounds on the
reproductive system.  It might sound like a wild idea, but from
an evolutionary perspective it makes sense.
         Since plants cannot escape predators by running away, they have
evolved a fascinating variety of defenses.  Some smell bad, taste
bad, or poison those that eat them.  Others have unpalatable
thorns, spines, or indigestible substances in their leaves.  When
insects attack, many plants fight back with a chemical arsenal
that can kill insects outright, make them stop feeding, or
disrupt their growth by mimicking insect growth regulator
hormones.  This growth disruption typically makes an insect
sterile, thus reducing the troubling insect population.
         The more Hughes explored the notion that plants might be making
contraceptives, the more evidence he found consistent with the
theory that this is indeed what plants are up to.  By lacing
their leaves with hormonally active substances, they suppress the
fertility of the animals that feed on them.  By Hughes's theory,
clover disease isn't simply an unfortunate livestock malady, it
is a subtle and previously unrecognized form of plant self-defense.  
The plants that make estrogen mimics, he notes, are
tasty ones sought out by animals and humans for food, not the
unappetizing plants that contain foul-tasting compounds-an
alternative defensive strategy.
         Hughes is a specialist in reproductive endocrinology at the
Bowman Gray School of Medicine, Wake Forest University, in Win-
ston-Salem, North Carolina, who holds an M.D. as well as a Ph.D.
in neuroendocrinology, the study of the interaction between the
brain and hormones.  As an undergraduate, he pursued research in
lant physiology.  He is also the son of a farmer and now raises
sheep on his own farm in North Carolina, so he brings firsthand
experience to the task as well.
         The thought that plants might be making chemicals aimed at un-
dermining the fertility of their predators first occurred to
Hughes while he was a doctoral student studying the impacts of
marijuana on the brain.  Humans have long used marijuana as a
drug because the chemicals it contains act in the brain to alter
mood and perception, creating a "high." But as Hughes and others
discovered, these chemicals do more than induce a pleasant
mellowness; they interfere with reproduction in a variety of
ways.  The same compound that makes a pot smoker high also acts
on the testicles to reduce the synthesis of testosterone and on
the brain to suppress lutenizing hormone, a key hormone that cues
ovulation in females and testosterone production in males. 
Studies have reported that marijuana feminized men who smoked it
heavily.
         Hughes's work focused on the way that marijuana interferes with
the hormone prolactin, which is produced in the brain and signals
the breast to produce milk.  Mother rats given marijuana produced
no milk, and their pups died of starvation.  Hughes later moved
on to investigate the effects of plant estrogens on the endocrine
system and the hormones that orchestrate reproduction, an area
few scientists had explored.
         For such a defensive strategy to work, he explains, the plant
would logically target females rather than males because a
predator's reproduction is limited. by the number of fertile
females.  If, for example, a plant managed to impair the
fertility of all the males save one, that single male can,
nevertheless, fertilize an entire flock of females.  But if only
a single female is fertile, she can produce only one or two lambs
         Plants containing estrogen mimics produce them according to a
seasonal pattern that fits perfectly with this strategy.  Clover
packs the greatest concentrations of estrogenic compounds into
the new growth in spring, and when a rabbit or a sheep injures it
by munching on these tender shoots, the plant responds by
producing even more estrogen at the site of injury, delivering an
added dose to predators that continue grazing.
         Humans long ago figured out that certain plants have
contraceptive powers, judging from references in classical
literature.  Historian John M. Riddle of North Carolina State
University reports that women throughout the ancient world used a
variety of plants to prevent pregnancies and precipitate
abortions, including a now extinct giant fennel called silphium. 
Researchers have confirmed that many plants in the fennel family
produce estrogenic substances or other hormonally active
compounds.  The ancients also used wild carrot, the beautiful and
delightfully common weed now known as Queen Anne's lace, which
the Greek physician Hippocrates, who lived in the fourth century
B.C., described as having similar powers.  Studies have shown
that its seeds contain chemicals that block the hormone
progesterone, which is necessary for establishing and maintaining
pregnancy.
         The pomegranate played a central role in both Greek myth and
their birth-control efforts.  According to the myth, Persephone,
the daughter of the fertility goddess Demeter, was told to eat
nothing during a visit to the underworld Hades, but she disobeyed
and ate a pomegranate.  As punishment, the gods sentenced her to
spend a part of the year in the underworld, and for this reason,
Earth experiences the barren season of winter until Persephone
returns each spring.  Riddle says the Greeks used pomegranate as
a contraceptive, and here again studies have found that it
contains a plant estrogen that acts like the chemicals found in
modern oral contraceptives manufactured by the pharmaceutical
industry.
         The presence of estrogenic compounds in so many foods raises
an important question.  Do these substances pose a hazard to
human health or to the development of babies?
         There is no simple answer to this question.  Plants containing
estrogen mimics may be beneficial in some instances and hazardous
in others, according to Patricia Whitten, an anthropologist
working at the Laboratory of Reproductive Ecology and
Environmental Toxicology at Emory University in Atlanta, Georgia. 
Scientists are just beginning to explore plant estrogens and how
these hormone mimics in food affect us, so fundamental 
questions-such as how much we actually ingest in our foods-remain as yet
unanswered.  Because humans eat a varied diet, it is not clear
whether we ingest sufficient quantities to worry about.  The dose
question is, moreover, inherently tricky when dealing with
hormones.  Depending on your age, sex, and hormonal status, the
same dose can have wildly different effects.  It will matter
whether you are a man or a woman; a postmenopausal woman or one
still in her reproductive years; an adult, a child, or a baby
developing in the womb.
         Whitten has found that exposure to plant estrogens early in
life can undermine the ability of rat pups to reproduce when they
grow up. In her experiment, the rat mothers were given low doses
of coumestrol, a plant estrogen found in sunflower seeds and oil
and alfalfa sprouts, which they passed on to their babies through
their milk.  Rats are considerably less developed than humans at
birth, so in the days after birth they are undergoing stages of
development that in humans occur in the womb.
         The pups in this experiment did not suffer obvious genital de-
fects or other physical abnormalities in the reproductive tract
