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Are We Threatening
Our Fertility, Intelligence,
and Survival?—A Scientific
Detective Story
Theo Colborn,
Dianne Dumanoski,
and John Peterson Myers
0
Little, Brown and Company
Boston
New York
Toronto
London
To all of you who contributed
to this effort, each in your own way with your expertise, your critical
assessment, your time, your
encouragement, and your patience - and for your children
and grandchild ren and their grandchildren.
A Little, Brown Book
First published in the United States of America by Dutton
an
pnnt o Dutton Signet, a division of Penguin Books USA Inc 1996
nrs. pobhshed
G„., B„„,„ by Li,„e Brown jntl C()mpany
Copyright © Theo Colbwn, Dianne Dumanoski and John Peterson Myers 1996
A pcion «f Cb.p.e, E.gb,
The moral right of the author has been asserted.
All rights reserved.
No part of this publication may be reproduced,
stored tn a retrieval system, or transmitted, in
any
form or by any means, without the prior
permission in writing of the publisher, nor be
otherwise circulated in any form of binding or
cover other than that in which it is published and
without a similar condition including this
condition being imposed on the subsequent purchaser.
book k dva.hibk
A CM,,, r„,rd
ISBN 0 316 87546 5
Printed and bound in Great Britain by Clays Ltd, St Ives pic
UK companies, institutions and other organisations wishing
to make bulk purchases of this or any other book
pub tshed by Ltttle, Brown should contact their local
oo s top or t e special sales department at the address below.
Tel 0171 911 8000. Fax 0171 911 8100.
Little, Brown and Company (UK)
Brettenham House
Lancaster Place
London WC2E 7EN
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FOREWORD
Vice President Al Gore
January 22, 1996
Last year I wrote a foreword to the thirtieth anniversary edition of
Rachel Carson’s classic work, Silent Spring. Little did I realize that I
would so soon be writing a foreword to a book that is in many re
spects its sequel.
Thanks to Rachel Carson’s clarion call, we developed new and
vital protections for the American public. Now Our Stolen Future
raises questions just as profound as those Carson raised thirty years
ago—questions for which we must seek answers.
Silent Spring was an eloquent and urgent warning about the
dangers posed by manmade pesticides. Carson not only described
how persistent chemicals were contaminating the natural world, she
documented how those chemicals were accumulating in our bodies.
Since then, studies of human breast milk and body fat have conHrmed the extent of our exposure. Human beings in such remote
locations as Canada’s far northern Baffin Island now carry traces of
persistent synthetic chemicals in their bodies, including such notorious
compounds as RGBs, DDT, and dioxin. Even worse, in the womb and
through breast milk, mothers pass this chemical legacy on to the next
generation.
As Carson warned in one of her last speeches, this contamina
tion has been an unprecedented experiment: “We are subjecting
whole populations to exposure to chemicals which animal experi
ments have proved to be extremely poisonous and in many cases cu-
vi
10R1W0RD
mulative in their effects. These exposures now begin at or before
birth and—unless we change our methods—will continue through
the lifetime of those now living. No one knows what the results will
be because we have no previous experience to guide us.”
We are only now beginning to understand the consequences of
this contamination. Our Stolen Future takes up where Carson left off
and reviews a large and growing body of scientific evidence linking
synthetic chemicals to aberrant sexual development and behavioral
and reproductive problems. Although much of the evidence these
scientific studies review is for animal populations and ecological ef
fects, there are important implications for human health as well.
A decade ago, the ozone hole provided shocking evidence of
the atmospheric effects of chlorofluorocarbons (CFCs). Last year,
scientists declared that human activity is changing the earth’s cli
mate. Today, reports in leading medical journals point ominously
to hormone-disrupting chemicals’ effects on our fertility—on our
children.
Our Stolen Future provides a vivid and readable account of
emerging scientific research about how' a wide range of manmade
chemicals disrupt delicate hormonjt systems. These systems play a
critical role in processes ranging from human sexual development to
behavior, intelligence, and the functioning of the immune system.
Although scientists are just beginning to explore the implica
tions of this research, initial animal and human studies link these
chemicals to myriad effects, including low sperm counts; infertility;
genital deformities; hormonally triggered human cancers, such as
those of the breast and prostate gland; neurological disorders in chil
dren, such as hyperactivity and deficits in attention; and develop
mental and reproductive problems in wildlife.
The scientific case is still emerging, and our understanding of
the nature and magnitude of this threat is bound to evolve as re
search advances. Moreover, because industrial chemicals have be
come a major sector of the global economy, any evidence linking
them to serious ecological and human health problems is bound to
generate controversy. However, it is clear that the body of scientific
research underlying Our Stolen Future raises compelling and urgent
questions that must be addressed.
FOREWORD
vii
Responding to the mounting evidence, the National Academy
of Sciences has established an expert panel to assess the threats.
That is an important first step. We must also expand research efforts
to learn more about how these chemicals may do their damage, to
identify how many other synthetic chemicals possess such proper
ties, and to discover the extent to which we and our children are ex
posed. We need to understand the often invisible damage they may
cause. We must find out if there are ways to protect children, who
appear to be at greatest risk for birth defects and developmental dis
orders from such hormonally active compounds. We need to explore
further the links between effects on humans and those on wildlife.
We can never construct a society that is completely free of risk.
At a minimum, however, the American people have a right to know
the substances to which they and their children are being exposed
and to know everything that science can tell us about the hazards.
It is now clear that we waited too long to ask the right questions
about the CFCs that eventually attacked the ozone layer, and we are
going too slow in addressing the threat of climate change. We cer
tainly waited too long to ask the right questions about PCBs, DDT,
and other chemicals, now banned, that presented serious human
health risks.
Our Stolen Future is a critically important book that forces us to
ask new questions about the synthetic chemicals that we have spread
across this Earth. For the sake of our children and grandchildren, we
must urgently seek the answers. All of us have the right to know and
an obligation to learn.
ACKNOWLEDGMENTS
II,
'
This book was a collaborative effort that extended well beyond us to
include scientists, scholars, and friends from around the world. It
would be impossible to name everyone who gave their time and ex
pertise in the development of this story. Rather than risk the chance
of omitting anyone, we have chosen not to produce a list of those
who deserve thanks. We hope that each one of you (you know who
you are), as you read the book, will be able to take satisfaction in
what we have produced. We are truly indebted to you.
In addition, this book would never have reached publication
without the initial and constant support of a number of foundations:
the W. Alton Jones Foundation, the Joyce Foundation, the C. S. Mott
Foundation, the Pew Scholars Program, Pew Charitable Trusts, the
Winslow Foundation, and the Keland Endowment of the Johnson
Foundation.
CONTENTS
Prologue
1: Omens..........................................
2: Hand-Me-Down Poisons............
3: Chemical Messengers.................
4: Hormone Havoc...........................
5: Fifty Ways to Lose Your Fertility
6: To the Ends of the Earth............
7: A Single Hit...................................
xi
14: Flying Blind...................................
1
11
29
47
68
87
110
122
142
167
198
210
231
239
Appendix: The Wingspread Consensus Statement
Notes............................................................................
Index............................................................................
251
261
295
8: Here, There, and Everywhere......
9: Chronicle of Loss.........................
10: Altered Destinies...........................
11: Beyond Cancer..............................
12: Defending Ourselves....................
13: Loomings.......................................
PROLOGUE
This is a most unusual book. The product of a collaboration by three
authors, it uses an untraditional style to present a message that tran
scends traditional knowledge concerning synthetic chemicals, their
safety, and how we perceive risk. The three of us who worked on this
book—Theo Colborn, Dianne Dumanoski, and Pete Myers—each
brought different talents and experience to the task and played a dif
ferent role in getting this book to press. We entered into this collabo
ration because the increasingly complex problems facing us at the
close of the twentieth century demand such cooperative efforts. They
require more than any single individual can bring to the challenge.
Theo Colborn’s seven years of work synthesizing the research
on endocrine-disrupting chemicals and her extensive data base pro
vided the scientific foundation for this effort. Dianne Dumanoski’s
challenge was to take the complex science and transform it into a
story that would be accessible to everyone, including those without
any scientific background. Dianne, who has reported and written
about environmental science and policy for twenty-five years, supple
mented this information through additional research and interviews.
Pete Myers brought a background in science, as well as extensive ex
perience in national and international environmental policy, adding
another valuable dimension to our thinking. The authors developed
and refined the book’s structure and argument together, working
closely and regularly in long sessions through much of the writing.
xii
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1
PROLOGUE
Since this is still an unfolding scientific mystery, it is told as a de
tective story with Theo Colborn and Pete Myers appearing as figures
in the text, as do the other scientists who have played key roles. The
first part of this story takes the reader through Theo’s process of dis
covery as she reviewed the scientific literature concerning the health
effects of synthetic chemicals on wildlife and humans. Theo is the
sleuth in this scientific mystery not only because she really played such
a role but also because we think this approach will engage the reader.
As the book moves beyond Theo’s early detective work, it begins to
discuss the evidence and reflects the thinking of all three of us.
We live in a complex world that is going to require innova
tive approaches to deal with the problems technology has created. It
has taken a nontraditional approach—involving extensive coopera
tion among experts from many disciplines—to reveal the nature of
the chemicals that are stealing our future. Just as scientists had to
break with convention to uncover this problem, we found we had
to break with literary convention to tell the story of their discovery.
OMENS
1952: Gulf Coast, Florida
In years of watching bald eagles, Charles Broley had never
seen anything like it, so he made careful notes in his field diary, a
record that would over time document the decline of the bird along
the eastern coast of Canada and the United States. Broley, a Cana
dian, made his Ijving as a banker, but he worked with equal intensity
at his passionate avocation—ornithology. Long before the abandoned
nests with broken eggshells appeared, he noticed the eagles were act
ing strangely.
Broley’s study of Florida’s bald eagles had begun in 1939 at the
suggestion of staff at the National Audubon Society. After his initial
surveys, he made enthusiastic reports about a robust eagle popula
tion that was nesting successfully all along the peninsula’s west coast
from Tampa to Fort Myers. In the early ’40s, Broley followed 125 ac
tive nests and, climbing aloft, he banded some 150 young eaglets
each year.
Then in 1947, the picture suddenly changed. The number of
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OUR STOLEN FUTURE
eaglets began dropping sharply, and in the succeeding years, Broley
witnessed bizarre behavior in many of the eagle pairs. The season
was early winter, the time when adult birds find mates and begin
their courtship by gathering sticks and building a nest together. But
at nesting sites he had visited for thirteen years, two-thirds of the
adult birds, easily recognized by their white heads, appeared indiffer
ent to the nesting ritual. They engaged in no courtship activity. As
Broley noted in his diary, they showed no interest whatsoever in mat
ing. The birds just “loafed.”
What had caused Florida’s eagles to lose their natural instinct to
mate and raise young? When Broley looked around for a possible ex
planation, his eyes fell on the large housing developments spawned by
Florida s postwar development boom. The new homes were gobbling
up hundreds of acres of prime coastal land, so Broley attributed the
declines and aberrant behavior to human intrusion. University-based
eagle researchers fully concurred in this initial diagnosis.
Broley later came to doubt this explanation. As he continued
his work through the mid-1950s, he became firmly convinced that 80
percent of Florida s bald eagles were sterile—a complaint that one
could hardly blame on bulldozers.
The late 1 9 5 0s: England
Although otters were no longer as plentiful as in earlier times, the
traditional sport of otter hunting continued into midcentury rela
tively unchanged from the days when Sir Edwin Landseer had cap
tured the kill in his nineteenth-century oil painting The Otter Hunt.
Devotees of the sport in Britain still kept at least thirteen packs of
shaggy, long-eared hounds for the chase and feisty little terriers to
flush the otters out. And those who had learned the habits of the
otter from fathers and uncles before them still knew where to seek
( out the otter s lair. On weekends during the hunting season, they
would scout along the stream banks looking amid the tangled roots
for the hollows that shelter otters by day. Once an otter was on the
run, the sounds of a horn and the baying of the hounds would res
onate through country glens as men pursued an ancient blood sport.
OMENS
3
By the end of the decade, however, hunters began to have trou
ble finding otters to hunt, and then in some areas otters disappeared
altogether for no apparent reason.
Other than the hunters, few noticed that the elusive and largely
nocturnal animals were vanishing from rivers and streams where they
had always been found. When conservationists finally took note of
the problem almost two decades after the decline had begun, they
looked to the huntsmen’s records for clues about why the otters had
disappeared.
Some suspected the pesticide dieldrin, but the cause of the de
cline would remain a mystery until the 1980s, when English scien
tists analyzed evidence from across Europe.
The mid- 1 960s: Lake Michigan
In the post-World War II economic boom, the consumer appetite
for new luxuries seemed insatiable. For Michigan mink ranchers,
these were good times indeed, as the wave of prosperity carried them
from one flush year to another through the 1950s. Pat Nixon might
be wearing a good Republican cloth coat, but other American women
wanted mink.
By the early 1960s, however, the mink industry that had grown
up around the Great Lakes because of the ready supply of cheap fish
began to falter—not because the demand for mink was flagging but
because of mysterious reproductive problems. Ranchers were mating
their domesticated mink as they always had, but the females weren t
producing pups. At first, the average number of pups had dropped
from four to two, but by 1967, many females never gave birth, and
the few that did inevitably lost those babies soon afterward. In some
cases the mothers died as well. The only mink ranchers escaping the
devastating losses were those who fed their animals with fish im
ported from the West Coast.
Michigan State University researchers, seeking to identify the
cause, immediately zeroed in on the pollutants carried in Great Lakes
fish, eventually linking the reproductive failure to PCBs, a family of
synthetic chemicals used to insulate electrical equipment.
4
OUR STOLEN FUTURE
Curiously, other mink ranchers in the Midwest had also faced
financial ruin because of reproductive failure a decade earlier. But in
their case, the mink herds crashed after the animals were fed with
scraps from chickens that had been given the synthetic drug diethyl
stilbestrol or DES, a man-made female hormone, to make them
grow faster. Although the symptoms were strikingly similar, the sec
ond crash among fish-fed mink could not be linked to DES, and the
connection between the two declines remained a mystery.
1970: Lake Ontario
r
The sight of the herring gull colony on Near Island was overwhelm
ing, even for a seasoned biologist like Mike Gilbertson. This was the
time when the gulls should be busily feeding their squawking, de
manding brood, but what the Canadian Wildlife Service biologist
found instead was a scene of devastation. As he walked through the
barren sandy expanse where the gulls breed and raise their young, he
encountered unhatched eggs and abandoned nests everywhere, and
here and there, dead chicks.
In a quick count, Gilbertson estimated that eighty percent of
the chicks had died before they hatched, an extraordinary number.
As he examined the dead chicks, he saw grotesque deformities. Some
had adult feathers instead of down, club feet, missing eyes, twisted
bills. Others looked shriveled and wasted, and they still had the yolk
sack attached, suggesting they hadn’t been able to use its energy for
development.
Something about the symptoms seemed vaguely familiar, but
Gilbertson knew he had never seen them in the field. Where had he
heard about this before? I he question nagged at him as he completed
his melancholy tour and headed back by boat to his laboratory.
A few days later, it suddenly came back to him. Chick edema
disease—an affliction he had read about as a student in England.
The same deformities and wasting had shown up in the offspring of
chickens exposed to dioxin in laboratory experiments. If the dead
gulls had all the symptoms of chick edema disease, he thought, there
must be dioxin contamination in the Great Lakes.
OMENS
6
Gilbertson’s colleagues and superiors greeted this theory with
skepticism bordering on derision. Some doubted his diagnosis be
cause dioxin had never been reported in the lake, and their doubt
only deepened when analysis of gull eggs with the methods then
available could find no trace of dioxin.
Gilbertson nevertheless remained convinced that Great Lakes
birds were showing signs of dioxin contamination, but he found no
support for pursuing his theory.
The early 1 970s: The Channel Islands,
Southern California
Even the trained eye finds it difficult to tell a male western gull from
a female. So if it hadn’t been for the extra eggs in the nests, it is pos
sible no one would have made the startling discovery that females
were nesting with other females.
Ralph Schreiber of the Los Angeles County Natural History
Museum first spotted nests with unusually large numbers of eggs on
San Nicolas Island in 1968. Gulls find it difficult to incubate more
than three eggs at a time, so he immediately suspected that more
than one female must be laying in these nests.
Four years later, George and Molly Hunt from the University
of California at Irvine discovered the same phenomenon on Santa
Barbara, a smaller island closer to shore. At least eleven percent of
the nests on that island had four to five eggs, and they found that in
these nests fewer chicks than normal actually hatched. The Hunts
saw thinning eggshells in the Santa Barbara gull colony as well, lead
ing them to suspect that the birds were suffering from exposure
to DDT.
The Hunts could not at first confirm whether females were, in
deed, sharing nests. In later work, however, the husband-and-wife
team did establish that the female gulls were setting up house
keeping together and producing the nests with extra eggs. In a 1977
paper in the journal Science, they explored possible natural explana
tions for such behavior, suggesting that same-sex pairings might be
an adaptation that conferred some evolutionary advantage.
6
OUR STOLEN FUTURE
Over the next two decades, female pairs would be found nest
ing in populations of herring gulls in the Great Lakes, among glau
cous gulls in Puget Sound, and among the endangered roseate terns
off the coast of Massachusetts.
The 1 980s: Take Apopka, Florida
Judging by the lush wetlands along its shore, Lake Apopka, one of
Florida’s largest water bodies, should be alligator heaven. The lake
was understandably high on the list when state and federal wildlife
researchers began looking for a source of eggs for the state’s multimillion-dollar alligator ranching industry, which raises the reptiles
for their handsome hides. To their surprise, however, the biologists
found that Apopka s alligators had no eggs to spare.
In some Florida lakes, the surveys showed that ninety percent
of the eggs laid by female alligators hatch. At Lake Apopka, the hatch
ing barely reached eighteen percent. Even worse, half of the baby
gators that hatched languished and died within the first ten days.
Lou Guillette, a University of Florida specialist on the repro
ductive biology of reptiles, could not make sense of the symptoms he
was seeing. There seemed little question that the problems found
in the lake’s alligators were somehow linked to the 1980 accident at
the Tower Chemical Company, located a quarter of a mile from the
lake s shore. Right after the spill of the pesticide dicofol, more than
ninety percent of the alligator population had disappeared. But why
were the alligators suffering reproductive problems long after water
samples suggested that the lake was again clean?
When researchers took to the water at night in airboats to trap
the lake s alligators and examine them more closely, they found a
strange deformity in many of the males: at least sixty percent of
them had abnormally tiny penises. Nothing like this-had ever been
reported before.
What kind of toxic effect could this possibly be?
OMENS
1
1988: Northern Europe
The first signs of the epidemic that would become the largest seal
die-off in history appeared in the spring on the island of Anholt in
the Kattegat, a narrow strait between Sweden and Denmark.
In mid-April, those conducting routine surveys of the seal pop
ulations began to find aborted harbor seal pups washed up on the
wet sand along with the debris from winter storms. Not long after,
the tides carried in the speckled silver bodies of older animals as well.
Because of the contamination in Europe’s coastal waters, some
immediately speculated that the animals were victims of pollution,
but Dutch virologist and veterinarian Albert Osterhaus was skeptical
from the start. All signs pointed to some infectious disease.
By the end of the month, reports of more dead seals were coming
in from Hesselp, a smaller, less accessible island to the south. From
there, the die-off spread at a gallop along the coastal areas throughout
the North Sea, hitting seals in the Skagerrak Strait between Denmark
and Norway in June, the herds in the Oslo Fjord in July, and the har
bor seals on England’s east coast in early August. By September, the
beaches of the remote Orkney Islands off the northern tip of Scotland,
the Scottish west coast, and the Irish Sea were also awash in dead
seals. The death toll by December came to almost eighteen thousand
seals, more than forty percent of the entire North Sea population.
Strangely, however, the plague victims showed different symp
toms in different locations—a clue that led Osterhaus to suspect that
the underlying cause must be a virus that suppresses the immune sys
tem. In time, the researchers found signs of infection with a distemper
virus in the stricken seals—one similar but not identical to the lethal
microbe that kills dogs and other members of the canine family.
At last it seemed that scientists had the answer to the appalling
die-off, but some in the environmental community remained uncon
vinced. What had made the seals so vulnerable? Was it more than
just coincidence that the disease had taken a much lighter toll along
the less polluted shores of Scotland?
8
OUR STOLEN FUTURE
The early 1990s: The Mediterranean Sea
Although fishermen and yachtsmen who venture offshore sometimes
encounter schools of striped dolphinjS surfing playfully in the bow
wakes of boats, these small, sprightly, high-jumping cetaceans gener
ally live and die out of human sight far from land. For this reason,
the massive die-off in the Mediterranean population was well under
way before wildlife researchers realized that yet another marine
mammal had been hit by some deadly plague.
The first few dead and dying striped dolphins came ashore one
by one near Valenciai on Spain s eastern coast in July 1990, causing no
suspicion that they were anything but isolated natural deaths. By mid
August, however, significant numbers of dead animals began hitting
the beaches—not only around Valencia, but in Catalonia to the north
and on Mallorca and the other Balearic Islands—as the disease ripped
through the dolphin schools inhabiting the deep, open waters a dozen
miles offshore. Physical examinations showed that the plague victims
suffered from partially collapsed lungs, breathing difficulties, and ab
normal movement and behavior. By the end of September, the death
toll was rising along the French coast, and sick animals were also be
ginning to wash up in Italy and Morocco. But as winter set in, the epi
demic slowed and finally stopped.
The following summer, the virulent disease broke out again in
southern Italy and move eastward toward the western edge of the
Greek islands. In the spring of 1993, it resurfaced in the Greek is
lands and spread to the east and northeast, claiming more and more
victims as it went.
By the time the epidemic had played itself out, the official body
count totaled more than eleven hundred. For every victim that
washed ashore, several more vanished into the deep.
Once again, the killer proved to be a virus in the distemper
family, but researchers found signs that contamination may have
also played a role in the die-off.
Beginning in 1987, Alex Aguilar, a marine mammal specialist
from the University of Barcelona, had been collecting fat samples from
striped dolphins off northeastern Spain by firing specially designed
darts from a crossbo or spear gun into animals riding the bow wakes.
OMENS
8
When he compared these samples with those taken from the beached
carcasses, he found that the victims of the die-off carried PCB levels
two to three times higher than what he had found in healthy dolphins.
1992: Copen ha gen , Denmark
Even a high school biology student could see the deformities in the
tiny tadpolelike human sperm as they swam about under the micro
scope. In a single sample, some sperm might have two heads and
others two tails, while another might have no head at all. Many didn’t
seem to swim right, showing total inactivity or frenetic hyperactivity
instead of a strong, steady motion.
Over the years, Niels Skakkebaek, a reproductive researcher at
the University of Copenhagen, had seen more and more sperm ab
normalities, as well as a drop in the typical sperm count. At the same
time, the rate of testicular cancer had tripled in Denmark between
the 1940s and the 1980s. Skakkebaek also noticed low sperm counts
and unusual cells in the testes of men who eventually developed this
type of cancer. Were the two findings connected7
Skakkebaek began to research the scientific literature, looking
for other studies on sperm count, especially for data on men who did
not suffer from infertility or other health problems. He and his col
leagues eventually reviewed sixty-one studies, most of them from the
United States and Europe, but also from India, Nigeria, Hong Kong,
Thailand, Brazil, Libya, Peru, and Scandinavia.
The researchers were stunned by what they found. According to
the data, average human male sperm counts had dropped by almost
fifty percent between 1938 and 1990. At the same time, the inci
dence of testicular cancer had jumped sharply, not just in Denmark
but in other countries as well. The medical data also suggested that
genital abnormalities such as tmdcscendcd leslicles and shortened
urinarv tracts were on the rise among young boss.
Because the changes in sperm counts and quality and the in
crease of genital abnormalities had occurred over such a short period
of time, the researchers ruled out genetic factors. Instead, the changes
appeared due to some sort of environmental factor.
10
OUR STOLEN FUTURE
«
❖
Beginning in the 1950s, these bizarre and puzzling problems
began to surface in different parts of the world—in Florida, the Great
Lakes, and California; in England, Denmark, the Mediterranean, and
elsewhere. Many of the disturbing wildlife reports involved defective
sexual organs and behavioral abnormalities, impaired fertility, the loss
of young, or the sudden disappearance of entire animal populations.
In time, the alarming reproductive problems first seen in wildlife
touched humans, too.
Each incident was a clear sign that something was seriously
wrong, but for years no one recognized that these disparate phenom
ena were all connected. While most incidents seemed linked some
how to chemical pollution, no one saw the common thread.
Then in the late ’80s, one scientist began to put the pieces
together.
••
HAND-ME-DOWN POISONS
From the corner of her eye, Theo Colborn caught sight of
another scientific paper shooting across the floor and settling on the
carpet. She didn’t even bother to turn her head. In hopes of slowing
the tide of paper that was swamping her office in the fall of 1987, she
had taken to closing her door, but it had done little good. With the
wrist action of a Frisbee champion, the project director simply flicked
them under the door. He had become so adept, he could wing a doc
ument to the center of the office. She let it sit there.
Flick. Another. Flick. Flick. Two more.
Sometimes, half a dozen documents would arrive in a single
hour. She barely had time to file the reports and papers that bore titles
such as “A Quantitative Assessment of Thyroid Histopathology of
Herring Gulls (Larus argentatus) from the Great Lakes and a Hypo
thesis on the Causal Role of Environmental Contaminants,” much
less read them. Colborn looked around at the listing stacks of reports
and studies and the bulging cardboard file boxes spread across the
floor. So much had accumulated since she had begun her review of
scientific papers concerning the health of wildlife and humans in the
*
12
OUR STOLEN FUTURE
Great Lakes region that the place was beginning to look like a landfill.
If it got much worse, she would have to apply for a permit. Working
late into the evening and on weekends had not solved the problem. As
hard as she was scrambling, she felt as if she were getting buried.
How was she ever going to make sense of all this stuff?
Despite two months of full-tilt work, she still could not get a
clear picture of how well the Great Lakes were recovering from
decades of acute pollution. Seeking to learn all she could, she had
gathered hundreds of papers, in addition to the ones that kept arriv
ing across the threshold. One couldn’t complain about a dearth of
studies, but nothing coherent seemed to be emerging from her in
tensive research. What she had seemed like a hodgepodge of discon
nected information, yet at the same time, she sensed that something
important was lurking beneath the confusing surface. The most
promising material seemed to be new data linking toxic chemicals to
cancer in fish. That made sense. That is what one would expect to
find in lakes reputed to be full of cancer-causing chemicals.
But how did the hundreds of other studies reporting all manner
of strangeness fit into the picture? Why were the terns in polluted
areas neglecting their nests? And what about the bizarre wasting syn
drome observed in tern chicks, which seemed normal at first but
then suddenly began losing weight until they withered away and
died? Then there were the reports of female herring gulls nesting to
gether instead of with males.
But even when the task seemed totally overwhelming, Colborn
still felt lucky. Landing the job as scientist on this project to assess
the environmental health of the Great Lakes had been a real break.
She had joined the team at the Conservation Foundation, a non
profit think tank in Washington, in early August 1987, feeling rather
proud of herself and her new career. After all, she had come to
Washington for the first time in her life just two years earlier, a fiftyeight-year-old grandmother with a brand-new Ph.D in zoology from
the University of Wisconsin. Her first stint had been as a Congres
sional Fellow at the Office of Technology Assessment, a policy analy
sis group that did studies at the request of Congress (until abolished
by the Republican majority in 1995), where she had worked on studies
related to air pollution and water purification. Then the Conservation
HANO-ME-OOWN POISONS
13
Foundation had approached her about the Great Lakes study—an
effort the group was undertaking with a Canadian counterpart, the
Institute for Research on Public Policy.
This certainly beat filling prescriptions at a small-town drugstore
in Carbondale, Colorado. Faced at fifty with the question of what she
was going to do with the rest of her life, Colborn had briefly consid
ered picking up her lapsed career as a pharmacist and opening a phar
macy in Carbondale, or she could have continued farming sheep, the
career she had pursued since moving to Colorado from New Jersey fif
teen years earlier. Either would have been the sensible course, but she
decided instead to finally do what she had long desired.
Through her lifelong passion for watching birds, she had been
drawn into the growing environmental movement and had spent years
working as a volunteer on western water issues. Despite all she had
learned on the front lines of various environmental battles, she still
felt handicapped by a lack of official credentials. Without a degree
behind you, it was easy for opponents to dismiss you as a do-gooder,
a “little old lady in tennis shoes,” even though she was tall, middleaged, and shod in cowboy boots. Of course, that wasn’t the whole
story; her intellectual appetite had been whetted as well by what she
had been able to learn on her own. So at fifty-one, Colborn plunged
into a new life as a graduate student trudging up and down the
mountains on the western slope of Colorado to take water samples
for her master’s work in ecology—a study of whether aquatic insects
such as stone flies and mayflies could serve as indicators of river and
stream health. Although some of her male advisers had been skepti
cal about investing energy in such an old graduate student, she had
persisted and continued on to get her Ph.D.
Flick. Another document landed a foot from her chair—a copy of
a speech by a governor from one of the states bordering on the Great
Lakes. Like many of the other speeches and reports, this one touted
the improvements in the Great Lakes and the signs of recovery. Public
officials on both sides of the border had all but declared total victory in
the battle against the severe pollution that had brought the Great
Lakes nationwide notoriety in the 1960s and 1970s.
The nadir had been the day in June 1969, when the Cuyahoga
River, which empties into Lake Erie in Cleveland, actually caught
i
14
OUR STOLEN FUTURE
fire and burned a bridge. Six months later, when Cleveland’s mayor
recounted the fire before a congressional hearing on the proposed
Clean Water Act, the city’s burning river made national headlines.
During this period, Lake Erie had been pronounced “dead” by the
news media, and scientists judged the other lakes to be seriously en
dangered. At the height of this degradation, huge, stinking mats of
rotting algae covered the beaches, bays and rivers were awash in oil
and industrial waste, and once-abundant bird and wildlife popula
tions collapsed.
The improvements since then were undeniable. Over two
decades, the pea-soup algae and egregious pollution had gradually
abated as local communities constructed sewage treatment plants,
states imposed bans on the phosphates in detergents that had fueled
runaway algal growth, and industries changed their practices to meet
new limits on what they could discharge into water bodies. Follow
ing the federal restrictions on the pesticide DDT in 1972, the prob
lem of thinning and broken eggshells that had devastated the bald
eagles and other birds began to disappear, and many badly depleted
bird populations rebounded dramatically. In fact, the numbers of
some previously threatened birds, such as the herring gull and the
double-crested cormorant, had climbed to an all-time high and now
constituted a nuisance in many places. Yet, such explosive increases
in opportunistic species could be something other than a sign of re
covery for the lakes. Paradoxically, such a population explosion could
signal a stressed ecosystem just as much as a population crash.
After two months of immersion in the wildlife literature and
lengthy conversations with biologists working in the Great Lakes, she
now had a strong gut feeling that the proclamations of recovery/ were
premature. She had come to
I doubt that the la^.es, however improved, were truly “cleaned up.” The broken eggs littering the bird
colonies may have disappeared, but biologists working in the field
were still reporting things that were far from normal: vanished mink
populations; unhatched eggs; deformities such as crossed bills, miss
ing eyes, and clubbed feet in cormorants; and a puzzling indifference
in usually vigilant nesting birds about their incubating eggs. Colborn’s eyes wandered across the file boxes lined up the length of her
office—forty-three of them, one for each species that had been stud-
HAND-ME-DOWN POISONS
15
ied in the Great Lakes. Everywhere in this wildlife data she was find
ing signs that something was still seriously wrong.
Whatever it was, the symptoms were not as visible and straight
forward as those that had prompted Rachel Carson to write Silent
Spring almost a quarter of a century earlier. Carson, a scientist and
writer whose 1962 book helped spark the postwar environmental
movement, could graphically detail the damage done by wanton use
of man-made pesticides. It was hard to miss the masses of dead birds
that littered suburban backyards after aerial spraying in the 1950s or
to forget the image of a bird dying in a convulsive spasm from pesti
cide poisoning. Abnormal parental behavior or poor survival of young,
on the other hand, are less immediately apparent but perhaps no less
important in the long run for a species’ survival.
And if something was still wrong, what were the implications
for humans living in the region? That was the ultimate question Col
born would be pursuing in the Great Lakes study.
She had already ordered public health reports from the United
States and Canada, and she had plans to survey data from several
cancer registries that had been set up in the Great Lakes basin in the
1970s—a time of increased public awareness of the pollution and
growing concern that the large numbers of toxic chemicals in the
lakes might be jeopardizing human health. There was a strong con
viction among many people living in the region that they were being
exposed to higher levels of toxic chemicals than those living else
where and were suffering from higher than normal cancer rates.
The Great Lakes region appeared to be a good place to look for
links between environmental contaminants and cancer. Colborn
planned to scour the scientific literature and health statistics and
ferret out any clue. If there was anything there, she was determined
to find it. For the time being, she would set aside the puzzle of the
female gulls nesting together and the other distracting anomalies
and go after the cancer connection.
Her project director, Rich Liroff, was even more excited about
the cancer question than Colborn herself. As a member of the Sci
ence Advisory Board of the International Joint Commission, which
advises the United States and Canada on lakes policy, he had been
16
OUR STOLEN FUTURE
hearing a great deal about new ffindings on fish tumors. It was the
hottest topic in Great Lakes research.
At his urging, Colborn was off a few weeks later to the Four
teenth Annual Aquatic Toxicity Workshop in Toronto, where the
much anticipated final session would focus on chemical contami
nants and fish tumors. Liroff’s final instructions were to get some
ugly pictures of cancer-ridden fish for the planned book that was
to be based on their work.
The session on fish tumors more than lived up to expectations,
as slides of grotesque fish tumors flashed across the screen in the
darkened meeting room. Clearly this was key evidence that would
give direction to her research on human and wildlife health, for the
researchers were making a persuasive cause-and-effect link between
specific chemicals found in the Great Lakes basin and cancer. Al
though common sense would suggest that the health problems in
wildlife and the contamination that had become pervasive must be
connected, it often proved impossible to pin an abnormality to a sin
gle chemical in part because the animals were being exposed to hun
dreds of chemicals, most of them still unidentified.
Some skeptics had questioned whether the cancer in fish was
related to chemical contamination at all. But presentations in the fish
tumor session put several alternative explanations to rest, including
the suggestion that the cancer outbreaks were not a new phenomenon
but a natural event caused by viruses.
John Harshbarger, a leading expert on cancer in wildlife from the
Smithsonian Institution, had responded that historical data showed
that large outbreaks of cancer in fish had been reported only since the
chemical revolution of the past half century, which had poured count
less tons of man-made chemicals into the environment. In all the
outbreaks except one, he added, viruses had been excluded as a cause.
The documented outbreaks had also followed a distinct pat
tern. The fish cancers showed up below discharge pipes from indus
trial operations or municipalities and affected fish species that spend
most of their time on the bottom mingling with the muds and sedi
ment. Moreover, scientists had gone on to demonstrate the link be
tween the contaminated sediments and the cancer in laboratory
experiments using confined fish. When researchers fed contami-
HAND-ME-00WN POISONS
17
nants extracted from the sediments to the fish or applied them to
the skin, the fish developed the same cancers seen in the wild.
A series of other talks followed, which made the case that the
chemicals causing the cancer were polyaromatic hydrocarbons, or
PAHs, a class of chemicals found in petroleum products or created
by the incomplete burning of any carbon-containing material rang
ing from gasoline to hamburgers on the outdoor grill.
A team from the U.S. Fish and Wildlife Service had ruled out
not only viruses but also metals and synthetic chlorine-containing
chemicals such as DDT in their studies of cancer in brown bullheads,
a type of catfish, in the Black and Cuyahoga Rivers, which flow into
Lake Erie. The slides of tumor-ridden fish from the notorious Cuya
hoga River were a sorry sight, with deformed, knobby whiskers and
oozing cancers on their smooth scaleless skin. The researchers had
found high concentrations of PAHs in the tissue of these cancer-ridden
fish and PAH breakdown products in the bile in their livers.
Other researchers reported on an international collaborative
effort that was shedding light on how PAHs did their damage inside
the body. Diseased fish showed changes in the liver caused by bond
ing between carbon-based organic chemicals such as PAHs and the
DNA in the nuclei of their cells. This phenomenon of bonding
between foreign chemicals and DNA, which carries an individual’s
genetic blueprint, had been associated with the earliest stage of can
cers caused by chemicals.