as seen in the DES experiments, but they showed evidence of
permanent changes that sabotaged their fertility.
         "We think we've altered the sexual differentiation of the
brain," Whitten says of the exposure, The females don't ovulate
and are sterile because their brains do not respond to the
hormone that triggers ovulation-an indication that they have been
masculinized.  The males, on the other hand, are feminized,
showing less mounting behavior and fewer ejaculations.  For a
rat, the first ten days after birth are the critical period for
the development of those areas of the brain linked to sexual
behavior.
         But the very same foods that disrupt development before birth
or early in life might help prevent'disease in an adult. 
Evidence that foods high in plant estrogens, such as soybeans,
might protect against breast and prostate cancer has sparked a
great deal of scientific interest and new research into plant
estrogens.  Numerous studies have linked estrogens, even those
naturally occurring in the body, to cancer, suggesting that the
greater a woman's lifetime exposure, the greater the risk. 
Researchers theorize that plant estrogens might be protective
because they are weaker than the natural estrogens made in the
body.  If they occupy estrogen receptors in the breast and
displace natural estradiol, they might reduce a woman's lifetime
exposure to estrogen.
         The thing to keep in mind, Hughes says, is that plants and the
animals that eat them, including humans, share a long
evolutionary history.  Over many generations, the most sensitive
individuals, those who became sterile from eating estrogenic
foods, dropped out of the population.  All those who were able to
produce at least some offspring passed on a certain degree of
resistance.  This sort of evolutionary winnowing occurs because
of individual differences.
         The discovery that DDT could act like an estrogen must have
seemed like a singular curiosity in 1950, but unfortunately, it
has proved far from unique.  Over the past half century, the same
chemical laboratories that produced this "miraculous" pesticide
created a host of other synthetic chemicals that can also
interfere with hormones.  We have been slow to recognize this
threat or to realize that the world has become permeated with
hormone-disrupting synthetic chemicals.
         When male workers in a chemical plant developed extremely low
sperm counts after exposure to the pesticide kepone, it became
clear that DDT was not the only synthetic chemical capable of
producing estrogenlike effects.  Others were quickly added to the
list.  Like DDT, these synthetic chemicals were not intended as
drugs or hormone mimics.  They were invented by chemists in
laboratories to kill insects threatening crops and to give
manufacturers new materials such as plastics.  Inadvertently,
however, the chemical engineers had also created chemicals that
jeopardize fertility and the unborn.  Even worse, we have
unknowingly spread them far and wide across the face of the
Earth.
         How many man-made chemicals scramble the body's chemical
messages?  No one knows and no one has systematically screened
the tens of thousands of synthetic chemicals created since World
War 11 for such effects.  As with kepone, which is now banned,
many of those that are known have been discovered by accident.
         To date, researchers have identified at least fifty-one
synthetic chemicals-many of them ubiquitous in the environment-that disrupt the endocrine
system in one way or another.  Some
mimic estrogen like DES, but others interfere with other parts of
the system, such as testosterone and thyroid metabolism.  This
tally of hormone disruptors includes large chemical families such
as the 209 compounds classified as PCBS, the 75 dioxins, and the
135 furans, which have a myriad of documented disruptive effects.
         Most discussions of hormone-disrupting chemicals inevitably
focus on DDT, the PCBS, and dioxin, but not because they
necessarily pose the only or the gravest threat.  These get the
lion's share of the attention because they happen to be the only
hormone-disrupting chemicals that scientists have studied in any
depth.  While admittedly far from the whole story, these 
well-known cases do, however, serve to illustrate a much broader
problem, so they will also receive considerable attention in this
book.  The magnitude of this problem is still unclear, but those
who have watched the list of hormone.disruptors grow think the
age of discovery is far from over.  "There are probably a lot
more," says John McLachlan.
         As the number of hormone-disrupting chemicals mounts, Claude
Hughes worries, emphasizing that humans lack evolutionary history
with these synthetic compounds.  These man-made estrogen mimics
differ in fundamental ways from plant estrogens, he notes.  The
body is able to break down and excrete the natural estrogen
mimics, while many of the man-made compounds resist normal
breakdown and accumulate in the body, exposing humans and animals
to low-level but long-term exposure. This pattern of chronic
hormone exposure is unprecedented in our evolutionary experience,
and adapting to this new hazard is a matter of millennia not
decades.  He worries that some portion of the population is bound
to be sensitive.  He worries about his daughter and son and the
grandchildren he anticipates in years hence.  What if his kids
are among the sensitive?  What if they can't reproduce because of
eating this stuff?
         Some might be tempted to jump to the conclusion that because
so many natural estrogens already exist in nature, there is
therefore no need to worry about synthetic chemicals that
interfere with hormones.  This kind of argument has surfaced in
the discussion about carcinogenic substances, since some
researchers have discovered that cancercausing substances can be
produced through natural processes as well as through industrial
ones, and it has left most ordinary people hopelessly confused. 
Many simply shrug and say why worry if everything can cause
cancer.  In this case, however, it is important to recognize the
crucial differences between natural and synthetic hormone mimics. 
Many of the man-made hormone mimics pose an even greater hazard
than natural compounds because they can persist in the body for
years, while plant estrogens might be eliminated within a day.
         Regardless of whether natural or man-made, there is reason to
be cautious with all hormone-disrupting chemicals.  It is true
that humans have adapted over millions of years to the presence
of hormone mimics in many food plants.  But while we may have
evolved ways to coexist with such compounds, this does not mean
they are harmless.  One should never lose sight of the reason
plants make them: to sabotage fertility.  Our ancestors took
advantage of these potent chemicals by using giant fennel, wild
carrot, and pomegranate for birth control and abortions.  Even
naturally occurring bormone mimics can disrupt development of the
unborn or young children.  Based upon animal studies concerning
the developmental effects of plant estrogens, Hughes questions
the wisdom of baby formulas containing soy, which harbors
estrogenic compounds, until more comprehensive studies are
completed.

         If some scientists are seeking to identify hormone-disrupting
chemicals, others are exploring the hazards they might pose.
         In the darkened laboratory at the U.S. Environmental Pro-
tection Agency's Health Effects Research Laboratory in Research
Triangle Park, North Carolina, slides showing rat genitals,
scrambled gonads, and all manner of sexual confusion flash onto
the screen.  The man at the control button is Earl Cray, a
reproductive toxicologist, who makes his living by studying how
chemicals disrupt sexual development.  He is describing all the
ways that synthetic chemicals wreak havoc with hormones and
showing the consequences to those exposed in the womb.  His
fascinating, and disturbing slide show brings to mind the title
of the Paul Simon song but with a slight revision.  There must be
fifty ways to lose your fertility-or more.
              He stops on a picture of a rat abdomen, that of a male
rat who looks like a female.  Gray points out the pink nipples
protruding through the rat's white fur.  Male rats in this breed
aren't supposed to have any nipples at all.  This male's sexual
development went awry because its mother was exposed during
pregnancy to vinclozolin, a synthetic chemical that is widely
used to kill fungus on fruit.  Vinclozolin was frequently
detected in the foods children commonly eat in the United States.
              Vinclozolin disrupts development as dramatically as DES
or other estrogen mimics but causes its havoc in a different way. 
First of all, it targets the androgen receptor, which is tuned to
the male hormone testosterone, rather than the estrogen receptor. 
Like the mimics, this chemical occupies the receptor, but unlike
them, it does not turn on the biological response normally
triggered by testosterone.  Instead, viiiclozolin simply blocks
the receptor and doesn't let the testosterone messages through. 
This is like jamming the line on a cellular phone so it is always
busy and the intended messages are blocked.  Without these
testosterone signals, male development gets derailed and boys
don't become boys.  Instead, they become stranded in an ambiguous
state, where they cannot function as either males or females.  In
scientific terms, these are "Intersex" individuals or her-
maphrodites-a term that comes from the Greek deity Hermaphrodite
whom classical sculptors portrayed as a figure with male genitals
and female breasts.
         Gray and his colleague William Kelce have also recently
discovered that DDE, a ubiquitous chemical and the DDT breakdown
product found most often in the human body, acts as an androgen
blocker.  Like vinclozolin, it binds to and blocks the androgen
receptor, so the body's own signals do not get through.  Gray
believes there are more anti-androgens to be discovered and more
out in the environment than anyone has suspected.
         Gray is trying to drive home a point that is often overlooked:
estrogen mimics are only one manner of hormone disruption, only
one of the hazards to sexual development and fertility.  All too
frequently, the threat from hormone-disrupting chemicals is seen
solely as a problem of estrogen mimics.  This is perhaps
understandable.  Because of the DES experience, scientists have
studied man-made chemicals that can bind to the estrogen receptor
for more than two decades, describing everything from the action
on the cellular level to lifelong impacts on humans exposed in
the womb.  In any discussion of the potential hazard, DES is
bound to serve as the principal reference point.  There is
certainty about how it works.
         The obliging nature of the estrogen receptor is another reason
estrogen mimics receive a good deal of attention,.  Scientists
never did find a simple structural characteristic common to all
the foreign chemicals that the estrogen receptor consorts with,
though they speak vaguely about the fact that these molecules are
flat or "planar." The fact remains, however, that the estrogen
receptor binds to many chemicals with strikingly different
structures.
         The politics of the breast cancer issue have also helped push
estrogen to center stage.  Since estrogen exposure increases the
risk of breast cancer, researchers have been exploring links
between breast cancer rates and estrogenic compounds that
accumulate in breast tissue and other fatty parts of the body. 
Some grassroots advocacy groups have seized upon synthetic
chemicals as the leading suspect for what is behind the steady
one percent a year increase in breast cancer rates since World
War II.
         But there are dangers in focusing so narrowly on estrogen,
warns Linda Birnbaum, the head of the environmental toxicology
division at the EPA's Health Effects Research Laboratory. 
Estrogen is just one component in the complicated, integrated
endocrine system, and, she says, synthetic chemicals target other
parts of the system more commonly than they disrupt processes
involving estrogen. The adrenal glands, which produce stress
hormones, get hit more than any other organ by man-made
compounds, followed by the thyroid gland.  Insults in any part of
one system tend to quickly ripple through other systems of the
body as well.  So while breast cancer could be linked to
estrogenic pesticides, it could also be linked to other kinds of
hormone disruption.  Birnbaum notes, for example, that depressed
thyroid levels have been linked to breast cancer just as
increased estrogen exposure has.
         However important, estrogen and the receptor mechanism are far
from the whole story on endocrine disruption.  Man-made chemicals
scramble all sorts of hormone messages, and they can disrupt this
communication system without ever binding with a receptor.  If
cellular phone messages aren't getting through, the problem isn't
necessarily with your phone.  There may be trouble somewhere else
in the system, such as in the satellite that relays the message
from continent to continent or the transmitter that sends the
message into space.  The same holds true with the endocrine
system.
         "If we're thinking only in terms of estrogenicity, we're
missing the boat," Earl Gray warns.
         For example, another large class of fungicides, members of the
pyrimidine carbinol family, inhibit the body's ability to produce
steroid hormones in the first place, so vital messages are never
sent.  Curiously, they interfere with hormone production for
exactly the same reason they prevent fungi from growing, by
inhibiting the synthesis of fatty compounds called sterols.  The
fungus needs these fatty substances to form cell membranes, and
without them, its growth screeches to a halt.  Humans and other
mammals form steroid hormones from a much talked about member of
this same chemical family, cholesterol.
         And even within the group of compounds known to disrupt es-
trogen levels, other mechanisms can be at work.  Although DDT is
regarded as a classic estrogen mimic that elevates hormone
levels, this is only one of its effects in the body.  According
to Gray, DDE, the form of DDT that persists the longest in the
body fat of humans and animals, has the opposite effect.  It
depletes hormones by accelerating their breakdown and
elimination, leaving the body short not just of estrogen but of
testosterone and the other  steroid hormones as well.  This can
lead to abnormally low hormone levels.  Since a developing fetus
is extremely sensitive to hormone levels, too little can be as
devastating as too much.
         On the other hand, foreign chemicals that do not act as hor-
mone mimics or blockers may boost the body's hormone levels by
interfering with the physiological processes that break down
hormones so they can be excreted.  Some chemicals deactivate the
enzymes involved in this process, according to Michael Baker, an
enzyme specialist at the University of California at San Diego. 
If some chemical interfered with the enzyme that helps break down
estrogen, for example, it would cause more estrogen to be
available to the receptors and indirectly create an estrogenic
effect without binding itself to the receptor.  Based on the
body's response, one might mistake such a chemical for a hormone
mimic.
         In Earl Gray's view, animal studies of hormone-disrupting chem-
icals have clear and immediate relevance to humans.  In the
broader environmental debate, some have challenged the predictive
value of rat studies to assess possible cancer risks posed by
synthetic chemicals to humans on the grounds that animals and
humans sometimes react differently to a chemical.  The use of
animals to study hormone-disrupting chemicals is, however,
fraught with less uncertainty, Gray explains, because scientists
understand far more about the role of hormones in development
than they do about the biological events that give rise to
cancer.  Moreover, the evidence shows that humans and animals
respond in generally the same way to hormone-disrupting
chemicals.  The available human data and the effects seen in lab
animals show "a perfect correlation." Earl Gray spells out the
bottom line with intensity and directness.
         "We know a lot about the process.  We know it can be altered
by chemicals.  It is important to take the effects you see in
animal studies seriously."