Taken together, this was the most sophisticated work to date
and something of a breakthrough. The studies—inducing the same
cancer in the laboratory as seen in the wild, isolating PAHs in fish tis
sue, and showing chemically induced cancer-related changes at the
cellular level—all showed that the link between fish cancer and con
taminated sediments was more than a coincidental association.
Amid the buzz of excitement about the growing evidence link
ing PAHs to fish tumors, the meeting’s keynote address added some
sobering perspective.
Those trying to discover links between ill health and contami
nants were losing the battle, declared Bengt-Erik Bengtsson, the
head of the Swedish Environmental Protection Board’s Laboratory
for Aquatic Toxicology. Despite noteworthy advances, toxicologists
18
OUR STOLEN FUTURE
were falling further and further behind in their ability to analyze and
identify the contamination they encountered in the environment.
In the Baltic Sea, he noted, biologists had reported a reduction
in the size of the testes of fish—a condition apparently related to
the amount of contamination from organochlorines, a class of man
made chemicals containing chlorine. But they had been at a loss to
discover which chemical was causing the problem, for current analyt
ical methods had been able to identify only six percent of the syn
thetic organochlorine chemicals found in Baltic waters. Chemical
companies were putting hundreds of new synthetic chemicals onto
the market each year—far faster than toxicologists and regulatory
agencies were able to develop new assays to detect them, Bengtsson
warned. It was a wonder researchers had succeeded in linking any
thing so many chemicals, so many effects.
Colborn intuitively sensed that Bengtsson’s speech contained
an important clue about how many chemicals were acting on wildlife
in the Great Lakes and elsewhere. But because of her immediate fo
cus on the cancer connection, she put it out of her mind. Months
would pass before she came to recognize its full importance.
When Colborn returned from Toronto with ugly pictures in hand
and renewed enthusiasm for the daunting task that lay ahead, the pub
lic health reports that she had ordered were waiting on her desk.
She dove into the health data, focusing especially on those areas
where wildlife researchers had found cancer in fish. If the wildlife were
providing warnings, she reasoned, then that was where one would first
expect to find humans with higher cancer rates.
To her dismay, the cancer registries that had been set up in the
Great Lakes basin proved useless, for none had been in operation
long enough to yield conclusions about trends or comparative risk
for those regions bordering the lakes. So Colborn turned to broader
reports on human cancer in the United States and Canada. She
pored over the computer printouts and reports for hours, analyzing
the data from various perspectives to see if she could tease out mean
ingful patterns. When nothing emerged, she went at it again from a
new direction. She looked for clusters of a single kind of cancer, higher
overall cancer rates, striking geographical patterns in the cancer inci
dence, or anything else out of the ordinary.
*>
HAND-ME-DOWN POISONS
19
Finally, after months of concerted effort, she had to admit that
no matter which way she cut the data, they yielded no support for
the belief that people in the Great Lakes basin were dying of cancer
more than people elsewhere in the United States and Canada. Sur
prisingly, the opposite appeared to be the case. The rates for some
cancers were actually lower in the Great Lakes area than in some
other regions. There was simply no evidence in the public health
records of elevated or unusual cancer patterns among those living
near the lakes.
Colborn was puzzled. The high cancer rates she had heard so
much about appeared to be more myth than reality. After months of
chasing the specter of cancer, she found herself at a dead end.
Faced with this major setback, she turned her mind again to
the wildlife literature and tried to think clearly about where she
should go next. Sitting there surrounded by the boxes of animal
studies, she was suddenly struck by the obvious. Why on earth hadn’t
she seen this before? The fish cancer research might be cutting-edge
work, but most of the problems being reported in wildlife were
not cancer. Except in fish in highly contaminated areas, cancer was
an extreme rarity. Yet a long list of fish and animals all across the
Great Lakes basin showed ill health that seemed to be impairing
their survival.
The phrase is automatic: “cancer-causing chemical.” The habit
of mind is so ingrained, we do not even recognize the conceptual
equation that has dominated our thinking about chemicals. For the
past three decades, the words “toxic chemical” have become almost
synonymous with cancer not only in the public mind but in the
minds of scientists and regulators as well. Colborn was no exception.
But now she recognized that this preoccupation with cancer and mu
tations had been blinding her to the diversity of data she had col
lected. Moving beyond cancer proved to be the most important step
in her journey, for as she looked at the same material with new eyes,
she gradually began to recognize important clues and follow where
they led.
Colborn wasn’t sure where to turn next. If the problem wasn’t
cancer, what was it? She was still floundering around in a morass of
20
OUR STOLEN FUTURE
undigested information. By this time, she had collected several hun
dred scientific papers and dozens of studies and reports, but each new
document seemed only to add to the confusion.
For want of a better idea, she decided to go back and again read
through the Ries on mink, otter, fish, and birds such as the bald eagle
and herring gull.
At the recommendation of her project director, Colborn had
traveled earlier to Hull, outside Ottawa, to meet with Mike Gilbert
son, Glen Fox, and other veteran researchers in the Canadian
Wildlife Service, who had been investigating the problems in Great
Lakes wildlife for more than a decade. The trip had been invaluable
both for the information she had gathered and for the professional
friendships that had developed from that initial encounter.
Gilbertson had given Colborn complete access to his meticu
lously organized collection of material on each animal species that
breeds in the Great Lakes basin—data that he had gathered over the
years and arranged in chronological order in three-ring binders. Col
born was awed by the elegance of the effort and by the years of dedi
cation and scholarly consideration that it reflected. With a sense of
history, Gilbertson had gone to great lengths to collect papers and
studies dating back a half century or more—literature documenting
that the problems seen today in the birds and wildlife along the lakes
had not been reported before World War II. In the bald eagle file, she
found evidence of parallel declines in the postwar period in the bald
eagle in North America and in its European cousin, the white-tailed
sea eagle, along with a collection of reports detailing the concentra
tions of synthetic chemical contaminants found in both species. Photo
copies from Gilbertson’s archive had greatly enriched Colborn’s files,
but their conversations, during which Gilbertson generously shared
his broad experience, had proved even more invaluable.
Over lunch in the Canadian Wildlife Service cafeteria, Col
born, Gilbertson, and Fox had discussed the Wildlife evidence con
tradicting the frequent claims that the lakes had been cleaned up.
The two Canadians shared the conviction the wildlife work had
likely implications for human health and constituted a warning hu
mans ought to heed. In her survey of the scientific literature, Col
born had been fascinated by some of Fox’s work, which reported
HAND-ME-DOWN POISONS
21
evidence of behavioral changes in the wildlife as well as signs of
physical damage.
In herring gull colonies, particularly in highly polluted areas of
Lakes Ontario and Michigan, Fox and his colleagues had found nests
with twice the normal number of eggs—a sign that the birds occupy
ing the nests were two females instead of the expected male-female
pair. The phenomenon, which persisted in some areas, had been par
ticularly prevalent in the mid to late 1970s. During this period, Fox
had collected and preserved seventeen near-term embryos and newly
hatched chicks from the affected colonies in hopes that he might
eventually discover what was causing this unusual behavior and
other reproductive problems.
A few years later, Fox encountered a scientist who might help
him find the answer. Michael Fry, a wildlife toxicologist at the Uni
versity of California at Davis, had investigated how the pesticide
DDT and other synthetic chemicals disrupt the sexual development
of birds after hearing reports of nests with female pairs in western
gull colonies in southern California. While some looked for an evo
lutionary explanation for the phenomenon, Fry had suspected conta
mination. Reports in the scientific literature indicated that a
number of synthetic chemicals, including the pesticide DDT, could
somehow act like the female hormone estrogen.
To test his theory, Fry had injected eggs taken from western
gull and California gull colonies in relatively uncontaminated areas
with four substances—two forms of DDT; DDE, the breakdown
product of DDT; and methoxychlor, another synthetic pesticide that
has also been reported to act like the hormone estrogen. The experi
ment showed that the levels of DDT reported in contaminated areas
would disrupt the sexual development of male birds. Fry noted a
feminization of the males’ reproductive tracts, evident by the pres
ence of typically female cell types in the testicles or, in cases of
higher doses, by the presence of an oviduct, the egg-laying canal nor
mally found in females. Despite all this internal disruption, the
chicks had no visible defects and looked completely normal.
As soon as he could make arrangements, Fox shipped the pre
served embryos and chicks off to Fry in California. In his examina
tion of the birds’ reproductive tracts, Fry found that five of the seven
22
OUR SIOHN FUTURE
males were significantly feminized and two had visibly abnormal sex
organs. Five of the nine females showed significant signs of disrupted
development as well, including the presence of two egg-laying canals
instead of the one that is normal in gulls. Such disruptions, Fry noted,
could indicate that the birds had been exposed to chemicals that
acted like the female hormone estrogen.
Earlier experiments by other researchers had shown that expos
ing male birds to estrogen during development affects the brain as
well as the reproductive tract and permanently suppresses sexual be
havior. When chicken and Japanese quail eggs received estrogen in
jections, the males that hatched never crowed, strutted, or exhibited
mating behavior as adults.
Taken together, the evidence in the Great Lakes suggested that
the females were nesting together because of a shortage of males,
which might be absent because they were disinterested in mating or
incapable of reproducing. Though most of the eggs in these samesex nests were infertile, these females sometimes managed to mate
with an already paired male and hatch a chick. The female pairs ap
peared to be an effort to make the best of a bad situation.
Fox and others had noticed other behavioral abnormalities as
well, particularly in birds that had high levels of chemical contami
nation. In Lake Ontario colonies, the birds showed aberrant parental
behavior, including less inclination to defend their nests or sit on
their eggs. In unsuccessful nests, the incubating eggs were unat
tended for three times as long as in nests where birds successfully
produced offspring. A study comparing reproduction in Forster’s
terns nesting in clean and contaminated areas reported that nest
abandonment and egg disappearance, often due to theft by preda
tors, was substantial in the contaminated area on Lake Michigan but
virtually nonexistent in the clean colony on a smaller lake in Wiscon
sin. Parental inattentiveness clearly diminished the chances that the
eggs would hatch and the chicks would survive.
What Colborn remembered afterward about the conversation
was how cautious they had all been. Despite the shared view that
wildlife findings had implications for humans, no one wanted to ac
knowledge the unspoken question hanging in the air. No one dared
ask whether synthetic chemicals might be having similar disrupting
HAND-ME-DOWN POISONS
23
effects on human behavior. Those were treacherous waters they all
preferred to avoid.
As Colborn tackled the wildlife files for a second time, her
mind kept returning to the female gulls nesting together. She pulled
out the papers by Fox and Fry and carefully reread them. She sensed
that the “gay gulls,” as someone had dubbed them, were an impor
tant piece of the puzzle, but she still didn’t know how to put it all
together. The feminization of the males was a consequence of dis
rupted hormones. That involved the endocrine system, which was
composed of various glands that controlled critical functions such as
basic metabolism and reproduction.
Well, that about summed up her knowledge of current en
docrinology. She had taken courses in pharmacy school, but the in
tervening decades had revolutionized the field. And endocrinology
was not standard fare in the training of ecologists. If she was going to
pursue this line of inquiry, she would have to know more.
Several new endocrinology textbooks joined the stacks of wildlife
files on the top of her desk. Her first efforts to master the basics of the
endocrine system proved frustrating in the extreme. The texts were
dense, unreadable, and full of acronyms that forced one to keep flip
ping back to earlier pages. Colborn only began making headway when
she found a practical, accessible text, Clinical Endocrine Physiology,
which she kept within reach through the months that followed.
As she focused on hormones, evidence that she had previously
passed over gained new meaning. She recalled the keynote address by
Bengtsson, the Swedish toxicologist who described how the size of fish
testicles had diminished as contamination from synthetic organochlorine chemicals increased in the Baltic. Was this a sign of hormone dis
ruption? She looked again at reports of abnormal mating behavior in
bald eagles, which had preceded the appearance of eggshell thinning
and the collapse of the eagle population. The birds had been disinter
ested in mating. Hormone disruption, Colborn now suspected.
Other things struck her, too, as she read through the wildlife
files. A pattern began to emerge. Birds, mammals, and fish seemed to
be experiencing similar reproductive problems. Although the adults
living in and around the lakes were reproducing, their offspring often
OUR STOLEN FUTURE
did not survive. Colborn began to focus on studies that compared
Great Lakes populations to others living inland. In every case, the
lake dwellers, who appeared otherwise healthy, were far less success
ful in producing surviving offspring. It seemed that the contamina
tion in the parents was somehow affecting their young.
It dawned on Colborn that the human studies investigating the
effects of exposure to synthetic chemicals had focused largely on can
cer in exposed adults. Only a handful had looked for possible effects
on the children of exposed individuals, but Colborn recalled reading
one that had studied the children of women who had regularly eaten
Great Lakes fish. She dug it out of her files and read it again. The
study by Sandra and Joseph Jacobson, psychologists from Wayne
State University in Detroit, had also found evidence the mother’s
level of chemical contamination affected her baby’s development.
The children of mothers who had eaten two to three meals a month
of fish were born sooner, weighed less, and had smaller heads than
those whose mother did not eat the fish. Moreover, the greater the
amount of PCBs, a persistent industrial chemical that is a common
pollutant in Great Lakes fish, in the umbilical cord blood, the more
poorly the child scored on tests assessing neurological development,
lagging behind in various measures, such as short-term memory, that
tend to predict later IQ.
The parallel between this human study and the offspring effects
in wildlife was interesting as well as troubling.
Colborn moved on, following wherever the investigation led,
but the Jacobson study hovered in the back of her mind, nagging at
her like an unanswered question. Had scientists been looking in the
right place in their search for effects? Perhaps the Jacobson studies
were more important than anyone had realized.
As she dug deeper, more parallels became apparent. In the tissue
analyses done on the wildlife, the same chemicals kept showing up in
the troubled species, among them the pesticides DDT, dieldrin, chlor
dane, and lindane, as well as the family of industrial chemicals called
PCBs, which had been used in electrical equipment and many other
products. Of course, these results might be a coincidence, or they
could well reflect technical limits and the small budgets for tracking
HAND-ME-DOWN POISONS
25
contaminants. These were the chemicals toxicologists knew how to
measure and the ones least expensive to analyze.
Whatever the reason for their repeated appearance, studies had
found the very same chemicals in human blood and body fat. Colborn was particularly shocked by the high concentrations reported in
the fat in human breast milk.
*
By the time the research deadline approached, Colborn had
plowed through more than two thousand scientific papers and five
hundred government documents. She felt like a beagle following its
nose. She wasn’t sure where she was headed, but propelled by her cu
riosity and intuition, she was hot on the trail. She had found so many
tantalizing parallels, so many echoes among the studies. Somehow,
she was certain, it all fit together, because she kept finding unex
pected links. Her latest discovery had come while she reexplored the
literature on the eerie wasting syndrome seen in young birds. The
chicks could look normal and healthy for days, but then suddenly
and unpredictably they would begin to languish, waste away, and fi
nally die. The wasting problem, scientists were learning, was a symp
tom of disordered metabolism. The young birds could not produce
sufficient energy to survive. Though one would not at first suspect
that this problem had anything in common with the gay gull phe
nomenon, it also stemmed from the disruption of the endocrine sys
tem and hormones.
But the elation of discovery passed quickly. The deadline was
looming. What did this all mean? She had pieces and patterns but
no picture.
Maybe she could gain perspective if she laid it all out. Colborn
began entering the findings from the studies on a huge ledger sheet,
the kind used by accountants. When that became unwieldy, she
turned to her computer and created an electronic spreadsheet, which
scientists call a matrix. As she made entries under columns headed
“population decline,” “reproductive effects,” “tumors,” “wasting,”
“immune suppression,” and “behavioral changes,” her attention came
to focus increasingly on sixteen of the forty-three Great Lakes species
that seemed to be having the greatest array of problems.
She sat back and looked at the list: the bald eagle, lake trout,
26
OUR STOlEN FUTURE
herring gull, mink, otter, and the double-crested cormorant, the
snapping turtle, the common tern, and coho salmon. What did they
have in common?
Of course! Each and every one of these animals was a top
predator that fed on Great Lakes fish. Although the concentrations
of contaminants such as PCBs are so low in the water in the Great
Lakes that they cannot be measured using standard water testing
procedures, such persistent chemicals concentrate in the tissue and
accumulate exponentially as they move from animal to animal up
the food chain. Through this process of magnification, the concen
trations of a persistent chemical that resists breakdown and accumuates in body fat can be 25 million times greater in a
top predator
such as a herring gull than in the surrounding water.
One other startling fact emerged from the spreadsheet. Accord
ing to the scientific literature, the adult animals appeared to be doing
.k*e l e, he‘1 th Problems were found primarily in their offspring Al
though she had been thinking about offspring effects, Colborn had
not recognized this stark, across-the-board contrast between adults
and young.
Now the pieces were beginning to fall together. If the chemicals
found ,n the parents' bodies were to blame, they were acting as
hand-me-down poisons, passed down from one generation to the
next. that victimized the unborn and the very young. The conclusion
was chilling.
But the host of disparate symptoms in everything from adult
erring gu Is to baby snapping turtles did not seem to add up Some
ammals like the gulls, exhibited strange behav.or such as same-sex
nests, while other species, including the double-crested cormorant
had visible gross birth defects such as club feet, missing eyes’
crooked spines, and crossed bills. Again a pattern emerged from the
confusing pieces of the puzzle as Colborn reflected on what she had
learned by following her nose.
These were all cases of derailed development, a process guided to
a sigmficant extent by hormones. Most could be linked to disruption
or the endocrine system.
This, naught pointed Colborn’s investigation in another direclon. She began reading everything she could find about the chemicals
Laki, Ontario 'Utimajn'i^cai'iOn cj PCfe
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As PCBs work their way up the food chain, their concentrations in animal
tissue can be magnified up to 25 million times. Microscopic organisms pick
up persistent chemicals from sediments, a continuing source of contami
nation, and water and are consumed in large numbers by filter feeding tiny
animals called zooplankton. Larger species like mysids then consume zoo
plankton, fish eat the mysids, and so on up the food web to the herring gull.
28
OUR STOLEN FUTURE
that showed up again and again in the tissue analyses of animals hav
ing trouble producing viable young. She quickly learned that the
testing and reviews done by manufacturers and government regula
tory agencies had focused largely on whether a chemical might cause
cancer, but she found enough in the peer-reviewed scientific litera
ture to prove that her hunch had been correct.