DEFENDING OURSELVES



THE THREAT EXPLORED IN THIS BOOK MAY SEEM OVERWHELMINg, ESPE-
cially to those confronting it for the first time.  Feelings of
fright and helplessness are, in our experience, not unusual. 
This is indeed a frightening problem.  No one should
underestimate its seriousness, even though the magnitude of this
threat to human health and wellbeing is as yet unclear.  It would
likewise be dangerous to retreat into denial, which can be a
strong temptation in the face of large, insidious problems that
leave individuals feeling helpless and hopeless.
         But however grim and unsettling the facts appear in this in-
stance, facts are not fate.  Trends are not destiny.  Three
decades ago, Rachel Carson's predictions about the impacts of
synthetic pesticides led to major changes in their use and thus
prevented much of the apocalyptic "silent spring" she envisioned. 
Today, the growing scientific knowledge about endocrine-disrupting 
chemicals gives us similar power to avert the hazards
outlined in previous chapters.  This should be reason for hope
rather than despair.
         Unfortunately, however, solutions to this problem will be nei-
ther quick nor easy.  Much of the concern qbout hormonally active
synthetic chemicals arises from the persistence that many of them
have in the environment.  Many don't readily degrade into benign
components.  A generation after industrial countries stopped the
production of the most notorious of these persistent chemicals,
their legacy endures in food and in human and animal bodies. 
Some will be in the environment for decades, and in a few cases
even centuries.  At the same time, other hormonally active
chemicals remain in production, and unexpected new sources of
exposure continue to come to light.  Most disturbing of all, many
of us already carry contamination levels that may put us and our
children at risk.
              Defending ourselves from this hazard requires action on
several fronts aimed at eliminating new sources of hormone
disruption and minimizing exposure to hormonally active
contaminants already abroad in the environment.  This will entail
scientific research; redesign of chemicals, manufacturing
processes, and products by companies; new government policies;
and efforts by individuals to protect themselves and their
families.  Tragically, there is no way to repair the damage done
to individuals who now suffer impairments stemming from
chemically caused disruption during their early development. 
Such damage cannot be undone.  But with diligent work by govern-
ment bodies, scientists, corporations, and individuals, we can
reduce the threat to the next generation.  Over time, the ill
effects now evident in wildlife and humans could diminish and
gradually disappear.
              That is the good news in this troubling picture.  Although
hormone-disrupting chemicals can cause grievous, permanent damage
to those exposed in the womb, they do not attack genes or cause
mutations that persist across generations.  They have not altered
the basic genetic blueprint that underlies - our humanity. 
Remove the disruptors from the mother and the womb, and the
chemical messages that guide development can once again arrive
unimpeded.
              Up to now, women have generally assumed that they could help
ensure the health of their children by being vigilant during
pregnancy about what they eat and drink and about exposure to X
rays, pesticides, and other toxic chemicals.  Such short-term
prudence will certainly protect the unborn child from many kinds
of permanent damage, including the devastating neurological
effects of alcohol.  But protecting the next generation from
hormone disruption will require a much longer vigilance over
years and decades-because the dose reaching the womb depends not
only on what the mother takes in during pregnancy but also on the
persistent contaminants accumulated in body fat up to that point
in her lifetime.  As discussed earlier, women transfer this
chemical store built up over decades to their children during
gestation and during breast-feeding.
              Thus, it is critical that we as individuals and as a society
make choices that reduce this chemical legacy that is being
passed from one generation to the next.  In the interest of the
coming generation and those that follow, we must limit what
children are exposed to as they grow up and keep the toxic burden
that women accumulate in their lifetimes prior to pregnancy as
low as possible.  Children have a right to be born chemical-free.
              Our day-by-day choices as consumers will have dramatic
effects on such exposure and, potentially, an impact that ripples
across generations.  The food we ourselves eat may help safeguard
our children.  The way we raise and feed our daughters may help
protect our grandchildren.
              There are admittedly many unknowns and uncertainties, but
until definitive answers are available, a few simple guidelines
can help prevent unneeded risk.



Know Your Water

You have a right to know what is in your water.  Consider the in-
tegrity of your water supply, and don't be lulled into false
assumptions about its safety.  If you drink well-water, be
concerned about groundwater contamination, especially if you live
in the Midwest or other agricultural areas.  The risk to drinking
water supplies may be greatest during and immediately after the
peak seasons for pesticide
application.
         If your water comes from a community source, find out about
your water authority's testing program and what it has found. 
Urge them to test at least monthly and to make the results
public.  They have a fundamental responsibility to tell you what
is in your water and allow you to make judgments about what ri
sks to take.  Tell your water officials you are interested in
whether they have tested for hormonedisrupting chemicals,
especially the herbicides atrazine and dacthal.  These chemicals
are often sentinels.  If either is found, other pesticides are
likely to be present as well, and weekly testing is warranted
during the growing season, when farmers are applying pesticides
to their fields.
              Testing your own water is expensive, and few laboratories
serving the consumer market are capable of making a thorough
assessment of hormone-disrupting chemicals.  But a new generation
of tests now under development may soon change the practical
options available to individual homeowners.  Until then,
consumers will have to make sure that their public water company
is doing sufficient testing to verify the safety of drinking
water.  Although many hormone-disrupting chemicals 
are chlorine-containing compounds, the treatment of drinking water with
chlorine is unlikely to contribute to the hazards of hormone
disruption.
              Do not count on filters that are designed primarily to remove
bacteria, microrganisms, and unpleasant tastes and odors.  They
may not remove the hormonally active synthetic chemicals.
              Do not assume that bottled springwater is properly regulated
or uncontaminated, especially-if bottled in plastic.
              People living in areas with questionable water supplies may
wish to distill their drinking water as they work to improve the
quality of their public water supply.  Home distilling units are
available.  But distillation is only a radical, short-term step. 
It is wholly impractical as a widespread solution to water
contamination.



Choose Your Food Intelligently

Clean fish is one of the most healthful sources of animal
protein.  Yet, as we've seen, fish can also be a source of
contamination.  For this reason, consumers should scrupulously
heed any warnings about fish contamination.  Because of concerns
about lost license revenues and tourist dollars, public officials
are seldom hasty about imposing warnings about contamination in
fish and rarely, if ever, do they do so without extremely good
cause.  In the United States, state fish and game departments are
usually the agencies that issue such fish advisories in
cooperation with health officials.  These public notices typi-
cally advise that pregnant women avoid consuming fish caught in
certain areas and that others limit their intake to a recommended
number of fish meals per month.
         If anything, these warnings are often insufficiently prudent. 
Children and. women who are not past the age of child-bearing
should avoid fish contaminated with persistent hormone-disrupting
chemicals such as dioxin, PCBS, and DDE.  And it is probably wise
for everyone else to forgo them as well.  Any fisherman tempted
to ignore the.warnings should recall the studies cited earlier
before delivering his catch to his family's dining table.  Human
studies-done by the Jacobsons have reported that children of
mothers who ate contaminated Great Lakes fish show evidence of
delayed neurological development and diminished head size at
birth.  Helen Daly found the offspring of female rats fed Lake
Ontario salmon to be less tolerant of stress, and parallel human
studies done by her colleagues showed evidence of reduced stress
tolerance in children of women who ate Lake Ontario fish.
         Avoid animal fat as much as possible.  As the journey of the
PCB molecule in Chapter 6 demonstrated, many of these chemicals
travel through the food web in fat and become more concentrated
as they move upward to the top predators such as polar bears and
humans.  In a 1994 report, the U.S. Environmental Protection
Agency found that meats and cheeses are a major source of dioxin
exposure in the United States today.  So eating less animal 
fat-found in foods such as butter, cheese, lamb, beef, and other
meats-will greatly reduce exposure to hormone-disrupting
chemicals.  Again, it is particularly important that women
minimize the consumption of animal fat from birth until the end
of their childbearing years.  They bear the next generation and
the responsibility to protect their children from contamination. 
Moreover, a family diet rich in vegetables, grains, and fruits
has a multigenerational benefit, for it will reduce the risk of
heart disease and cancer for adults and may help protect your
children and grandchildren from prenatal hormone disruption.
         Buy or raise your own organically grown fruits and vegetables. 
If they aren't available at your supermarket or are too
expensive, look to see if your grocer offers produce that has
been tested and found to have "no detectable sk your grocer if
the grocery chain screens its food for contaminants or buys from
suppliers that do.  You have the right to know what is in the
food you buy.  Encourage your grocers to stock and promote
organic produce.  Give them a copy of this book.  Supporting
organic agriculture may help safeguard water supplies as well as
reduce your family's exposure to pesticide residues.
         Minimize contact between plastic and food and avoid heating or
microwaving food in plastic containers or with plastic wrap.  Use
glass or porcelain for microwave cooking.  It is entirely
possible that some plastics will turn out to be harmless.  But
with the discovery that hormone-disrupting chemicals leach out of
some plastics, caution is warranted, at least until the research
is completed or until the sellers of plastic ware can guarantee
their products do not release chemicals into food and beverages.
          Researchers are only beginning to appreciate the myriad
benefits of breast-feeding, which not only aids in mother-baby
bonding but also provides infants with important immune
protection and a host of substances that enhance development.  At
the same time, breastfeeding exposes infants to disturbing levels
of chemical contaminants, including a number of known hormone
disruptors.  According to various studies of breast milk
contamination, nursing babies take in the highest doses of
contaminants they will experience in their entire lives-levels
ten to forty times greater than the daily exposure of an adult. 
It is indeed tragic that breast-feeding is the only efficient way
to remove these persistent chemicals from the human body.
         We know too little to judge how the undeniable benefits of
breast-feeding balance against the risks of transferring
hormonally active contaminants.  While we have great concern, it
is premature to advise women against breast-feeding.  Moreover,
some studies suggest that the transfer of contaminants in the
womb before birth may have a far greater impact than any transfer
taking place during nursing.  Thus, by the time'of breast-feeding
much of the potential impact may have occurred.  There is a
pressing need for research to determine whether the
concentrations of hormone-disrupting chemicals in human milk pose
enough of a hazard to make breast-feeding inadvisable for some
women, perhaps those having their first child later in life. 
These older women will generally carry a much higher burden of
per-
sistent chemicals than first-time mothers who are twenty.  Though
cow's milk lacks some of the specific benefits of human milk, it
contains only one-fifth the concentration of persistent
contaminants because cows are shorter-lived animals, vegetarians,
and are constantly eliminating contaminants from their body as
they are milked daily.  We cannot afford to ignore the pressing
issue of persistent contaminants when weighing the merits of
breast-feeding against alternatives such as bottle feeding with a
formula based on cow's milk.

Avoid Unnecessary Uses and Exposure

Wash your hands frequently.  Studies show that many synthetic
chemicals vaporize and then settle on indoor surfaces-counters,
tables, furniture, clothes-where they can be readily picked up by
those who touch them.  In fact, indoor air experts now sample for
contaminants in buildings by wiping surfaces with special
equipment.  Developing the habit of handwasbing, especially in
the case of children who often sit or play on the floor, is a
simple,,effective way to reduce exposure.
         Never assume a pesticide is safe.  Anything designed to
disrupt living organisms-plant or animal-may also prove harmful
to humans or other animals in unexpected ways.  Recall EPA
researcher Earl Gray's discovery that products designed to kill
fungus on fruits and vegetables can interfere with the synthesis
of steroid hormones in animals and most likely in humans as well. 
The casual use of pesticides around homes and gardens for
frivolous, cosmetic purposes is risky and irresponsible.  In the
United States, greater quantities of pesticides are applied per
acre in the suburbs than on agricultural land, much of it to
support the national obsession with green, weed-free lawns. 
Studies have found higher rates of cancer in children and dogs
living in households that use pesticides in the home and garden. 
The epidemiological studies done to date have not looked for the
kinds of functional and developmental problems described in this-
book.
         Make your own lawn pesticide-free and encourage your neigh-
bors to do so.  If they persist in their use of pesticides,
insist that they post their lawns at the time of treatment.  Keep
your children and pets away.  Organize within your neighborhood
to set strict standards for chemical treatment of lawns.  Lawn
care services sometimes try to reassure uneasy customers by
telling them that the pesticides used are "EPA approved." The
Environmental Protection Agency has never screened most of the
pesticides now on the market for hormonedisrupting activity, and
U.S. Environmental Protection Agency registration is no measure
of safety.  In fact, chemical companies register with the EPA
precisely because a product is potentially harmful.  Labeling
reduces the legal liability of the manufacturer in lawsuits
brought by people harmed by using the pesticide.  If necessary,
stop growing plants or shrubs that require such chemical support
to look presentable and replace them with insect- and 
disease-resistant alternatives.  Pesticides should be used only in
genuine emergencies.
              Don't be blase about the risks that come along with household
pest control, whether you do it yourself or hire a professional
exterminator.  Following the label won't eliminate the risks to
you and your children, but it will reduce them.  Use pesticides
in your home only if absolutely necessary and, if you do so,
follow the label instructions very carefully.  It is also
important to keep in mind that most pesticides are mixtures of
active and "inert" ingredients, and some compounds used as
"inerts," such as the nonylphenols and bisphenol-A-are recognized
endocrine disruptors.  The pesticide labeling law unfortunately
does not require manufacturers to list inert ingredients, and
legal "trade secrets" provisions allow them to avoid disclosure
to consumers.  So you cannot tell by looking at a product label
whether a pesticide con tains an endocrine-disrupting ingredient.
              Make a concerted effort to control fleas on pets without
insecticides.  This is safer for your pet and your family. 
Moreover, many flea control products have become increasingly
ineffective because heavy use has hastened the evolution of
pesticide-resistant superfleas.  Frequent grooming, use of a flea
comb, and regular baths with a noninsecticidal shampoo can help
keep fleas off your dog or cat.  You can prevent fleas from
gaining a foothold in your house by vacuuming regularly and
thoroughly, especially around cracks and baseboards, and by
washing your pet's bedding often.  Some recommend sprinkling
diatomaceous earth, a natural inert product found on the shelf in
garden stores, in your pet's favorite areas to discourage fleas.
         Find out how your local merchants treat their stores or
facilities for pests.  It has come to light that, some
supermarkets in the United States have been fogging their produce
with pesticides.  Few states provide effective guidance for
pesticide application in retail areas or in hotel rooms. 
Pesticide-free hotel rooms should be a regular option for 
health-conscious consumers, just as smoke-free rooms now are.  Asking
for them shows there is a consumer demand.
         Be aware that golf courses present a great potential for expo-
sure.  By one conservative estimate, based on a report of
pesticide use on Long Island golf courses, golf course managers
use at least four times more pesticide per acre than farmers. do
on food crops.  Seven of the fifty-two pesticides used on the
Long Island golf courses surveyed disrupt the endocrine system
and hormones.  Other pesticides in use there have been classified
as probable or possible carcinogens.  Find out what your local
course applies and when, so you can play at other times.  Keep
your hands away from your mouth while golfing, don't chew on
tees, and wash your hands after leaving the course.  Do not fish
on golf courses or downstream of them.
         Give babies unpainted, unvarnished toys made of wood or nat-
ural fibers.  If your young children must have plastic toys, make
sure t hey do not chew on them.