The hand-me-down poisons found in the fat of the wildlife had
one thing in common: one way or another, they all acted on the en
docrine system, which regulates the body’s vital internal processes
and guides critical phases of prenatal development. The hand-medown poisons disrupted hormones.
CHEMICAL MESSENGERS
Pushing on with her research on hormones, Theo Colborn Dis
covered a central piece of the puzzle in the world of Frederick vom
Saal, a biologist at the University of Missouri. Vom Saal’s exploration
of how hormones help make us who we are is a fascinating scientific
adventure in its own right. In a series of experiments with mice, he
showed that small shifts in hormones before birth can matter a great
deal and have consequences that last a lifetime. His work helped
highlight the hazard posed by synthetic chemicals that can disrupt
hormonal systems.
Vom Saal’s investigation of the wondrous world of hormones
began in 1976 during his postdoctoral days at the University of Texas
in Austin, inspired by the behavior of the lab mice. Like most post
doctoral biology students, vom Saal was spending the better part of
his life in the lab, where his regular chores included breeding mice.
As he played mouse matchmaker, arranging encounters between
eager males and receptive females, he became intrigued by the inter
play between the animals as he moved them from cage to cage.
In the beginning, the small, white, pink-eyed creatures had all
3D
OUR STOLEN FUTURE
seemed like cookie-cutter copies of each other. But as he watched the
females scurrying about in the breeding cages, individuals quickly
emerged from the crowd. Whenever he returned a female to a group
cage holding half a dozen females, there always seemed to be one
mouse who would attack the intruder. These were mice with an atti
tude—tough cookies who rattled their tails threateningly and lashed
out at their mild-mannered companions.
Such a difference between the behavior of one female and an
other was striking—and puzzling. The mice were all from a single labo
ratory strain that had been inbred for generations. When it came to
genes, they were virtually identical.
This simple observation set the course for vom Saal’s life’s work
in reproductive biology. In the years that followed, he designed
dozens of experiments to probe the mystery of how two mice with al
most the same genetic blueprint could behave so differently.
The notion persists that genes are tantamount to destiny and
that one might explain everything from cancer to homosexuality by
locating the responsible genes. But in a series of scientific papers,
vom Saal demonstrated that there are other powerful forces shaping
individuals—females as well as males—before birth. Genes, it turned
out, are not the whole story. Not by a long shot.
What vom Saal saw during those long hours observing mice in
the lab contradicted everything he had read. According to the scien
tific literature of the period (which reflected prevailing human as
sumptions as much as it described animal behavior), aggression was
strictly a male behavior. But if tail-rattling, chasing, and biting among
the females weren’t aggression, what would one call it?
Eventually, vom Saal’s colleagues had to concede that the be
havior did look like aggression, but they tended to shrug it off
as unimportant. Males were the center of the action in animal soci
eties according to the prevailing wisdom in the field of animal behav
ior, so what females did simply didn’t matter. They were just passive
baby makers.
Vom Saal wasn t so sure. His intuition told him what he was
seeing was probably important as well as interesting. His doctoral
work had centered on the role played by testosterone in development
J
w.
CHEMICAL MESSENGERS
■■■
*>
31
before birth, and he knew that this hormone—found at much higher
levels in males—drives aggression.
From his observations, the tough females weren’t common, but
they weren’t rare either. There seemed to be roughly one aggressive
female for every six mice in the colony—something he noticed be
cause the mice were housed six to a cage. If the mice were clones,
something besides genes had to be shaping the aggressive females.
Since birth the sisters had been raised identically, so living condi
tions could not explain the differences. Could the cause be some
thing in their prenatal environment?
That set him to thinking about how mice are carried before
birth. Their mother’s womb isn’t a single compartment like the hu
man womb, but two separate compartments or “horns” that branch
off to the left and the right at the top of the vagina or birth canal.
The baby mice are tucked in the narrow horns like peas in a pod as
many as six on a side. This arrangement means that some of the fe
males will develop sandwiched between two males.
Vom Saal began calculating probabilities. If there were twelve
mice in the typical mouse litter and if the placement of males and fe
males in the womb was random, how many females would end up be
tween two males? Roughly one in six, he figured. That supported the
theory taking shape in his head. Some of the females are markedly
more aggressive, he suspected, because they had spent their prenatal
life wedged between two males. A week before birth, the testicles in
a male pup begin to secrete the male hormone testosterone, which
drives his own sexual development. The female pups might be bathed
in testosterone washing over from their male neighbors.
Maybe, vom Saal thought, the answer to the mystery of how
genetically identical females could be so different lay in hormones—
chemical messengers that travel in the bloodstream, carrying mes
sages from one part of the body to another.
In the body’s constant conversation with itself, nerves are just
one avenue of communication—the one employed for quick, dis
crete messages that direct a hand to move away from a hot stove. A
large part of the body’s internal conversation, however, is carried on
through the bloodstream, where hormones and other chemical mes
sengers move about on the biological equivalent of the information
32
OUR STOLEN FUTURE
superhighway, carrying signals that not only govern sex and repro
duction but also coordinate organs and tissues that work in concert
to keep the body functioning properly.
Hormones, which get their name from the Greek word mean
ing to urge on, are produced and released into the bloodstream by
a variety of organs known as endocrine glands, including the testi
cles, the ovaries, the pancreas, the adrenal glands, the thyroid, the
parathyroid, and the thymus. The thyroid, for example, produces
chemical messengers that activate the body’s overall metabolism,
stimulating tissues to produce more heat. In addition to eggs, a
woman s ovaries release estrogens—the female hormones that travel
in the bloodstream to the uterus, where they trigger growth of the
tissue lining the womb in anticipation of a possible pregnancy.
Yet another endocrine gland, the pituitary, which dangles on a
stalk from the underside of the brain just behind the nose, acts as a
control center, telling the ovaries or the thyroid when to send their
chemical messages and how much to send. The pituitary gets its
cues from a nearby portion of the brain called the hypothalamus, a
teaspoon-size center on the bottom of the brain that constantly
monitors the hormone levels in the blood in much the way that a
thermostat monitors the air temperature in a house. If levels of a
hormone get too high or too low, the hypothalamus sends a message
to the pituitary, which signals the gland that produces this hormone
to gear up, slow down, or shut off.
The messages travel back and forth continuously. Without this
cross talk and constant feedback, the human body would be an un
ruly mob of some 50 trillion cells rather than an integrated organism
operating from a single script.
As scientists have delved deeper into the nervous, immune, and
endocrine systems—the body’s three great integrating networks—
they have encountered profound interconnections: between the
brain and the immune system, the immune system and the en
docrine system, and the endocrine system and the brain. The links
sometimes seem utterly mystifying. How, for example, could a
woman suffering from multiple personality disorder play with a cat
for hours while she was one personality and suffer violent allergic reactions to cats when she took on another?
CHEMICAL MESSENGERS
33
MypMaJamu.$~
Pineal body
Hippocampus — "a
Pituitary gland
Parathyroid gland
Thyroid gland
Thymus yland
4
JCid/w
Adrenal gland
Female Reproductive Organs
&
** j
&rM>t
/
*
s J
i- I
\ w 'Uierui \
(tl®
■ ProsMcI Mile Keprvdactive
Penis
__
Teslis — I Organs
'Vagina
Some important glands, organs, and tissues sending or receiving hormonal
messages in the human body.
Nobody knows the answer to this question, but it certainly lies
in this internal conversation and the constant babble of chemical
messengers. Changes in one part of this complex, interconnected
system can have dramatic and unexpected consequences elsewhere,
often where one might least expect, because everything is linked to
everything else. A brain tumor, for example, might show up as dis
rupted menstrual cycles and hypersensitivity of the skin rather than
as headaches.
If hormones are vital to maintain proper functioning in adults,
they are perhaps even more important in the elaborate process of de
velopment before birth.
But how could vom Saal test his theory?
Mouse Caesarean sections.
34
OUR STOLEN FUTURE
Just before the females were ready to give birth at the end of
their nineteen-day pregnancies, vom Saal removed the tiny babies,
who were approximately an meh long and about the size of an olive'
He marked them based on their position relative to their neighbors
in the womb. In this way, he could discover where aggressive females
had spent their prenatal lives. Thus began vom Saal’s exploration of
what some in the held playfully refer to as the “wombmate” effect,
known formally as intrauterine position phenomenon.
Although vom Saal is now forty-nine and a professor at the Uni
versity of Missouri, he still looks youthful enough to be mistaken for
a graduate student. In a scientific world where many seldom venture
beyond narrow specialities, vom Saal embraces the big picture, un
abashedly declaring that he is interested in “womb-to-tomb biol
ogy. He moves easily between elegant, tightly focused studies and a
arger more encompassing pursuit of fundamental questions- Why
does this happen? What is the evolutionary significance?
Those first studies in Austin confirmed his theory. As the mice
removed by Caesarean section matured, the aggressive females were,
as predicted, the ones who had developed between brothers. Each
intriguing finding raised new questions, leading to more studies and,
in time, observations on thousands of mice delivered by Caesarean
section. Aggression proved just the most obvious sign of profound
differences between mouse sisters that could be predicted to a re
markable degree by their position in the womb.
At first blush, vom Saal’s results sound like a tale of the ugly sister
and the pretty sister. Not only was the ugly sister-the mouse that had
developed between males-nrore aggressive, but vom Saal discovered
she was signrficantly fess attractive to males than the pretty sisters who
had spent then womb trme between other females. Eight times out of
ten, a male given a choice would chose to mate with the pretty sister
What's attractive to males isn't the female’s tiny pink eyes or
the curve of her tail. The social life of mice is governed by the nose
and the attractiveness of females depends on the socral chemicals'
they give off, which are called pheromones. The pretty sisters smell
sexier to males because they produce different chemicals than their
less attractive sisters. The prenatal hormone environment leaves a
CHEMICA4 MESSENGERS
35
Oviduct
tlieriM hom
Amniotic soc
KEY
(TMalc
Q Female Fa
) I (
■-
I
Vagina
Behavioral and reproductive differences in mice can be predicted to a re
markable degree by their position, which is related to hormone exposure, in
the womb. (Adapted from vom Saal and Dhar, 1992)
A
permanent imprint on each sister that is recognized by males for the
rest of her life.
The sisters also showed dramatic differences in their reproduc
tive cycles. Besides finding mates more readily, the pretty sister also
matured faster than her ugly sister and came into heat—a period of
sexual receptivity—more often. As a consequence, she had more op
portunities to get pregnant and was more likely overall to produce
more offspring in her lifetime than her aggressive, unattractive sister,
who experienced puberty later and came into heat less frequently.
Even more amazing, studies by other researchers, including
Mertice Clark, Peter Karpiuk and Bennett Galef of McMaster Uni
versity, and the team of John Vandenbergh and Cynthia Huggett of
North Carolina State University, have found that the wombmate ef
fect even influences whether a female will give birth to more males
or more females when she has pups of her own. This is mysterious in
deed, since scientists up to now believed that the mother has no role
36
OUR STOLEN FUTURE
in determining the sex of her offspring. Based on current under
standing, it is the sperm contributed by the father that dictates
whether the egg develops into a male or female, so how a mother in
fluences sex ratio is still unknown. However it happens, the pretty
sisters tend to have litters made up of sixty percent females, while
the ugly sisters generally give birth to litters that are roughly sixty
percent male. As Vandenbergh wrote of this transgenerational
wombmate influence: “Brothers beget nephews.”
After hearing the tale of the two sisters, one might easily con
clude that it would be wise to be a pretty sister if one had to be
a
mouse. They have lots of mates and babies and, judged by the evolu
tionary imperative of producing offspring, seem more successful
than their ugly sisters.
Not so fast, vom Saal cautions. When one considers how these
srsters live their lives within a mouse population that goes through
boom and bust cycles, the pretty sister begins to lose her obvious
e ge. Typically, a mouse population builds to a very high peak and
hen it crashes. In ordinary times when the population isn’t too
ense the pretty sisters definitely have the advantage, but as condi
tions become overcrowded the pretty sisters’ ability to produce ba
bies diminishes because the females respond to scent cues in urine
that inhibit reproduction.
But these overcrowded times are precisely when the ugly sisters
come into their own. Because they are relatively immune to the in
hibiting cues, they are likely to be the only ones to produce offspring,
n
ie ug y sisters are the only ones tough enough to protect their
babies from attack and infanticide.
Interestingly, some studies have shown that the mother’s phys
ical condition can also alter hormone levels in the womb and in-
M°USe m°therS that exPenence continuous
e atter part of their pregnancies give birth to fees who have all the physical and behavioral characteristics of
fema es who develop between males. Maternal stress seems to over
ride the ordinary wombmate variations and produce a litter composed solely of tough cookies.
So what s the evolutionary lesson L.
in this tale?
In vom Saal s view, the real lesson iis the value of
variability.
stresTthro6 h
CHEMICAL MESSENGERS
37
The acute sensitivity of developing mammals such as mice to slight
shifts in hormone levels in the womb has been shaped by evolution.
This characteristic helped insure wide variation in the offspring, even
wider variation than that produced by genetic shuffling alone. Varia
tion is the way mammals have hedged their bets in the face of a
rapidly shifting environment. If you don’t know what the conditions
will be for your offspring, the best thing to do is produce many dif
ferent kinds in the hope that at least one of them will be suited to
the emerging moment.
Vom Saal’s early investigations into the wombmate effect fo
cused solely on females. The decision to look at males to see if female
wombmates had any influence on them was almost an afterthought.
Though the results would round out this line of research, vom Saal ad
mits he frankly did not expect to find anything remarkable. It was
widely assumed that male development was driven exclusively by
testosterone, so being next to females should make little difference.
In fact, the results of his experiments astonished him. The
wombmate effect shaped the destinies of males as well as females and
in ways that no one would have ever predicted. In a major paper in the
prestigious journal Science in June 1980, vom Saal and his associates
laid out the case that it was exposure to the female hormone estrogen
before birth that increased a male’s sexual activity in adult life.
Inside and outside the world of science, many have regarded
the level of male sexual activity as an index of masculinity and a
product of the male hormone testosterone. Indeed, the findings were
so counterintuitive and so contrary to assumptions about the “male”
hormone testosterone and the “female” hormone estrogen that one
of his collaborators protested that they must have somehow mixed
up the samples. Vom Saal found, however, that estrogen and testos
terone each influence males—and in ways that run counter to our
conventional notions of “maleness” and “femaleness.” The effect of
wombmates on males proved an even more provocative vein of re
search than his earlier work on females.
If the females seem a story of the pretty and ugly sisters, then
vom Saal’s findings on the males sound like a tale of the playboy and
the good father.
As adults, the playboy males, exposed to higher levels of estrogen
38
OUR STOLEN FUTURE
by their female wombmates, showed another surprising characteristic
besides their higher rates of sexual activity. It would seem logical to
assume that exposure to estrogen might make males more solicitous
toward the young, but in fact, the opposite proved true. When placed
with young mice, these males were more likely to attack and kill ba
bies. The high-testosterone males who had had brothers for womb
mates turned out to be the good daddies, who surprisingly showed
almost as great an inclination to take care of pups as mouse mothers.
The playboy males were standouts in one other respect as well—
the size of their prostate, the small gland that wraps around the ure
thra, through which urine is eliminated. The males exposed to higher
levels of estrogen had prostates that were fifty percent larger than those
seen in brothers who had had male wombmates. In addition, these
larger prostates are more sensitive to male hormones in adulthood be
cause they contain three times the number of testosterone receptors
found in the prostates of brothers with male wombmates. More recep
tors generally means that the gland will grow more quickly in response
to male hormones circulating in the bloodstream in adulthood.
Although human babies don’t usually have to share the womb
with siblings, their development can nevertheless be affected by
varying hormone levels, which occur in the womb for reasons scien
tists don’t completely understand. Medical problems such as high
blood pressure can drive up estrogen levels, for example. Or perhaps
eating tofu, alfalfa sprouts, or other foods that are high in plant es
trogens during pregnancy could boost estrogen exposure. There is
also the possibility that the mother’s body fat contains synthetic
chemicals that disrupt hormones.
Whatever the source, a recent study on opposite-sex human
twins showed that wombmate effects can be detected in people as
well. The study, which focused on an obscure difference in the audi
tory systems of males and females that exists from birth, found that
girls who had developed with a boy twin showed a male pattern, sug
gesting that they, like vom Saal’s female mice, had been somewhat
masculinized by the hormones spilling over from a male wombmate.
In the midst of all these surprises, the male wombmate studies
in mice yielded only one expected result—on male aggression. Males
CHEMICAL MESSENGERS
«<
39
with male wombmates and the highest testosterone exposure before
birth were indeed the most aggressive toward other adult males, and
males with female wombmates were the least aggressive.
Scientists working in this field are still debating how estrogen
shapes the development of males and females, particularly the devel
opment of the brain and behavior, but vom Saal believes that estrogen
is helping to masculinize males by acting to enhance some effects of
the male hormone testosterone. Together the two hormones influ
ence the organization of the developing brain to increase the level of
sexual activity the male mouse will exhibit as an adult. Vom Saal had
demonstrated that this is a prenatal effect rather than a consequence
of adult hormone levels by castrating the mice shortly after birth and
then in adulthood administering an identical amount of male hor
mone to brothers with male and female wombmates. Even with
identical hormone exposure these male mice showed different levels
of sexual activity—evidence that adult hormone levels are not the
cause of these behavioral differences.
Those who hear about vom Saal’s work typically ask him, Which
is the “normal” mouse: the pretty sister or the ugly sister? The playboy
or the good father?
“They’re all normal,” vom Saal says emphatically.
The question itself seems to stem from our dualistic notion of
maleness and femaleness, which sees the two sexes as mutually exclu
sive categories. In fact, there are many shades of gray and overlap be
tween behaviors thought of as typically male or female. Seen in this
light, there is nothing abnormal about an aggressive female or a nur
turing male. In this strain of mice, whose genetic variability has been
reduced by generations of inbreeding, these individuals reflect the
variability created by the natural influence of hormones before birth.
What is “normal,” vom Saal says, returning to an evolutionary theme,
is not one type of individual or another but the variability itself.
But variability is just one of the larger lessons emerging from
vom Saal’s work. It has also opened a window on the powerful role of
hormones in the development of both sexes and the extreme sensi
tivity of developing mammals to slight shifts in hormone levels in
the womb. The wombmate studies have also underscored that hor
mones permanently “organize” or program cells, organs, the brain, and
OUR STOLEN FUTURE
behavior before birth, in many ways setting the individual’s course for
an entire lifetime.
It is important to remember that hormones do this without al
tering genes or causing mutations. They control the “expression” of
genes in the genetic blueprint an individual inherits from its parents.
This relationship is similar to that between the keys on a player
piano and the prepunched music roll that runs through and deter
mines the tune. Though the piano can theoretically play many tunes,
it will only play the one dictated by the pattern of holes in the music
roll. During development, hormones present in the womb determine
which genes will be expressed, or played, for a lifetime as well as the
frequency of their expression. Nothing has been changed in the indi
vidual’s genes, but if a particular note hasn’t been punched into the
music roll during development, it will remain forever mute. Genes
may be the keyboard, but hormones present during development
compose the tune.
What is astonishing about vom Saal’s wombmate studies is
how little it takes to dramatically change the tune. Hormones are ex
ceptionally potent chemicals that operate at concentrations so low
that they can be measured only by the most sensitive analytical
methods. When considering hormones such as estradiol, the most
potent estrogen, forget parts per million or parts per billion. The
concentrations are typically parts per trillion, one thousand times
lower than parts per billion. One can begin to imagine a quantity so
infinitesimally small by thinking of a drop of gin in a train of tank
cars full of tonic. One drop in 660 tank cars would be one part in a
trillion; such a train would be six miles long.
The striking lifelong differences between a pretty sister and ugly
sister stem from no more than a thirty-five parts per trillion differ
ence in their exposure to estradiol and a one part per billion difference
in testosterone. Using the gin and tonic analogy, the pretty sister’s
cocktail had 135 drops of gin in one thousand tank cars of tonic and
the ugly sister’s 100 drops—a difference that might not be detectable
in a glass much less in a tank car flotilla.
This is a degree of sensitivity that approaches the unfathom
able, a sensitivity, vom Saal says, beyond people’s wildest imagina
tion. If such exquisite sensitivity provides rich opportunities for
CHEMICAL MESSENGERS
If
■
*
41
varied offspring from the same genetic stock, this same characteristic
also makes the system vulnerable to serious disruption if something
interferes with normal hormone levels—a frightening possibility that
first dawned on vom Saal when Theo Colborn called him to talk about
synthetic chemicals that could act like hormones.
To appreciate vom Saal’s concern, one must understand more
about the intricate choreography of events before birth known as
sexual differentiation and the key role played by hormones in this
developmental ballet. In mice, elephants, whales, humans, and all
other mammals as well as in birds, reptiles, amphibians, and fish, the
process that creates two sexes from initially unisex embryos is guided
by these chemical messengers. They are the conductors that give the
cues at the right moment as tissues and organs make now-or-never
choices about the direction of development. In this central drama in
which boys become boys and girls become girls, hormones have the
starring role.
Our understanding of what determines whether a fertilized egg
becomes a male or female is very recent. Before the twentieth cen
tury, it was widely assumed that the sex of the baby was determined
by environmental factors such as temperature.
It was only in 1906 that two scientists—Nettie Marie Stevens
and Edmund Beecher Wilson—independently noted that each cell
in women had two X chromosomes while men always had an X and a
Y, an observation that led to the theory that the number of X chromo
somes determined sex. In the past decade, researchers have finally
established that it is a gene on the Y chromosome rather than the
number of X chromosomes that determines sex.
As most of us learned in high school biology, the eggs produced
by the mother all carry one X chromosome, and the sperm from the
father carry either an X or a Y chromosome. The sex of the baby hangs
in the balance as the sperm burst out of the starting gate and race
against each other in the reproductive marathon. If this most pri
mordial of athletic events were broadcast like the Boston Marathon,
we might hear that three Ys are neck-and-neck at the entrance to the
cervix, but an X is making a move on the outside in the push into
the uterus. A field of 75 million sperm have been pushing hard, sweep
ing their tails back and forth in steady swimming motions, but in the
n
OUH STOLEN FUTURE
biological equivalent of Heartbreak Hill, many are beginning to flag
as they enter the fallopian tube leading from the top of the uterus.
It’s a tight race right to the finish line as the competitors crowd to
ward the goal. At the finish line of this race, an egg awaits the victor,
rather than a crown of laurel, as it crashes through. If the Y-carrying
sperm gets to the egg first, the baby, who has XY chromosomes, will
be a boy. If the first sperm to the egg carries an X, the XX chromo
some will produce a girl.
Such stories about the race between the Xs and the Ys for the
egg left many of us with the impression that the outcome was all in
the genetic instructions carried by the sperm. If the sperm delivered a
Y, bingo, it was a boy—what unfolded between conception and birth
was all more or less automatic and dictated by that genetic blueprint.
In fact, the process is much more complex. The sex-determining gene
in that Y chromosome has only a quick walk-on part in the elegant and
wondrous process through which boys become boys.
In animals such as birds and humans, one sex is the basic model
and the other is what might be described as a custom job, since the
latter requires a sequence of additional changes directed by hormones
to develop properly into the opposite sex. In birds, this basic model
happens to be male. In mammals, including humans, the opposite is
the case, and an embryo will develop into a female unless male hor
mones override the program and set it off on the alternative course.
Although the sperm delivers the genetic trigger for a male when
it penetrates the egg, the developing baby does not commit itself to
one course or another for some time. Instead, it retains the potential
to be either male or female for more than six weeks, developing a
pair of unisex gonads that can become either testicles or ovaries and
two separate sets of primitive plumbing—one the precursor to the
male reproductive tract and the other the making of the fallopian
tubes and uterus. These two duct systems, known as the Wolffian and
Mullerian ducts, are the only part of the male and female reproduc
tive systems that originate from different tissues. All the other essen
tial equipment—which might seem dramatically different between
the two sexes—develop from common tissue found in both boy and
girl fetuses. Whether this tissue becomes the penis or the clitoris,
the scrotal sack that carried the testicles or the folds of labial flesh
CHEMICAI MESSENGERS
A
'1
43
around a woman’s vagina, or something in between depends on the
hormonal cues received during a baby’s development.
The big moment for the ¥ chromosome comes around the sev
enth week of life, when a single gene on the chromosome directs the
unisex sex glands to develop into male testicles. In doing this, the ¥
chromosome throws the switch initiating the very first step in male
development, the development of the testes, and that is the begin
ning and end of its role in shaping a male. From this point on, the re
mainder of the process of masculinization is driven by hormone
signals originating from the baby’s brand-new testicles. In adult life,
the testicles produce sperm to fertilize a woman’s eggs, the male’s
contribution to reproduction and posterity. But the testicles play an
even more important role in a male’s life before birth. Without the
right hormone cues at the right time—cues emanating from the tes
ticles—the baby will not develop the male body and brain that go
along with the testicles. It might not even develop the penis required
to deliver the sperm the testicles produce.
In girls, the changes that turn the unisex glands into ovaries,
the part of the female anatomy that produces eggs, begin somewhat
later, in the third to fourth month of fetal life. During this same pe
riod, one set of ducts—the Wolffian ducts that provide the option
for a male reproductive tract—wither and disappear without any spe
cial hormone instructions. While the development of the female
body isn’t as dependent on hormone cues as the development of
males, animal research suggests estrogen is essential for proper de
velopment and normal functioning of the ovaries.
The process of laying the groundwork for the reproductive tract
is more complicated in males and is marked by critical stages where
hormones direct now-or-never decisions. Shortly after they are formed,
the testicles produce a special hormone whose function is to trigger
the disappearance of the female option—the Mullerian ducts. To ac
complish this milestone, the hormone message must arrive at the
right time, because there is only a short period when the female
ducts respond to the signal to disappear. Then the testicles have to
send another message to the Wolffian ducts, because they are pro
grammed to disappear automatically by the fourteenth week unless
they receive orders to the contrary.
44
OUR STOLEN FUTURE
The messenger is the predominantly male hormone testos
terone, which insures the preservation and growth of the male Wolf
fian ducts. Under the influence of testosterone, these ducts form the
epididymis, vas deferens, and seminal vesicles—the sperm delivery
system that leads from the testicles to the penis.
A potent form of testosterone guides the development of the
prostate gland and external genitals, directing the genital skin to
form a penis and a scrotum that holds the testicles when they finally
descend from the abdomen late in a baby’s development. A naturally
occurring defect dramatically illustrates what can happen if these
messages do not get through.
From time to time, a young patient will show up in a gynecolo
gist s office because the teenager still hasn’t had her first period al
though all the other girls in her class have passed this milestone.
Usually nothing serious is wrong.
But once in a rare while, the physician will deliver an utterly
shocking diagnosis. The patient isn’t menstruating because despite
all appearances, she is not female. Although such individuals have
grown up as normal-looking girls, they have the XY chromosomes
of males and testicles in their abdomen instead of ovaries. But be
cause a defect makes them insensitive to testosterone, they never
responded to the hormone cues that trigger masculinization. They
never developed the body and brain of a male.
The pictures in medical textbooks of these unrealized males are
fascinating, for there is nothing about their unclothed bodies that looks
the least bit odd or unusual. As hard as one searches for a hint that a
genetic male lurks inside these bodies, there is no sign of development
derailed. These genetic males look like perfectly ordinary women with
normally developed breasts, narrow shoulders, and broader hips.
These completely feminized males are the most extreme exam
ple of what happens when something blocks the chemical messages
that guide development. If anything interferes with the testosterone
or the enzyme that amplifies its effect, the common tissue found in
boy and girl fetuses will develop instead into a clitoris and other
external female genitals. In less extreme cases of disruption, males
may have ambiguous genitals or abnormally small penises and unde
scended testicles.
CHEMICAL MESSENGERS
-x
45
But sex is more than a purely physical matter. According to
physicians who treat them, these feminized males not only look like
women, they act and think of themselves as women. There is noth
ing the least bit telling in their behavior to suggest that they are
really male. In most animals, the development of a properly func
tioning male or female involves the brain as much as the genitals,
and research such as vom Saaks shows that hormones permanently
shape some aspects of behavior before birth as much as they sculpt
the penis. If an individual is going to act like a male as well as look
like one, the brain must receive testosterone messages from the testi
cles during a critical period when brain cells are making some of their
now-or-never decisions.
An individual who gets the wrong hormone messages during
this critical period of brain development may show abnormal behav
ior and fail to mate even though it has the right physical equipment.
In an influential 1959 study, Charles Phoenix of the University of
Kansas found that female guinea pigs exposed to high levels of
testosterone in the womb acted like males. They would not show the
classic female mating posture, a raised posterior, known as “lordo
sis,” as adults or respond normally to the female hormones that stim
ulate sexual behavior and reproduction.
No one debates that hormones act to give males and females
different bodies and that their role in the development of animals
and humans is pretty much the same. But how hormones influence
the development of the human brain is hotly debated. Do they
shape the brain and behavior in humans as dramatically as they do in
mice or rats or guinea pigs? Are there structural differences between
the brains of men and women, and is there anv evidence that the differences stem from hormone influences before birth?
These questions are difficult to answer. Not only is human be
havior more complex than that of vom Saal’s mice, but we aren’t free
to give pregnant women various doses of hormones to see the effect
on the brain development of their babies.
Those who have probed the question of whether the behavioral
differences between men and women have a biological basis or are
purely cultural have found evidence of some structural differences
linked to hormones, but so far these sex-linked areas are fewer and
OUR STOLEN FUTURE
less pronounced than those seen in rats. Psychologists have also re
ported certain general differences in the way men and women think,
reporting that women have greater verbal skills as a rule and men tend
to be better at solving spatial problems. Many also believe that the
rough-and-tumble play and fighting seen to a much greater degree in
young boys than in girls stems from biology rather than from culture
or child-rearing methods.
At the same time that hormones are guiding at least some as
pects of sexual development of the unborn child, these chemical mes
sengers are also orchestrating the growth of the baby’s nervous and
immune systems, and programming organs and tissues such as the
liver, blood, kidneys, and muscles, which function differently in men
and women. Normal brain development, for example, depends on thy
roid hormones that cue and guide the development of nerves and their
migration to the right area in this immensely complex organ.
For all these systems, normal development depends on getting
the right hormone messages m the right amount to the right place
at the right time. As this elaborate chemical ballet rushes forward at
a dizzying pace, everything hinges on timing and proper cues. If
something disrupts the cues during a critical period of development,
it can have serious lifelong consequences for the offspring.
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HORMONE HAVOC
As WE PURSUE THE MYSTERY OF HAND-ME-DOWN POISONS, TWO TRAGIC
A
episodes in medical history contain important lessons and immedi
ate relevance to our quest. They leave no doubt that humans are vul
nerable to hormone-disrupting synthetic chemicals and demonstrate
that animal studies had repeatedly provided an early warning about
the hazards for humans.
From the very beginning, these warnings were clear and omi
nous. As early as the 1930s, researchers at Northwestern University
Medical School showed that tinkering with hormone levels during
pregnancy was dangerous business, particularly for the fetus under
going rapid development in the womb. In some of the experiments,
the researchers simply gave an extra dose of estrogen to pregnant rats,
who already have this female hormone in their bodies. The impact on
their pups proved dramatic. At birth, the rat offspring showed strik
ing abnormalities stemming from disrupted sexual development. The
female pups exposed to extra natural or synthetic estrogen in the
womb suffered structural defects of the uterus, vagina, and ovaries;
males had stunted penises and other genital deformities.
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48
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OUR STOLEN FUTURE
I
In contrast to Fred vom Saal’s work, which explores the effect
of tiny natural variations in hormone levels in the womb, these ear
lier experiments boosted a female’s hormone levels beyond the nor
mal range by adding estrogen from outside the body. They showed
t at larger shifts in hormone levels scrambled the chemical messages
and derailed sexual development. Although estrogen at normal levels
is essential for development, too much of it can wreak havoc.
This cautionary evidence was timely indeed. In 1938 British
scientist and physician Edward Charles Dodds and his colleagues
had announced the synthesis of a chemical that somehow acted in
e body like natural estrogen, and the medical community was abuzz
with excitement. Leading researchers and gynecologists hailed the
man-made estrogen, known as diethylstilbestrol or DES, as a wonder
drug with a host of potential uses. Almost immediately, researchers
began giving DES to women experiencing problems during preg
nancy in the belief that insufficient estrogen levels caused miscar
riages and premature births. What would prove to be a massive
uman experiment—one that eventually involved an estimated five
million pregnant women in the United States, Latin America, and
elsewhere was just getting under way.
In the decades that followed, doctors not only prescribed DES
to prevent miscarriages, they began to recommend it for untroubled
pregnancies as if it were a vitamin that could improve on nature
Prestigious publications, among them the Journal of Obstetrics and
Oynecology carried drug company ads such as one from Grant
Chemical Company that appeared in June 1957, which touted the
use of DES for “ALL pregnancies,” boasting that it produced “bigger
and stronger babies.”
&&
DES also found a broad market beyond pregnant women. Doc
tors used it liberally to suppress milk production after childbirth to
alleviate hot flashes and other menopausal symptoms, and to treat
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acne prostate cancer, gonorrhea in children, and even to stunt the
grow in teenage girls who were becoming unfashionably tall For
years college climes doled out DES as a “morning after” contracep' . Fa™erS We7buIlisl> on DES and used tons of it as an
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HORMONE HAVOC
51
-
demonstrated again and again as scientists explored the power of
chemicals to disrupt development. A small dose of a drug or hor
mone that might have no effect at one point in a baby’s develop
ment, for example, might be devastating just a few weeks earlier.
Americans largely escaped this tragedy, thanks to a skeptical
physician at the Food and Drug Administration, Frances Kelsey, who
had demanded more safety data and held up its general sale. Never
theless, the thalidomide experience had a profound impact on the
public and on scientists in the United States as well as elsewhere.
Though it had taken an incident as subtle as a sledgehammer to
drive the point home, the medical and scientific community finally
accepted without question what some animal researchers had been
trying to tell them for decades: chemicals can cause birth defects in
humans as well as in rodents.
For ordinary people, the pictures of babies without limbs shook
the technological optimism that had reigned since the end of World
War II like a California earthquake and caused growing skepticism
about the wonder drugs and “miracle” chemicals pouring onto the
market and about the adequacy of government regulation. In the
summer of 1962, through the news magazines such as Life, many
shared the nightmare of Sherri Finkbine, a twenty-four-year-old
mother and television host from Arizona who had taken thalidomide
tranquilizers brought home from England during the critical early
phase of her pregnancy. Convinced that her unborn baby had been
severely damaged, Finkbine and her husband searched for a place in
the United States to obtain an abortion, which was then illegal ex
cept to save the life of the mother. Their desperate quest finally
ended in Sweden.
By chance, Silent Spring—Rachel Carson's now classic book on
the dangers posed by synthetic pesticides to humans and the ecosys
tem—began appearing in serial form in The New Yorker just before
the thalidomide story broke. The book caught the cresting wave of
public anxiety and rode it to the best-seller list.
If thalidomide exploded the myth of the inviolable womb for
ever, the DES experience toppled the notion that birth defects have
to be immediate and visible to be important. r < H
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52
DUR STOLEN FUTURE
Every parent prays for a normal, healthy baby.
When their daughter Andrea was finally born in September
1953, Eva and David Schwartz, a couple living in Boston’s Roxbury
neighborhood, felt they had been blessed with even more than they
had prayed for. Their baby was not only normal and healthy, she was
beautiful. Eva, who had suffered two miscarriages after the birth of
her son Michael eight years earlier, was ecstatic. She often declared
that the baby girl was the most gorgeous thing she had ever seen.
Chubby, pink, blond, Andrea was the kind of baby you saw in baby
food ads.
In a baby picture, Andrea’s inquisitive eyes peek out from un
der the brim of a sunbonnet, suggesting intelligence as well as
beauty. The face is framed by a delicate lace collar, and her mother’s
pride is evident in the impeccably ironed dress. As she grew, the little
girl was tough and robust and never seemed to be anything but per
I
fectly healthy.”
Then in April 1971, the Schwartzes’ lives suddenly changed
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forever.
Andrea, then seventeen, was a high school senior, bubbling
over with plans and dreams that started with college in the fall and
eventually included marriage and a family. She had always wanted
children, always. She remembers being captivated when she was just
hve, by her cousin’s new baby and the thrill of being allowed to sit on
the couch and hold it. Andrea didn’t have overly grand ambitions;
she just wanted a happy, normal life.