Improving Protection

While individuals can do a great deal to protect themselves,
these efforts must be matched by broad government action to
eliminate synthetic chemicals that disrupt hormones.
         It is beyond the scope of this book to provide a detailed
critique of the laws and regulations relevant to this problem. 
Nonetheless, it is possible to identify several basic principles
that can inform future efforts to improve the laws protecting
people and ecosystems.
         Following the model of the 1987 Montreal Protocol, an interna-
tional treaty that mandates the phase-out of chlorofluorocarbons
and other ozone-depleting chemicals, the United States and other
nations should move quickly to implement comprehensive
international treaties to halt the use and ecological dispersal
of biologically active persistent compounds such as PCBS, DDT,
and lindane.  While negotiating such international environmental
agreements is admittedly challenging, past experience has shown
that governments can come together and act in the face of a
genuine threat to human welfare.  These protocols on persistent
hormone-disrupting chemicals should phase out the production and
use of these compounds worldwide and provide institutional and
financial support for their containment, retrieval, and cleanup.
         As a first step, these protocols should require the prior in-
formed consent of countries that are importing chemicals that be-
come persistent contaminants.  The exporting business or agency
should be required to notify an international monitoring body of
each trade and to notify the importing country of the nature of
the compounds and the associated risk.
         At the same time, individual nations should move to revise do-
mestic laws governing environmental health standards to ensure
that they provide protection from chemicals that interfere with
hormones.  Such revisions should include the following key
points:

         Shift the burden of proof to chemical manufacturers.  Chemical
         materials continue to be regulated with very inadequate and in-
         complete information.  To a disturbing degree, the current sys-
         tem assumes that chemicals are innocent until proven guilty. 
         This is wrong.  The burden of proof should work the opposite
         way, because the current approach, a presumption of innocence,
         has time and again made people sick and damaged ecosystems.  We
         are convinced that emerging evidence about hormonally active
         chemicals should be used to identify those posing the greatest
         risk and to force them off the market and out of our food and
         water until studies can prove their impact to be trivial. 
         Every new compound should be subjected to this test before it
         is allowed to enter into commerce.  The tool of risk assessment
         is now used to keep questionable compounds on the market until
         they are proven guilty.  It should be redefined as a means of
         keeping untested chemicals off the market and eliminating the
         most worrisome compounds in an orderly, timely fashion.

.        Emphasize prevention of exposure.  Many hormone disrupting
         chemicals alter normal developmental processes, causing perma-
         nent consequences that cannot be reversed or even mitigated
         through later treatment.  Because these effects are usually
         irreversible, treatment after the fact is an unsatisfactory
         solution.  The goal must be to prevent exposure to such
         chemicals in the first place by eliminating the use and release
         of hazardous compounds.

Set standards that protect the most vulnerable, namely children
and the unborn.  Today's standards have been developed based on
the risk of cancer and gross birth defects and calculate these
risks for a 150-pound adult male.  They do not take into consid-
eration the special vulnerability of children before birth and
early in life.

         Consider the interactions among compounds, not just the effects
         of each chemical individually.  Government regulations and tox-
         icity testing methods currently assess each chemical by itself. 
         In the real world, we encounter complex mixtures of chemicals. 
         There is never 'ust one alone.  Scientific. studies make it
         clear that chemicals can interact or can act together to
         produce an effect that none could produce individually. 
         Current laws ignore these additive or interactive effects. 
         Regulating as if chemicals act only individually is as
         unrealistic as assuming that a batter in a baseball game can
         only score a run for his team if he hits a home run.  In real
         life and in baseball, the bases may already be loaded and a
         single could well be enough.

         Take account of cumulative exposure from air, water, food, and
         other sources.  The current legal structure, which includes a
         number of laws addressing pesticides, food safety, water
         safety, and air pollution, encourages regulators to focus on
         one avenue of exposure at a time, such as the contaminant
         levels in drinking water or pesticide residues on food.  This
         type of approach often fails to consider how the exposure from
         all the different sources-air, water, food, dust, etc.-adds up. 
         Although exposure from any single source may be tolerable, the
         total from all sources may be unsafe.  For this reason,
         contaminant levels from any single source must be assessed
         within the context of total cumulative exposure.

. Amend trade secrets laws to make it possible for people to
protect themselves against undesired exposure while preserving
any real need for confidentiality.  Trade secrets laws have been
enacted to prevent business competitors from gaining an unfair
economic advantage by adopting a company's methods without having
borne the cost of product research and development.  In practice,
these laws are routinely used by manufacturers to deny the public
access to information about the composition of their products. 
Since, a skilled chemist can discover what a product contains, we
are skeptical that, trade secrets laws are keeping such
information from business competitors determined,to find out. 
One has to ask who is being kept in the dark by trade secrets
provisions, save for consumers, who do not have the money to do
the chemical analysis.  Until manufacturers provide honest and
complete labels for their products, consumers will not have the
information they need to protect themselves and their families
from hormonally active compounds. -

. Require companies selling products, especially food but also
consumer goods and other potential sources of exposure, to
monitor their products for contamination.  This should begin in
the grocery store.  Grocers should be able to tell you, when you
want to know, whether your food is contaminant-free.  The current
testing system, implemented by the Food and Drug Administration,
is simply inadequate.  It doesn't have the money or the manpower
to do the job responsibly.  The burden for testing should be
shifted to the manufacturer and distributor, with the FDA charged
with monitoring to ensure compliance.

. Broaden the concept of the Toxic Release Inventory.  This
powerful right-to-know law, enacted in 1986, now requires com-
panies in the United States to disclose the amount of toxic
contaminants that escape from their facilities into the envi-
ronment in the course of normal operations.  As the hazards
explored in this book make clear, many hormone-disrupting
chemicals enter the environment through "purposeful" release in
agricultural pesticides, through detergents, and in plastics. 
The reporting under the Toxic Release Inventory should include
this, deliberate release through products as well as inadver tent
releases during manufacturing.  Companies should, therefore, be
required to report the quantity of known endocrine. disrupting
compounds incorporated into products sold or transferred from
each facility.

         Require notice and full disclosure when pesticides are used in
settings where the public might encounter them.  This would in-
clude multifamily dwellings; lawns; places of worship; motels and
hotels; places where food is stored, sold, or prepared; and 
day-care centers, schools, colleges, and other places of learning.