As Eva Schwartz paged through the Boston Globe one morning,
she began reading a story that took her breath away. According to a
new study in the New England Journal of Medicine, doctors at Massa
chusetts General Hospital had linked a rare vaginal cancer showing
up in young women to a drug their mothers had taken during preg
nancy—the synthetic estrogen DES. Her mind flashed on the pills,
hundreds of pills, she had taken religiously while pregnant with An
drea. She had never missed a day, even though she often suffered
from extreme nausea. On such days, she would wait until her roiling
stomach settled a bit before taking the pills the doctor had ordered.
Even before her medical records confirmed it, Eva Schwartz knew.
She was one of those mothers.
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HORMONE HAVOC
53
Although that last pregnancy was an untroubled one, her physi
cian at the neighborhood health clinic in Roxbury had nevertheless
prescribed a regimen of DES, no doubt because of her history of mis
carriages. Eva began taking the DES pills when she was just six weeks
pregnant and continued to take increasingly larger doses of the drug
as her pregnancy advanced, following a program recommended by a
husband-and-wife research team from Harvard Medical School,
George van Siclen Smith, a physician, and Olive Watkins Smith, an
endocrinologist. The Smiths were the nation’s leading advocates for
prescribing DES for pregnant women, especially for those who had
already lost pregnancies.
Andrea Schwartz would escape the worst ravages of DES. Un
like the most unfortunate ones, she did not die of cancer while still
in her teens or undergo mutilating surgery that excised the uterus and
vagina in the process of trying to excise the cancer. But medical tests
over the next decade would show that despite outward appearances,
Andrea was far from normal. DES had already stolen some of her
dreams.
As one explores the DES experience, one nagging question re
curs. It is a question that arises not just with DES, but with all handme-down poisons that cause damage across generations.
Would doctors have ever linked the medical problems suffered
by young women with a drug their mothers had taken decades earlier
if it hadn’t been for a striking cluster of extremely rare cancers and a
chance question posed by a patient’s mother? Some specialists are
confident they would have recognized the problem, saying that DES
exposure causes other unique symptoms besides cancer, such as mal
formed vaginal tissue. Sooner or later, someone would have made
the connection. Still, it is possible no one would have ever figured
out that DES was doing profound but invisible damage to those ex
posed in the womb. Until DES, most scientists thought a drug was
safe unless it caused immediate and obvious malformations. They
found it hard to believe that something could have a serious long
term impact without causing any outwardly visible birth defects.
And even when one recognizes that prenatal events can lead to
medical problems years later, the long lag time between cause and
54
OUR STOLEN FUTURE
effect makes it difficult to prove connections or even verify that the
mother had been exposed to the suspected drug or substance. In the
case of DES, fears of liability on the part of doctors have only added
to the difficulties for those exposed to the synthetic estrogen. DES
daughters and sons joke bitterly about the epidemic of fires and
floods that they say hit doctors’ offices when they have sought to ob
tain their mothers’ medical records.
The most painful aspect of the DES tragedy is that the drug
did not even prevent miscarriages. By 1952, at least four separate
studies had reported that women treated with DES for threatened
miscarriages did no better than those treated with alternatives such
as bed rest or sedatives. Later that same year, Dr. William Dieckmann and his colleagues from the University of Chicago presented a
damning indictment of DES’s efficacy at the annual meeting of the
American Gynecological Society. In the largest and most carefully
designed trial to date, the team enlisted two thousand pregnant
women, treating half of them with DES and the rest with an identi
cal-looking pill that contained no drug. The researchers attempted
to eliminate bias by using double-blind methods that keep both pa
tients and doctors ignorant of who got DES and who got the fake
pill. Their conclusions were unambiguous: this wonder drug made
no difference at all in the outcomes of pregnancies. Those who took
DES did not have fewer miscarriages, fewer premature babies, or
fewer infant deaths. Even worse, a later analysis of this same data
concluded that DES had caused significant increases in miscarriages,
premature births, and deaths among newborn infants.
Despite the studies showing DES to be ineffective, the federal
Food and Drug Administration took no action to restrict its use
during pregnancy. The University of Chicago study did, however,
dampen enthusiasm somewhat, and some physicians stopped using
DES. But many did not, and for almost two decades, hundreds of
thousands of women still took DES during pregnancy, hoping to pre
vent miscarriages.
When the cluster of cancer cases began showing up at Mas
sachusetts General Hospital in Boston, doctors were alarmed and
utterly baffled. Between 1966 and 1969, specialists there had seen
seven cases of clear-cell cancer of the vagina—an extremely rare can-
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cer that almost never occurred in women under fifty. But the pa
tients referred to the Harvard University teaching hospital for treat
ment during this period were all young women between fifteen and
twenty-two. Prior to this rash of patients in one Boston hospital, only
four cases had ever been reported in women under thirty in the
world’s medical literature.
Even the most radical treatment, which included removing the
uterus and vagina, didn’t always spare the young women’s lives. One
of those first patients died in 1968 at eighteen.
At first, Dr. Howard Ulfelder, a professor of gynecology at Har
vard Medical School, had shrugged off the question posed by the
mother of one of these young patients. She had taken DES during
her pregnancy, she said. Did he think that could have anything to do
with her daughter’s illness?
Ulfelder just couldn’t see how this could be possible. Neverthe
less, when the next mother came in with a daughter suffering from
clear-cell cancer, he decided to ask whether she had taken DES dur
ing pregnancy. He was stunned when she said yes.
Ulfelder and his Mass General colleagues Arthur Herbst, an ob
stetrician, and David Poskanzer, a medical epidemiologist, had been
sifting through the histories of these young patients looking for some
common factor that might explain why this rare cancer was suddenly
showing up in these young women. At last, they had a possible clue.
In April 22, 1971, they published a paper in the New England Journal
of Medicine reporting that seven of the eight young women treated
for clear-cell cancer of the vagina had mothers who had taken DES
during the first three months of pregnancy.
Eva Schwartz couldn’t bring herself to tell Andrea about DES
and the danger of cancer for five months. Then just before Andrea
was going to start college in the fall, she made an appointment to
have her daughter examined by a gynecologist and broke the news.
Sitting at her kitchen table in the Boston suburb of Canton al
most a quarter century later, Andrea Schwartz Goldstein cannot re
call the words of that conversation. She only remembers the feelings,
the sensation of being ripped from a sunny shore and sucked into
a violent whirlpool of fear and uncertainty. Her mind raced. She
56
OUR STOLEN FUTURE
thought about what she had confidently assumed about the life that
stretched ahead of her. Maybe she would die of cancer before she
ever had a chance to marry. Maybe she would never have the chance
to have kids. Again and again after that day, the thought returned:
“I’m not going to live a whole life.”
She was still wrestling with the specter of cancer four years
later, when she married Paul Goldstein, whom she had met through
a friend when she was sixteen. The following year they bought a threebedroom house in Canton, and Andrea took out a life insurance policy
that was renewable without a physical, just in case. The insurance
policy would help out if she died and left Paul with little kids.
At forty, Andrea is still blond and the green eyes still have the
same intensity as in the baby pictures. She is an attractive woman
who bears deep psychological as well as physical scars from her DES
legacy. At times, she has battled depression, and even after all these
years, the pain hovers just beneath the surface as she speaks, raw and
unhealed. After thirteen years of working as an assistant to a physi
cian specializing in infertility, she recently returned to school to get a
nursing degree. DES took many things from her, she reflected, in
cluding the time of her life that should have been carefree and fun.
Although there were plenty of indications in animal studies
that prenatal exposure to DES or estrogens might cause other dam
age, medical specialists focused for the most part on clear-cell cancer
of the vagina and on tissue abnormalities in the vagina, which they
feared might lead to cancer. It never occurred to Andrea that invisi
ble damage caused by DES might make it impossible to have chil
dren. Even her doctors did not suggest the possibility.
Andrea puts another picture on the kitchen table not far from the
baby picture of the blond girl in the sunbonnet. This picture, however,
reveals the reality hidden beneath the appearance of health and nor
malcy. She holds the X ray up to the light, recalling the day she picked
it up at the radiologist’s office. The secretary handed it over, reporting
that the doctor had said it was “the funniest uterus he had ever seen.”
The previous year Andrea had suffered an ectopic pregnancy,
an abnormal event in which the fertilized egg fails to descend prop
erly into the uterus. Instead, it begins developing in the fallopian
tube that leads from the ovary to the uterus—a dangerous situation
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57
that often ruptures the tube, causing severe bleeding and sometimes
death. After Andrea was rushed to the hospital, doctors had oper
ated, stopped the bleeding, and cut out the damaged tube. That left
her with only one fallopian tube.
In the months that followed, she and Paul tried again to start a
family, but to no avail, so she finally consulted a fertility specialist.
When he learned that she was a DES daughter, her doctor had or
dered a special X ray of the uterus because a new study had found
that forty out of sixty daughters examined using a special dye and
X-ray technique had abnormally formed uteri.
The eye searches the patterns of light and dark on the X ray
looking for the familiar triangular space, theAipside down pear seen
so often in schematic diagrams of the female reproductive tract. There
is nothing recognizable as a uterus. The area highlighted by the dye
is a narrow, ragged tube containing no cavity at all.
Andrea liked her doctor because he didn’t sugarcoat the diag
nosis. He put it to her straight. Her uterus was “severely misshapen.”
She was never going to be able to have a baby.
Just as it had done to the rat pups in the experiments decades
earlier, DES had left her with severe reproductive tract deformities.
Regardless of the compelling association between DES and
vaginal cancer reported by the team from Mass General, some in the
medical and scientific communities remained skeptical that DES
could really cause vaginal cancer in those exposed before birth, even
though animal studies a decade earlier had signaled possible links
between early estrogen exposure and later cancers. In a 1963 study
published in the Journal of the American Cancer Institute, Thelma
Dunn, a pathologist with the National Cancer Institute, found that a
variety of pathological changes, including cysts and cancers, devel
oped in mice that had received estrogen injections as newborns. She
warned that the results showed “the vulnerability of the immature
animal to the harmful effects of exposure to a naturally occurring
hormone.” Dunn urged that when clues to the cause of cancer are
sought in human populations, “every effort should be made to ob
tain the prenatal and early postnatal history of patients with cancer.”
A year later in the same journal, Noboru Takasugi and Howard Bern
58
OUR STOLEN FUTURE
reported parallel findings, including permanent changes in the vagi
nal tissue of mice treated with estrogen shortly after birth. They,
too, warned about the serious implications: “We feel that abnormal
hormonal environments during early postnatal (and antenatal) life
should not be underestimated as to their possible contribution to ab
normal changes of neoplastic [cancerous] significance later in life.”
Although these animal studies proved to hold clinically relevant
warnings for humans, doctors and drug makers paid no heed.
The argument about whether DES had caused the rare vaginal
cancers was still raging in the early ’70s when John McLachlan, a
young researcher who specialized in the transfer of drugs and other
environmental chemicals into the uterus, arrived at the National In
stitute of Environmental Health Sciences at Research Triangle Park,
North Carolina, to set up a new group to investigate substances that
disrupted development. The DES cancer question was one of the
first challenges the developmental toxicology group took on.
Before long, the group had its first important finding. The vagi
nal cancer, which was rare in humans, had never been seen in mice.
Nevertheless, McLachlan’s team was able to induce adenocarcinoma
of the vagina in female mice by giving DES to their pregnant moth
ers. The study helped settle that argument at least, but it was just
the beginning of a still continuing debate about whether DES is re
sponsible for a variety of medical problems and abnormalities seen in
DES daughters and sons.
McLachlan and his colleagues then began to explore the effects
of DES on male offspring. They demonstrated clearly that male mice
exposed to DES in the womb were no less damaged than their sisters
by this synthetic estrogen. These males had a variety of genital de
fects, including undescended testicles, stunted testicles, and cysts in
the epididymis, a portion of the reproductive tract adjacent to the
testicles where sperm mature. They also had abnormal sperm, reduced
fertility, and genital tumors. The researchers found signs that DES
had somehow interfered with the hormone messages during develop
ment. In normal male development, the testicles in the developing
fetus produce a chemical messenger that triggers the disappearance
of the female option, the Mullerian duct. The male mice exposed to
DES still had parts of the female reproductive system. In 1975, the
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team published a major paper in the journal Science detailing the dam
age done to male mice exposed to this synthetic estrogen before birth.
Those were heady times, McLachlan recalls, full of excitement
and discovery. It was cutting-edge science, and he loved being out
there. His team kept in close touch with Dr. Arthur “Hap” Haney, a
physician at the Duke University Medical Center in nearby Durham,
who was treating humans exposed to DES. Time and time again,
McLachlan would End something in a mouse and discover, when
he called Haney, that the physician had seen the same problem in
humans as well. Once in a while, the mouse findings would signal
problems long before they emerged in humans. The developmental
toxicology team warned about the possibility of undescended tes
ticles three years before the problem was reported in boys whose
mothers had been exposed to DES.
No doubt because they never developed a striking cancer, DES
sons have been studied far less than DES daughters. While McLach
lan and Haney repeatedly saw parallels between the damage found in
mouse studies and the problems showing up in humans, this dearth
of extensive human studies has made it impossible to establish con
clusively that DES sons do indeed have such problems more fre
quently than those who were not exposed to estrogen prenatally.
Some larger studies, such as those done at the University of Chi
cago, have reported higher rates of underdeveloped testes, stunted
penises, and undescended testicles as well as a greater frequency of
abnormal sperm in DES sons, but other studies haven’t confirmed all
these findings. Conflicting results have also emerged from studies ex
ploring links between DES exposure and testicular cancer, although
researchers have anticipated such a connection based on animal
studies. In the eyes of the medical establishment, the question re
mains officially unresolved.
Despite the medical skepticism, many DES sons are convinced
that they are suffering from DES damage, including greater rates
of testicular cancer and fertility problems. Rick Friedman is one of
those who is certain that DES has permanently marked his life.
For Friedman, youth hadn’t been a time of robust good health.
But he had forged ahead, ignoring as much as possible the arthritis
and physical problems that plagued him In his twenties, he had
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married and taken over the management of the family business, an
International House of Pancakes that his father had built almost two
decades ago in Ardmore outside of Philadelphia. If it wasn’t one
thing, however, it seemed to be another. After unsuccessful attempts
to start a family, Friedman and his wife, Sachi, consulted a fertility
clinic in 1987. While his wife suffered from reproductive difficulties,
tests showed that he was part of the problem, too: he had abnormal
sperm and a low sperm count.
It had never occurred to him that his growing litany of ailments
might somehow be connected—the chronic allergies, the strange
arthritis that hit when he was seventeen, the undescended testicle,
the epididymal cysts in his reproductive tract, and the infertility that
made it unlikely that he and his wife would have children. And then
in 1992, a freakish tumor. The discovery that his problems could
stem from a single cause, from something that happened to him be
fore he was born, was sheer accident. How unexpected that a com
mon thread might tie together all this pain and grief.
If Friedman had suspected he might be at special risk, perhaps he
wouldn t have ignored the fatigue and breathing problems for so long.
Perhaps he would have taken himself to a doctor before the tumor had
mushroomed into “a mass the size of a child’s football.” Those were the
words the doctor used to break the news that he was suffering from
something more than overwork. At thirty-one years of age, Friedman
found himself in the intensive care unit fighting for his life against can
cer and the severe lung damage that the tumor had caused. The doc
tors gave him only one chance in three of pulling through.
Nevertheless, he beat the odds. He survived the operation and
endured four rounds of aggressive chemotherapy. It was during his
long recuperation in early 1993, a time when he could do little more
than rest on the couch and read, that Friedman happened to pick up
McCall s magazine. With long hours to pass, he found himself read
ing anything and everything, and on this day, he started perusing an
article about the health problems of men who were exposed in the
womb to a drug taken by their mothers to prevent miscarriages.
“Damn, this sounds like me,” Friedman thought as he began to
read through the problems reported in males exposed to DES in the
womb—abnormal sperm, immune system problems such as arthritis,
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and the classic symptoms found in DES sons: undescended testicles
and epididymal cysts. He read on. The article featured several young
men who had been stricken with testicular cancer, which they are
convinced is yet another legacy of DES. Because of the dearth of
studies on DES sons and the difficulty of determining whether preg
nant women took the drug deca,des earlier, however, researchers
haven’t firmly established this connection. Although the football
size tumor had grown in his chest, not his testicle, the doctors had
told Rick it was a germ-cell tumor related to testicular cancer.
Rick pursued his hunch. At first his mother couldn’t recall tak
ing anything called DES, but that isn’t uncommon. In one study, re
searchers found that only twenty-nine percent of the women whose
medical records indicated they had taken DES during pregnancy
could recall whether they had taken the drug or not. Another eight
percent firmly stated that they had not, although their medical
records reported the contrary. Then as his mother searched her
memory, she told him that she had had a miscarriage before conceiv
ing him and had shown signs of threatening another early in her
pregnancy with him. Yes, she remembered, it was just after his
grandmother had passed away. Her doctor had given her a shot and
then put her on pills, but she didn’t know if they were DES.
Friedman decided to track down his mother’s medical records
and met with the same frustration experienced by cancer researchers
at Memorial Sloan-Kettering Cancer Center, who have tried to link
testicular cancer with prenatal DES exposure. His mother’s doctor was
now dead and the records long gone. The pharmacy where his mother
had bought the pills had moved and dumped their old records. The
hospital where he was born did eventually come up with records, but
they didn’t contain information on his mother’s prenatal care.
But Friedman really didn’t need records to confirm in his own
mind that he was indeed a DES son. Regardless of the continuing de
bate in the medical community, the circumstantial evidence seemed
overwhelming, in his view. As he explored medical surveys and hu
man and animal studies on DES effects, he found that he didn’t
have just one or two of the problems reported in males exposed to
DES. He had half a dozen. “I am a textbook case,” he concluded.
«
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OUR STOLEN FUTURE
In the case of DES daughters, on the other hand, there is ample
evidence that DES has caused clear-cell cancer and deformities of
the reproductive tract. Because of these structural abnormalities,
DES daughters are much more likely to have ectopic pregnancies,
miscarriages, and premature babies. Although the majority of DES
daughters eventually bear a child, often only after repeated attempts,
the odds are stacked against them, with two out of three pregnancies
ending in failure.
As was the case with thalidomide, the timing of the DES expo
sure appears more important than the dose. Women whose mothers
took DES after the twentieth week of pregnancy do not suffer from
the reproductive tract deformities, while those exposed before the
tenth week of pregnancy have a greater chance of developing vaginal
or cervical cancer.
This issue of timing also adds an element of confusion for those
investigating how DES has affected humans. Lumping together in
dividuals exposed early and late in pregnancy may mask the magni
tude of the drug’s impact on those exposed during critical periods of
development. Many studies have treated DES-exposed individuals
as a single group without addressing the question of timing.
But animal studies indicate that DES acts on other parts of the
developing fetus besides the reproductive tract, including the brain,
the pituitary gland, the mammary glands in the breast, and the im
mune system, causing permanent changes there as well. Researchers
have found evidence that prenatal and neonatal exposure to DES or
other estrogens can sensitize the developing fetus to estrogens and
perhaps make it more vulnerable later in life to certain cancers, such
as those in the breast, uterus, and prostate, that have been linked to
elevated estrogen exposure.
In immune system studies on mice, scientists have found that
DES exposure before birth reduces the number of T-helper cells,
which are sometimes described as the heart of the immune sys
tem because they coordinate the overall immune response by telling
other immune cells when to come into play. The importance of the
T-helper cells has been vividly demonstrated recently by the arrival
of the AIDS virus, which knocks out these key cells, thereby making
the body incapable of mounting a coordinated immune response.
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The devastation of the T-helper cells allows all kinds of invaders
from cancers to fungus to run amok, which is why AIDS patients
typically battle one disease after another. DES also affects another
important part of the body’s defense system, the natural killer cells,
which are thought to act as a tumor patrol, alerting the immune sys
tem to the presence of tumor cells and controlling the spread of
these cells to other parts of the body—a process known as metas-’
tasis. Given this decreased tumor defense, it is not surprising that a
number of studies have found that DES-exposed mice show an in
creased sensitivity to chemical carcinogens in adult life and develop
more cancers as they age.
Although DES-exposed mice have been reported to develop
cancers in the breast, uterus, and ovaries, nothing is known about
the incidence of these cancers in women exposed to DES before
birth. But in the past decade, researchers have confirmed that women
exposed to DES before birth show similar permanent changes in the
function of their T and natural killer cells. Despite these impair
ments, DES offspring have generally not shown a greater vulnerabil
ity to infection, although one study did find an increased incidence
of rheumatic fever. There is growing evidence, however, that DESexposed women have a greater likelihood of developing autoimmune
diseases, such as Hashimoto’s thyroiditis, Graves’ disease, rheuma
toid arthritis, and other diseases stemming from defects in the regu
lation of the immune system. Based on animal studies that show
that the severity of immune defects increases with age, researchers
are concerned that humans exposed to DES will also experience
more immune system problems as they get older.
Has DES had as dramatic an impact on the brain as it has had
on the body? This is perhaps the most intriguing question stemming
from the inadvertent human DES experiment, and it remains largely
unanswered. Although studies have found that DES disrupts the
physical development of humans and animals in identical ways, it
isn’t clear that these striking parallels hold when it comes to its im
pact on the development of the brain. Studies have found some dif
ferences between species in the balance of hormones at work during
this process, making it difficult to extrapolate directly from rodents
to humans.
64
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OUR STOLEN FUTURE
In animals, exposure to DES or higher than normal levels of es
trogen causes “dramatic and permanent changes in brain structure
and behavior,” according to Melissa Hines, a researcher at Goldsmiths’
College, University of London at New Cross, who specializes in the ef
fect of hormones on the development of the brain and behavior. And
here again the effects are surprising and counterintuitive. As strange
as it might seem, female rats, mice, hamsters, and guinea pigs ex
posed to excess estrogen before or just after birth show a more mascu
line pattern of reproductive behavior. They mount other animals
more frequently and are less inclined to display the female mating
posture. Early estrogen exposure also alters other behavior that differs
between the sexes, such as rough-and-tumble play, maze learning,
and aggression, causing females again to act more like males. So while
small amounts of estrogen appear necessary for normal female devel
opment, higher doses result in masculinization. Across a wide range of
species, including amphibians, songbirds, rodents, dogs, cattle, sheep,
and rhesus monkeys, researchers have found that exposing developing
females to increased estrogens or male androgens will increase mascu
line behavior and decrease feminine behavior.
In male mice whose mothers are treated during pregnancy with
low doses of DES, scientists have observed increased rates of terri
torial behavior, notably the marking of their territory with urine, and
obvious increases in activity levels as adults. At high doses, one gets
the opposite effects and impaired masculine behavior.
The animal studies raise provocative questions about possible
effects in humans, but unfortunately most of them have never been
carefully investigated, Hines notes.
The best evidence suggesting a link between DES exposure and
human behavior comes from studies on sexual orientation, the ques
tion of which sex an individual finds sexually attractive. The vast
majority of men are attracted to women and the vast majority of
women to men, an evolutionarily unsurprising arrangement since it
facilitates reproduction. But the classic Kinsey studies on human
sexual behavior found that this difference is not absolute. The Kin
sey surveys done in the late ’40s and early '50s reported that about
ten percent of the men were sexually attracted to other men and
three to five percent of the women to other women.
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Hines summarized several studies comparing DES-exposed
women with their unexposed sisters or with other unexposed women
and found an association between prenatal DES exposure and homo
sexuality and bisexuality. In one of these studies, researchers re
cruited and interviewed sixty women from a medical clinic—thirty
who had been exposed to DES and thirty presumably unexposed
women who showed abnormal Pap smears (although this condition is
also associated with DES exposure). The researchers conducted inter
views with these women and assessed their sexual orientation using a
seven-point heterosexual to homosexual gradient developed by Kin
sey. While none of the women with abnormal Pap smears indicated a
homosexual or bisexual orientation, twenty-four percent of the DES
women reported a lifelong bisexual or homosexual orientation. These
researchers also compared twelve DES daughters with sisters who had
not been exposed to the synthetic estrogen and found that fortytwo percent of the DES-exposed women had a lifelong bisexual ori
entation, but only eight percent of their sisters. A second study of
thirty DES-exposed women and thirty unexposed controls who were
matched based on such characteristics as age, race, and social class
reported similar differences. Studies on DES sons so far have found
no indication that DES influences the sexual orientation of sons.
The research team that recruited women at the medical clinic
also interviewed them to see if they could detect differences in other
behaviors that typically vary between male and females, such as par
enting interests, degree of physical activity, and aggression and delin
quency. An initial study reported that those exposed to DES showed
less interest in parenting, but a second failed to find such an associa
tion with DES exposure.
Researchers have also found surprisingly high rates of major de
pression in both men and women exposed to DES before birth as
well as other psychiatric disorders such as anxiety, anorexia nervosa
(an eating disorder in which individuals starve themselves by refus
ing to eat), and phobic neurosis. Studies have reported such differ
ences even when DES sons and daughters were unaware that they
had been exposed. In one series of studies of the DES-exposed, forty
percent of the women and seventy-one percent of the men had ex
perienced major depression that impaired the individuals’ ability to
66
OUR STOLEN FUTURE
function at home, work, or school, required taking medication for
depression, or required professional help.
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The DES experience is rich in lessons.
This tragic and unintended experiment demonstrated that chem
icals could cross the placenta, disrupt the development of the baby,
and have serious effects that might not be evident until decades later.
This was a previously unrecognized medical phenomenon: delayed
long-term effects that did not emerge until the child reached puberty
or anytime later in life.
It warned that appearances are not always coincident with real
ity. One had to worry not just about gross and immediately apparent
birth defects such as missing limbs but about invisible damage done
during development to tissue and cells—damage that can, neverthe
less, have a lifelong impact and undermine survival.
It dramatized the dangers of interfering with the delicate bal
ance of hormones during development. It showed how fragile the fetus
is and how it passes through critical stages when it is particularly
vulnerable. It underscored that an unborn baby is not just a small
adult. Drugs and chemicals that have little effect on adults can cause
serious and permanent damage to a baby during its rapid prenatal
development.
Again and again, the DES experience brought home the com
mon fate of mice and men. Rodents and humans exposed to DES in
the womb suffer identical damage to the genitals and the reproduc
tive tract, a parallel that also holds true not just for mammals but for
many other animal types as well. To an astonishing degree, evolution
has conserved through hundreds of millions of years a basic strategy
in vertebrates for embryonic development that is dependent on hor
mones. Regardless of whether the offspring is a human or a deer
mouse, a whale or a bat, hormones regulate its development in fun
damentally the same way.
“There are so many apparent differences in these species,” John
McLachlan noted. “Yet the strategy for sexual development is remark
ably similar, and the effect of estrogen is remarkably similar. That
sounds simple,” he reflected, “but to my thinking it’s profound.”
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The DES experience offered another critical lesson as well that
is relevant not just to those exposed to DES but to all of us. The
developmental effects of DES made it clear that the human body
could mistake a man-made chemical for a hormone. In the mid1970s, researchers began to discover that other man-made chemi
cals, such as the pesticides DDT and kepone, showed hormone effects
as well. It would take time for McLachlan and others to recognize
the potential importance of this observation.
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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 surpris
ingly 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 mes
sengers. 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 Muller,
discovered a powerful new pesticide, and both synthetic chemicals
made their debut amid great acclaim in 1938. Just as DES was her
alded as a “wonder drug,” DDT was hailed as a “miraculous pesticide.”
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Chemical structures of the natural female hormone (estradiol), generically
called “estrogen,” and the natural male hormone, testosterone, compared
with the structures for DDT, an insecticide, and diethylstilbestrol (DES), a
synthetic female hormone drug with estrogen-like effects. Surprisingly, DDT
and DES proved to be effective mimics of natural female hormones, de
spite their dissimilar appearance.
Dodds received a knighthood for his efforts in synthesizing sex hormones, and Muller 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 struc
ture 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 hor
mones that help carry on the body’s never-ending internal conversa-
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OUR STOLEN FUTURE
tion all share a common architecture based on four rings. The male
and female hormones, testosterone and estrogen, may have power
fully different effects, but in diagrams of their chemical structure,
they are remarkably similar. The divergent destinies of male and fe
male hinge on an atom here and there. By contrast, DDT and DES
have a two-ringed configuration. The difference between this arrange
ment 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.
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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 commu
nicates through hormones. Like many natural teachers, he has a the
atrical 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 sci
entists 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
in the air. A receptor isn’t supposed to receive all the chemical sig-
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nals 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 identifled.
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, reality is proving considerably messier and unpredictable,
DUR STOLEN FUTURE
72
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Under normal conditions (top), a natural hormone bmds(to lt7e^°r
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tivates genes in the nucleus to produce the appropriate biological response.
Hormone mimics (middle) can also bind to the receptor and mduce> jesponse.
Hormone blockers (bottom) do not induce a response but prevent natural hormo™ from attaching to the receptor. Certain synthet.c chemicals rel a ed
into the environment can behave like hormone mimics and hormone blocke
contributing to disruption of cellular activity. The compound that outnumbers
or outcompetes for receptor sites determines the response by the cell.
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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 un derstand how DES was able to
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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 develop
ing fetus contain special proteins that soak up almost all the estro
gen circulating in the blood and make it unavailable to receptors.
But these proteins—called sex steroid binding globulin—do not rec
ognize 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. With
out 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 estro
gen receptor. Some scientists have therefore suggested that these
“weak” estrogens are probably not powerful enough to cause prob
lems. 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 ma
jor figure in experimental DES research.
“The real issue is the special sensitivity of the developing or-
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74
OUR STOLEN FUTURE
ganism,” Bern says. It may be particularly vulnerable not only be
cause it is undergoing rapid development but also because its hor
mone 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 oper
ate 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 ef
fects across an astonishing range of species. Classic accounts of evo
lution 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, es
pecially elements of basic design, such as the endocrine system.
As scientists have explored hormone receptors in different ani
mals, they have marveled at the lack of change over millions of years
of evolution. Whether in a turtle, or mouse, or a human, the en
docrine 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 inter
nal communication system based on hormones and receptors is an
ancient adaptation that arose early in the evolution of vertebrates—
the evolutionary branch of animals with backbones that includes hu
mans. 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
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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 phenom
enon, but the mystery of hormone mimics would not yield to such a
simple explanation. To their bewilderment, they found that the es
trogen receptor binds to chemicals with a variety of strikingly differ
ent 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.
•
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The early 1940s seemed like a particularly promising time for the
sheep ranchers in the gently rolling hills south of Perth in western Aus
tralia. 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 fi
nally 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
OUR STOLEN FUTURE
76
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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 chemi
cals, 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 labora
tory, 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. Hor
mone mimics lurk in parsley, sage, and garlic; in wheat, oats, rye, bar
ley, 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 com
pounds 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 hormonethe renroductive
reproductive system.
* ~°«nipounds on the.
svstem. It might sound like a
evolutionary perspective it makes sense.
k escape predators by running away, they have
/riety of defenses. Some smell bad, taste bad, or
nem. Others have unpalatable thorns, spines, or
/s in their leaves. When insects attack, many
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FIFTY WAYS ID LOSE YOUR FERTILITY
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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 previ
ously 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 plant
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 chemi
cals 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 sig
nals the breast to produce milk. Mother rats given marijuana pro-
78
m SHIH Flint
duced no milk, and their pups died of starvation. Hughes later
moved on to investigate the effects of plant estrogens on the en
docrine 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 ex
ample, a plant managed to impair the fertility of all the males save
one that single male can, nevertheless, fertilize an entire flock of fe
males. 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 preda
tors that continue grazing.
Humans long ago figured out that certain plants have contracep
tive 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 preg
nancies 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 ac
tive 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 nec-
essary 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 experi-
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FIFTY WAYS TO LOSE YOUR FERTILITY
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cnees 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
many foods
foods raises
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 Toxi
cology 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 hu
mans eat a varied diet, it is not clear whether we ingest sufficient
quantities to worry about. The dose question is, moreover, inher
ently 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 post
menopausal 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
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OUR STOLEN FUTURE
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because their brains do not respond to the hormone that triggers
ovulation—an indication that they have been masculinized.
males, on the other hand, are feminized, showingless
havior and fewer ejaculations. For a rat, the first ten days ter b h
are the critical period for the development of those areas of the brain
bram
hnke Bu°t the ver^e foods that disrupt development before birth or
early in life might help prevent disease in an adult. Evidence t a
foods high in plant estrogens, such as soybeans, might protect agains
breast and prostate cancer has sparhed a great deal of scientific interest
and new research into plant estrogens. Numerous stud.es have finked
estrogens, even those naturally occurring in the body, to cancer, sug
gestmg that the greater a woman's lifetime exposure the greater the
nsk. Researchers theorize that plant estrogens might be protective
because they are weaker than the natural estrogens made n the body^
If they occupy estrogen receptors in the breast and displace natura
estradiol, they might reduce a woman’s lifetime exposure to estrogen.
The thing to keep in mind, Hughes says, is that plants an
e
animals that eat them, including humans, share a long eyolyt.ona^
history. Over many generations, the most sens.fve• md.viduals those
who became sterile from eating estrogenic foods, dropped out o
population. All those who were able to P™du“^.,easttXolu
spring passed on a certain degree of resistance. TTus sort of evolu
tionary winnowing occurs because of individual differences.
Tire discovery that DDT could act like an estrogen must have
seemed like a singular curios.ty in 1950, but unfortunately it has
proved far from unique. Over the past half century, the same chemica
Faboratones that produced this “miraculous” pesticide created a host
of other svnthetic chemicals that can also interfere wrth hormones
We have been slow to recognize this threat or to realize that the wor d
has become permeated with hormone-d^rupting synthetic ehem.cak
When male workers in a chemical plant developed extreme y
low sperm counts after exposure to the pesticide kepone, it became
clear that DDT was not the only synthetic chemical.capable.of pre
ducing estrogenlike effects. Others were quickly added to the list.
I ike DDT these synthetic chemicals were not intended as drugs or
hormone mimics. They were invented by chemists in laboratories to
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kill insects threatening crops and to give manufacturers new materi
als 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 II
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 dis
rupt the endocrine system in one way or another. Some mimic estro
gen 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 com
pounds 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 necessar
ily 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 admit
tedly 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 dis
ruptors 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 evolution
ary history with these synthetic compounds. These man-made es
trogen mimics differ in fundamental ways from plant estrogens, he
notes. The body is able to break down and excrete the natural es
trogen 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
IL/
62
OUR STOLEN FUTURE
chronic hormone exposure is unprecedented in our evolutionary
experience, and adapting to this new hazard is a matter of millen
nia 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 carcino
genic substances, since some researchers have discovered that cancer
causing substances can be produced through natural processes as well
as through industrial ones, and it has left most ordinary people hope
lessly 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 hor
mone 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 pomegran
ate for birth control and abortions. Even naturally occurring hor
mone 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 for
mulas
mulas containing
containing sov.
soy, which
which harbors
harbors estrogenic
estrogenic compounds, until
more comprehensive studies are completed.
I)’
If some scientists are seeking to identify hormone-disrupting
chemicals, others are exploring the hazards they might pose.
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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 Gray, a reproductive toxicolo
gist, 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 revi
sion. 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. Vinclo
zolin 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 testos
terone. Instead, vinclozolin 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 Hermaphro
dite whom classical sculptors portrayed as a figure with male genitals
and female breasts.
Gray and his colleague William Kelce have also recently discov
ered that DDE, a ubiquitous chemical and the DDT breakdown
.;^S
84
OUR STOLEN FUTURE
product found most often in the human body, acts as an androgen
blocker. Like vinclozolin, it binds to and blocks the androgen recep
tor, 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 envi
ronment 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 fre
quently, 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 discus
sion 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 pla
nar.” 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 es
trogen 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 di
vision at the EPA’s Health Effects Research Laboratory. Estrogen is
just one component in the complicated, integrated endocrine sys
tem, and, she says, synthetic chemicals target other parts of the sys
tem more commonly than they disrupt processes involving estrogen.