         Reform health data systems so they provide the infor7nation
needed to make sound and protective policies.  A lack of,crucial
data on the national and international level cripples our ability
to make timely, intelligent decisions.  Our ignorance about
trends in many areas of human health is truly appalling.  We must
undertake a concerted effort to build better records of birth
defects and symptoms of impaired function with particular
attention to reproductive and neurological disorders.  This can
be done in ways that protect patient confidentiality while
satisfying the health research community's need for better, more
comprehensive data.  Until this kind of scientific data are
available, it will be impossible to determine whether important
changes are occurring and to respond appropriately to new
hazards.



. Research Directions

Changes to laws and regulations must go hand in hand with an on.
going scientific research effort to discover more about the
impact of hormone-disrupting chemicals, how they do their damage'
and how damage can be avoided.  The research should be driven by
the need to answer a small number of crucial questions:



         How much are we exposed?
    How is the human body really responding to these chemicals? 
    What is the impact on ecosystems?
   When and how should the government act?

         FORENSIC RESEARCH

A comprehensive research program is needed to determine the ef-
fects of hormonally active synthetic chemicals on human health
and well-being.  Are we indeed seeing more genital defects,
increased infertility, and more children with learning
disabilities such as hyperactivity and deficits in attention, as
reports suggest?  Probing such questions will require a
sophisticated integration of epidemiology on human populations,
animal studies, and laboratory investigations of how these
chemicals act at the cellular and molecular level.
              Epidemiological studies, which are never easy, will be
particularly difficult in this instance.  First, researchers face
the lack of an uncontaminated population for comparison.  No
young person alive today has been born without some in utero
exposure to synthetic chemicals that can disrupt development. 
There are only the less exposed and the more exposed.  Then,
there is the additional problem of a long lag time between
exposure to these chemicals and the emergence of ill effects.  If
problems become evident only years or decades after birth,
reconstructing patterns of exposure will be difficult at best. 
Epidemiologists may find that the best opportunities for teasing
out human health effects are in developing countries, where
exposure to agricultural pesticides is generally far greater than
in the United States today.  Anecdotal reports from some of these
countries suggest that hormone-disrupting chemicals may be
causing pervasive, transgenerational damage, but the lack of
basic health data currently makes it impossible to document these
reports.
              A systematic assessment of plastics and their possible
contamination of food should be a high priority.  Over the past
thirty years, plastic has become central to our food delivery
system, so virtually all our food-from springwater to peanut
butter-arrives encased in some form or another of plastic
packaging.  To what extent and under what circumstances are
biologically active compounds leaching from plastics into food
and beverages?  Is this contamination sufficient to pose a health
hazard?  Are there safe, inert forms of plastic that do not leach
synthetic chemicals when foods are packaged or stored in them?
Recent studies have implicated widely used synthetic compounds
such as phthalates, an ingredient in plastics, and alkylphenol
polyethoxylates, which are found in plastics, detergents, and
many other products, in hormone disruption.  We need a better
understanding of what happens to such compounds in the
environment.  How do they break down, and what are the possible
consequences for ecosystems of the original compound or of the
chemicals created as it undergoes degradation by light, bacteria,
and other natural processes?
         Serious detailed assessments should be undertaken to consider
the role of hormone disruptors in several disturbing ecological
trends, especially the dramatic decline and loss of frog
populations around the world, the series of epidemics that have
hit marine mammals, and other notable biological disruptions. 
Some classic wildlife crashes should be revisited to ask whether
hormone disruptors contributed to the declines or perhaps are
impairing recovery.  The dramatic ninety percent decline in the
waterbird population in Florida's Everglades coincided with
profound disruption in the natural water flow but also with the
burgeoning use of agricultural chemicals in south Florida.  The
waterfowl along the major U.S. flyways, which have suffered a
decades-long decline, spend their winters in habitats that
include farmland and wetlands that receive pesticide-contaminated
runoff.



RESEARCH ON BIOLOGICAL MECHANISMS AND
EXPOSURE



We need a better understanding of how the undisturbed physiologi
cal system works in humans, including the normal levels of hor-
mones and how even natural variations contribute to differences
among individuals.  There is a pressing need for more information
on human exposure to synthetic hormone disruptors.  How does the
mother's exposure translate into what reaches the fetus, and what
does this prenatal exposure mean to that individual's
development?



RESEARCH FOR REGULATION AND PREVENTION

A research program must be undertaken to establish standards that
protect human and ecological health from hormone-disrupting
chemicals.  Are there permissable exposures?  Do they vary from
one compound to another?
         Any effort to regulate synthetic chemicals that disrupt
hormones will depend on improving our ability to detect
hormonally active compounds.  What types of screening methods
allow for quick, efficient, and cost-effective identification of
such chemicals?  How quickly can researchers develop them for
broad use?
         The body does not react to hormone impostors as it does to or-
dinary poisons, as we noted in Chapter I 1. A high dose may in
some cases have less impact than a low dose-a phenomenon
scientists call a nonmonotonic response.  Is this a general
phenomenon with hormone systems?  If it is, this finding will
have profound implications for toxicological testing and
regulation.  Industry representativ,es often complain 
that high-dose testing overestimates the risks at low levels, but such
testing might, on the contrary, completely miss damaging effects.
         The significance of infant exposure to hormone-disrupting
chemicals through breast milk should be a top research priority. 
Nursing mothers transfer substantial amounts of chemical
contaminants to their babies, but how much does this matter? 
Children born to mothers with contaminated breast milk have
already been exposed in the womb.  Will the additional exposure
through breast milk greatly increase the risk they run?  Are
there breast-feeding regimens that can lower the transfer rate of
contaminants from mother to baby while maintaining the benefits?



Redesigning Manufacture and Use of Chemicals

Hormone-disrupting synthetic chemicals are today an inescapable
fact of life.  They are in our food and water.  They reach us
through the air and through consumer goods we bring into our
homes.  They have spread across the face of the Earth and
insinuated themselves into virtually every nook and cranny of the
food web.  There is no way to recall them.  That is the dilemma
we face.  We can, though, as suggested above, reduce the risks of
exposure by personal choice and through government action, but
such after-the-fact remedies are inevitably disruptive,
difficult, and incapable of eliminating the problem.  Once
problematic chemicals are at large, there is only one option-to
manage and cope.
         Ultimately, one arrives at the question of how to prevent such
hazards in the first place.  How can we enjoy the benefits of
synthetic chemicals without putting ourselves and our children at
risk?  What can we do to make sure we don't repeat this kind of
mistake in the future?  Traditional regulations and pollution
prevention practices provided are only partial solutions.
         To answer the question-how to achieve protection-we must
rethink how we make and use synthetic chemicals.  We must re-
design the practices, processes, and products that create the
problem.  Here and there, efforts' that move in this direction
are already under way.  Two advocates for fundamental rethinking
and redesign-Dr.Michael Braungart, a German chemist, and William
McDonough, an American architect-have also been working on a set
of overall criteria to guide such efforts, criteria for the
synthetic chemicals themselves as well as for the processes and
products that contain them.  While this movement is still in its
infancy, it signals the direction for changes that will diminish
hazards by reducing waste and the contaminants reaching the
environment.
         Braungart identifies several guidelines for the production of
chemicals that will make them easier to track and recycle:


Greatly reduce the number of chemicals on the market.  With one
hundred thousand synthetic chemicals in commerce globally and one
thousand additional new substances coming onto the market each
year, there is little hope of discovering their fate in
ecosystems or their harm to humans and other living creatures
until the damage is done.

Reduce the number of chemicals used in a given product; make them
simpler.

Make and market only chemicals that can be readily detected at
relevant levels in the real world with current technology . Some
compounds currently in broad use are very hard to measure in the
world at large, making it difficult, economically and practi-
cally, to study human expqsurqpr, their fate in the environment.

Restrict production to only products that have a completely
defined chemical makeup and stop production of products
containing unpredictable mixtures of chemicals.  Such mixtures-for 
example the 209 PCBs-are difficult to test for safety and to
track once released in the environment.

Do not produce a chemical unless its degradation in the environ-
ment is well understood.  In some instances, chemicals released
into the environment can break down into'substances that pose a
greater hazard than the original chemical.



         Braungart and McDonough also advocate a major change in ihe
way we use synthetic chemicals in products and industrial
processes, guided by the axiom that there should be "no such
thing is waste." This notion borrows from natural systems, where
chemi.Cals, nutrients, and organic matter are continuously
recycled.  The 'waste from one creature or process becomes
resources or food for another.  One can see this principle at
work in the backyard compost pile where worms, insects, and
bacteria transform leaves, gtass clipPings, carrot peels, and
wilted lettuce into crumbly rich black soil to nourish new trees,
grass, and vegetables.
         Waste from one process could feed another in the industrial
realm as well, McDonough and Braungart argue.  But whether in the
compost pile or the factory, such recycling will become possible
only if "waste" is not contaminated by substances that make it
unusable by living things or for subsequent industrial
activities.  Through proper design of the manufacturing process
and products, McDonough and Braungart believe that most discarded
material can "feed" the next process.  In a well-designed system,
solvents should clean again and again, not just once.  Worn-out
televisions and other appliances could be returned to the makers,
where components would be disassembled and the materials recycled
and used again in parts for new televisions.
         Although systems designed according to this principle are pro-
foundly different from current approaches, they are not
infeasible or impractical, even right now.  This concept is
already having a profound impact on the automobile industry
worldwide.  Spurred in part by proposals in Europe to require
manufacturers to take back whatever they make, a new 
trend-products designed for disassembly, or DFD-is taking off at a
gallop.  Outside of Detroit, the Big Three auto makers are
working jointly to design cars that can be easily taken apart at
the end of their life and truly recycled into new automobile
parts.  Products designed without thought for recycling often
contain an assortment of different synthetic materials that make
true recycling impossible.  Mixed plastics in an auto dashboard,
for example, might end up "down-cycled" into a park bench, but
they cannot make an encore in a new dashboard.  Closing the loop
and using materials again and again eliminates the demand for new
raw materials and reduces the contaminated waste disposed of in
the environment.  The key to such closed loop recycling is
intelligent design. .
              In a similar pioneering effort with the textile industry,
Mc,Donough and Braungart have helped design a line of upholstery
fabso the manufacturing process and the final product are free of
hazardous chemicals.  The effort, undertaken with Design Tex, New
York-based textile designers and distributors, began with a
survey of the 7,500 chemicals used to dye or process fabrics that
aimed to eliminate those that pose hazards because they are
persistent, mutagenic, carcinogenic, or known to interfere with
hormone -systems.  Only 34 chemicals survived this screening
process, The fabric, which is now in production in Switzerland,
is a mixture of wool and the plant fiber ramie that comes in a
normal range of colors and sells for a price competive with that
of comparable fabrics manufactured using conventional methods and
design.
         Our use of pesticides is also ripe for approaches based on
rethinking and redesign rather than the continual use of ever
more new chemicals.



Over the past forty years, crop losses have remained constant
despite greatly increased pesticide use, in large part because of
changes in agricultural practices and standards and because of
pests' remarkable adaptability.  Armed with a chemical arsenal,
farmers abandoned common-sense agricultural practices that had
been used for millenia to discourage pests, including crop
rotation, carefully timed planting, crop diversity, and field
sanitation.  During this period, farm operations have moved into
areas where pest problems had previously made farming infeasible.
         Consumers, food processors, wholesalers, and supermarkets
increasingly demand picture-perfect produce that is free of cos-
metic blemishes caused by insects, fungus, or disease.  Such
flaws are not harmful, nor do they make a fruit or vegetable less
nutritious, but expectations for picture-perfect produce greatly
increase pesticide use.  In oranges, for example, sixty to eighty
percent of the pesticide use takes place to improve the cosmetic
appearance of the skin.  It can't be argued, in this or any
similar case, that pesticide use is necessary to achieve more or
better food.
         Garden designers, garden writers, and homeowners need to
take up the challenge of creating a new standard of suburban
beauty, one that moves away from the green-carpet aesthetic and
revels in a diversity of plants adapted to local conditions. 
Because this ideal of a homogeneous, flawless greensward fights a
natural tendency toward diversity, it is demanding by its very
nature, requiring fertilizers and pesticides, frequent watering,
and a great deal of time and effort.  Like flawless fruit
flawless lawns come at a high price.  The time has come to change
our attitudes and redesign our yards and gardens with plantings
that.grow comfortably in the place we live and with mowed play
areas that will flourish without constant chemical support.  A
pioneering team from Yale University recently published a
manifesto for this suburban revolution, titled Redesigning the
American Lawn: A Search for Environmental Harmony , which
includes practical guidance for nonspecialists seeking to make
their yards safe, saner havens.

         The synthetic pesticides developed over the past half century
are powerful weapons that should be used sparingly and only when
essential.  The other tragedy of pesticide use-one distinct from
the focus of this book-concerns the growing problem of pesticide
and antibiotic resistance among insects and disease-causing
organisms.  Through casual and excessive use of pesticides and
drugs, humans have accelerated the evolution of insects, weeds,
and bacteria that are increasingly immune to our miracle
pesticides and wonder drugs.  The bugs are not only fighting
back, they are winning this evolutionary struggle.  Within a few
years of DDT's introduction, new superbugs had appeared that were
invulnerable to its poison.  Two decades later, Rachel Carson
warned in Silent Spring about ever increasing resistance among
pests and the ominous implications for human health.  Now, at a
time when some public health scientists fear an increasing threat
of tropical diseases in the United States, the pesticides we need
to control disease-carrying insects may no longer be effective. 
Resistance has become so widespread that we may soon find
ourselves as defenseless in the face of disease and health-
threatening pests as we were half a century ago.  What we thought
was a stunning technological conquest of nature is proving only a
temporary victory.  By using our wonder drugs and miracle
pesticides in excess, we have squandered their benefits.