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The adrenal glands, which produce stress hormones, get hit more
than any other organ by man-made compounds, followed by the thy
roid 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 chemi
cals 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 syn
thesis 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 hor
mones 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 accel
erating their breakdown and elimination, leaving the body short not
just of estrogen but of testosterone and the other steroid hormones
OUR STOLEN FUTURE
86
as well. This can lead to abnormally low hormone levels. Since a de
veloping 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 ho mone mimics or blockers may boost the body’s hormone levels by in
terfering with the physiological processes that break down hormones
so they can be excreted. Some chemicals deactivate the enzymes in
volved in this process, according to Michael Baker an enzyme spe
cialist at the University of California at San Diego. If some chemical
interfered with the enzyme that helps break down estrogen, for ex
ample, it would cause more estrogen to be available to the receptors
and indirectly create an estrogenic effect without binding itself
the receptor. Based on the body’s response, one might mistake such
a chemical for a hormone mimic.
vl.,/,: animal studies of hormone-disrupting chemIn Earl Gray’s, view
d immediate relevance to humans. In the broader
icals have clear am-----have challenged the predictive value of
environmental debate, some —
.
rat studies to assess possible cancer
risksrisks
posed
by synthetic
chem<----cancer
posed
by synthetic
cals to humans on the grounds that animals and humans sometimes
react differently to a chemical. The use of animals to study hor
mone-disrupting chemicals is, however, fraught with less uncer
tainty. Gray explains, because scientists understand far more about
the role of hormones in development than they do about the bio ogical events that give rise to cancer. Moreover, the evidence shows
that humans and animals respond in generally the same way to ho mone-disrupting chemicals. The available human data and the effects
seen in lab animals show “a perfect correlation. Earl Gray spells ou
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the bottom line with intensity and directness.
“We know a lot about the process. We know it can be altere
by chemicals. It is important to take the effects you see m animal
studies seriously.”
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TO THE ENOS OF THE EARTH
After more than three months of darkness and teasing Twi
light, the sun hnally shoulders its way above the horizon, signaling
the approach of spring on Kongspya Island, high above the Arctic
Circle in Norway’s Svalbard archipelago. As the days quickly lengthen,
ringed seals begin to venture out of the water and dig nursery lairs in
the snowdrifts on the ice near shore. One by one, the polar bears stir
in their dens beneath the deeply drifted snow. Only pregnant fe
males hole up for the winter, while females that are not pregnant
and males spend the months of darkness wandering great distances
over the shifting pack ice that surrounds this part of Svalbard for
most of the year.
Kongspya, a rocky, treeless island lying east of Greenland at sev
enty-nine degrees north latitude, is something of a maternity ward
for the great white bear. Pregnant females often seek out the island’s
Bogen Valley, digging their nursery dens on its south-facing slopes as
winter sets in. There, in hibernation during the long winter night,
they give birth to one-pound cubs and nurse them for several months
before reemerging with twenty-pound youngsters in spring.
88
OUR STOLEN FUTURE
Twelve hundred miles to the south in Oslo, Oystein Wiig, a po
lar bear researcher, keeps tabs on more than a dozen of Svalbard s
pregnant bears from the warmth of his office at the Zoological Mu
seum. Much about these bears has remained a mystery because of
the cold, the darkness, and the remoteness of the high Arctic. But
now, with the help of modern technology such as helicopters and
satellites, scientists like Wiig can probe their previously hidden lives.
On held trips to Svalbard, he has fitted the female bears with radio
collars that beam signals to passing satellites that then transmit the
information to Wiig. As the bears leave their dens in March, Wiig
and his assistants head for Svalbard to track the new mothers and
learn more about the two thousand bears who roam the archipelago.
Based on what researchers had already learned, Wiig expected
at least twelve of the hibernating females to produce offspring, most
likely twins. But to his surprise, only Eve of the pregnant bears
emerged from their dens with young in 1992.
A single bad year should be no cause for alarm, for a female s
success in producing offspring can depend on many things, including
ice conditions, weather, the supply of seals for food, and the density
of the bear populations. The age at which female polar bears Erst re
produced in Svalbard had increased by a year over the past decade or
so, reflecting, Wiig speculates, that the bear population is reaching its
limit given the available food supply. But the failed pregnancies were
nevertheless worrisome, given what Norwegian researchers are finding
in the fat of the polar bears. Though Svalbard is remote and seems
pristine, the bears there are highly contaminated with industrial
chemicals, including PCBs, the pesticide DDT, and several other per
sistent man-made compounds that are known to disrupt reproduc
tion in wildlife. Wiig and his colleagues collect the fat from live bears
by shooting them with a dart containing a tranquilizer. Once a bear
becomes immobilized, Wiig might fit it with a radio collar and bore
into its blubber using a device similar to an apple corer.
Some Svalbard bears carry as much as ninety parts per million
of PCBs in their fat—an infinitesimal amount by normal measures,
but biologically a potent dose. Researchers studying declining seal
populations have found that seventy parts per million of PCBs is
enough to cause serious problems for females, including suppressed
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89
immune systems and deformities of the uterus and of the fallopian
tubes that transport the eggs from the ovaries. But those seals were
living in Wadden Zee, off the Netherlands, where industrial waste
has poured in for decades from Europe via the Rhine-Meuse estuary.
Svalbard, on the other hand, lies at the end of the Earth, hundreds of
miles from cities, chemical factories, farm fields, and dump sites.
Where was this stuff coming from, and how was it getting into
bears roaming the Arctic wilderness?
The story of PCBs and how they have spread throughout the
planet and into the body fat of almost every living creature is one
of the most fascinating and instructive chapters in the history of the
era of synthetic chemicals. Of the fifty-one synthetic chemicals that
have now been identified as hormone disruptors, at least half, in
cluding PCBs, are “persistent” products in that they resist natural
processes of decay that render them harmless. These long-lived
chemicals will be a legacy and a continuing hazard to the unborn for
years, decades, or in the case of some PCBs, several centuries.
Introduced in 1929, PCBs became the first big commercial suc
cess for a new elite of chemical engineers who would eventually syn
thesize tens of thousands of novel chemicals that exist nowhere
in nature. The engineers created PCBs by adding chlorine atoms to
a molecule with two joined hexagonal benzene rings known as a
biphenyl. The result of their tinkering was a family of 209 chemicals
known collectively as polychlorinated biphenyls, or PCBs, which soon
proved to be immensely useful compounds.
In early assessments, PCBs seemed to have many virtues and no
obvious faults. They are nonflammable and extremely stable. Toxic
ity tests at the time did not identify any hazardous effects. Con
fident of their safety as well as their utility, the Swann Chemical
Company, which would soon become a part of Monsanto Chemical
Company in 1935, quickly moved them into production and onto
the market.
With the issuance of federal regulations requiring the use of
nonflammable cooling compounds in transformers used inside
buildings, PCBs quickly found a steady major market in the elec
trical industry. Other industries put PCBs to use as lubricants, hy
draulic fluids, cutting oils, and liquid seals. In time, these chemicals
V
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OUR STOLEN FUTURE
also found their way into a host of consumer products and thus into
the home. They made wood and plastics nonflammable. They pre
served and protected rubber. They made stucco weatherproof. They
became ingredients in paints, varnishes, inks, and pesticides. In ret
rospect, it is clear that the very characteristics that made them a run
away commercial success also made them one of our most serious
environmental pollutants.
Although some evidence of toxic effects in workers began emerg
ing as early as 1936, indicating that PCBs were not as safe as previously
believed, PCBs were on the market for thirty-six years before serious
questions surfaced publicly about this wonder chemical. In the
meantime, manufacturers kept coming up with new uses. From 1957
through 1971, paper companies put PCBs in their carbonless copy pa
per, enabling typists, in an era before widespread use of the copying
machine, to make duplicates of documents without carbon paper. •.
The person to first recognize that PCBs had become a pervasive
contaminant was the Danish-born chemist Soren Jensen. In 1964
Jensen, who worked at the Institute for Analytical Chemistry at the
University of Stockholm, kept encountering mysterious chemical
compounds as he tried to measure DDT levels in human blood.
Whatever it was, Jensen found it wherever he looked—in wildlife
specimens collected three decades earlier, in the Swedish environ
ment, in the surrounding seas, in hair samples from his wife and in
fant daughter. The presence of the mystery contaminant in wildlife
samples taken in 1935 indicated it could not be a chlorine-based pes
ticide, which came into broad use only after World War II. It took
Jensen more than two years of investigation to identify the synthetic
pollutant as PCBs. A report of Jensen’s findings first appeared in the
British journal New Scientist in 1966.
As other scientists began to look for PCBs, they, too, found
them everywhere—in soil, air, water; in the mud of lakes, rivers, and
estuaries; in the ocean; in fish, birds, and other animals. Chemists
had long puzzled about the elusive peaks that showed up repeatedly
on their gas chromatograph charts when they were analyzing sam
ples taken from the environment. The peaks, which looked similar to
those made by DDT, registered the presence of some chemical, but
until Jensen compared the peaks using a chemical sample provided
TO THE ENDS OF THE EARTH
91
by a German manufacturer, they did not know what the contami
nant was. Finally, they had the answer—PCBs.
Ten years later, in 1976, the United States banned the manufac
ture of"PCBs, and other industrial countries eventually followed. In
half a century of production, however, the synthetic chemical industry
worldwide (excluding the USSR) had produced an estimated 3.4 bil
lion pounds of PCBs, and much of it was already loose in the environ
ment and beyond recall. Moreover, the ban did not address existing
PCBs, allowing their use to continue in closed applications—such as
transistors, electric ballasts, and small appliances—even today.
There is no way to discover exactly how the PCBs in the polar
bears made their way to the Svalbard archipelago or where they came
from. But research over the past two decades has given scientists a
good understanding of how PCBs travel through ecosystems and mi
grate over long distances. Based on this knowledge, it is possible to
imagine the journey of an individual PCB molecule. Though the
specific route and events in the journey we are about to describe are
hypothetical, the plot is a plausible scenario built from historical
accounts and a myriad of scientific studies.
'f
*<
Our imaginary PCB molecule—a chemical known among scien
tists as PCB-153 because of the arrangement of its chlorine atoms—
had already been around for some time before it set off on its global
wanderings just after World War II ended. As the market for PCBs be
gan to grow in the 1930s, the Monsanto Chemical Works expanded
production at its plant in Anniston, Alabama, where it heated a mix
ture of the chemical biphenyl, a particular form of chlorine, and iron
filings to create PCBs. During the spring of 1947, the workers at the
Anniston factory made up a batch of PCBs containing fifty-four per
cent chlorine. As the chlorine gas bubbled through the heated biphe
nyl, six atoms of chlorine bonded to one of the biphenyls in the tank,
and PCB-153 came into being. After an alkali wash and some dis
tillation to purify the newly formed PCBs, Monsanto often sold the
compound—which contained not only PCB-153 but dozens of other
members of the large PCB family—under its brand name Aroclor-1254.
Almost half a century later, the PCBs made on that spring day
might be found virtually anywhere imaginable: in the sperm of a
92
OUR STOLEN EUTURE
man tested at a fertility clime in upstate New York, in the finest
caviar, in the fat of a newborn baby in Michigan, in penguins in
Antarctica, in the bluefin tuna served at a sushi bar in Tokyo, in the
monsoon rains falling on Calcutta, in the milk of a nursing mother in
France, in the blubber of a sperm whale cruising the South Pacific,
in a wheel of ripe brie cheese, in a handsome striped bass landed off
Martha’s Vineyard on a summer weekend. Like most persistent syn
thetic chemicals, PCBs are world travelers.
Our imaginary molecule of PCB-153 that would end up in a po
lar bear in the high Arctic might have made its first trip by train. A
few weeks after the manufacture of this molecule, the freight train
carrying a shipment of Aroclor-1254 rumbled over the rails in New
York State headed for a plant in western Massachusetts where Gen
eral Electric manufactured electrical transformers.
These ubiquitous metal cans attached to electrical poles were
an essential component in the growing grid that sent electricity from
generating systems over high voltage power lines and into homes to
power lights, radios, vacuum cleaners, and refrigerators—the won
derful new twentieth-century electric conveniences. The transformers
made at GE’s Pittsfield, Massachusetts, plant reduced the high-voltage
current from the transmission lines into the lower voltage required
by lights and appliances.
From General Electric’s perspective, the PCBs were an ideal in
sulating coolant for their capacitors and for transformers used in sit
uations where flammability was a concern. Because PCBs did not
catch fire and burn, they offered a safer alternative to the flammable
oil used in transformers before this new synthetic product was devel
oped. The company had developed its own custom formula for trans
formers called Pyranol, containing Aroclor and oils which it blended
at the Pittsfield plant.
With the postwar economic boom, the demand for transform
ers and other electrical equipment seemed insatiable. America was
building new houses for returning GIs as fast as it could—houses
that needed new appliances and increased electrical service. While it
would be very difficult to retrace the precise sequence of events that
led to the escape of our PCB molecule into the environment, we can
imagine that the next step in its journey took place at Pittsfield, and
■■■
i
k
TO THE ENDS OF THE EARTH
*
I
!
I-
|
93
from interviews with a former plant employee and public records, we
can reconstruct what might have taken place on a typical summer
day. That summer the production line in Pittsfield was working at
full tilt, and the Pyranol in the factory storage tanks did not sit
around for long. On a steamy day in June, a worker reached for a
hose at his workstation that was connected through underground
pipes to storage tanks. After making a final check on the transformer
he had been finishing, he opened the valve and filled it to the top
with Pyranol. In a few days, our molecule of PCB-153, sealed tightly
inside that new transformer, was heading back south by train.
'4
!
I
The oil refineries in the west Texas city of Big Spring were also
scrambling that summer to keep up with the postwar economic
boom, for the explosive growth of suburbs was creating a new class of
commuters who needed new cars and gasoline to power them. One
of the city’s smaller oil and chemical companies, now no longer in
business, was moving as quickly as possible to build a new refinery
complex, but the project had stalled for several months while the
contractors awaited the arrival of back-ordered electrical equipment.
The shipment of transformers from GE to the refinery finally arrived
in July. Within a week, the distribution transformer containing the
molecule of PCB-153 was installed and in service in a building that
housed the control room for the new installation.
Not even a month had passed before a fierce August thunder
storm tore through Big Spring, filling the air with exploding thunder
and leaping lightning that struck at several places during the short,
violent storm, including the power lines supplying the refinery. As
the power surge hit the transformer near the control room, it re
sponded with a metallic thump and the building went dark.
The following morning, the refinery’s maintenance supervisor
lifted the cover of the transformer to inspect the damage. Seeing
twisted, crumbled coils, he decided that the unit was beyond repair,
so he asked one of his men to empty the unit and send it off to the
dump. The maintenance worker complied, hauling the transformer
to the parking lot. As he tilted the transformer, its oily contents
oozed out onto the red dirt of the parking lot, and PCB-153 slipped
into the greasy puddle. The worker reckoned the oil might help keep
94
OUR STOLEN FUTURE
down the insufferable dust. Since PCBs have an affinity for organic
matter, the molecule quickly attached itself to a dust particle.
But with the roaring winds of west Texas, dust never stays put
long. Four months later, a winter storm roared through and swept
the molecule aloft. Stampeding curtains of dust drove toward the
town of Tarzan, where they beat against barns and houses as the
winds howled. The dust particle with PCB-153 rode the whirlwind,
bouncing with the turbulence like a cowboy on a bronco. The wild
ride ended when the dust particle sifted through the fine cracks
around a doorsill and settled in a drift on the kitchen floor.
When the windstorm passed, the woman of the house'surveyed
her kitchen with a sigh. The fine red dust coated the windowsills and
lay two inches deep before the door. With a weary efficiency, she took
up her com-straw broom and whisked the dust particle with our itiner
ant molecule into a dustpan. As it fell into the wastebasket, the dust
particle sifted down into a crumpled, grease-stained newspaper page
that the housewife had used to drain her bacon that morning.
By the end of the week, PCB-153 was buried under trash in a lo
cal dump, an informal affair in a ravine with a parched creek bed.
Despite the rivulets that flowed down through the growing moun
tain of trash during summer thunderstorms, the molecule stayed put
for more than two years, for unlike many chemicals, PCBs don’t dis
solve readily in water.
The late winter of 1948 brought a spell of heavy rains to west
Texas. After intermittent downpours, the creek surged to life in the
beginning of March and roared toward the trash that tumbled down
the side of the ravine. The roiling waters took a bite out of one edge
of the trash mound, exposing a cross section of the town’s recent his
tory and sweeping the greasy newspaper and the molecule from the
transformer spill downstream. The floodwaters subsided the follow
ing morning, leaving the soggy newspaper sheet stranded on a sand
bar five miles away. PCB-153 was clinging to a greasy blotch on the
page, shielded from the light but exposed to warm spring air.
As the sun climbed higher and winter turned to spring, the lump
of paper dried and slowly warmed. With the sun beating down on the
paper in early April, PCBs suddenly began disengaging from the, dust
particle moving upward, floating into the air as a vapor. The PCB-153
TO THE ENDS OF THE EARTH
i
i
i
95
was suddenly free. The journey that would end in the rump fat of a
Norwegian polar bear had begun.
The molecule caught a warm gentle breeze from the southwest,
wafting north and east over the shrub-covered expanse of east Texas
toward the fragrant pine forests of Arkansas. As the breeze stiffened,
it sailed on unimpeded into Missouri. A rising current of spring air
pushed it higher into the atmosphere, and the molecule soared up
ward, higher and higher on the thermal. When the air mass collided
with a cold front moving down from the north, the journey ended
abruptly. The clouds released their moisture in a hard, cold rain, and
PCB-153 washed back to earth and landed on a bluff overlooking the
Mississippi River north of St. Louis.
During three weeks of unusually cool and cloudy weather, the
molecule clung to a rotting leaf in a hollow on a rocky outcropping,
but as soon as the sun reemerged and the temperature climbed,
the molecule floated off again. It lingered over St. Louis for several
days and sloshed about in a stagnant air mass. Then, as a Bermuda
high developed off the southern Atlantic coast, a torrent of air
rushed through from the south and swept the PCB molecule north
ward over the radiant green cornfields of southern Illinois toward
the Great Lakes.
The air flow generated by the Bermuda high pushed north with
the speed of a freight train. The molecule tumbled onward in a great
white bank of cumulus clouds. But as the warm winds rushed through
Chicago and out over Lake Michigan, they met a wall of cooler air
because the Great Lakes, like any large body of water, warmed more
slowly in spring than the surrounding land. In the night chill, the
PCB-153 suddenly condensed back into a liquid state for the first
time since it had left Missouri.
The breeze died just before midnight and the molecule settled
on the dark water near the lakeshore city of Racine, Wisconsin. Like
all PCBs, the molecule had a predilection for surfaces, so it lingered
about on the boundary between the air and water, bumping now and
again into other wandering members of its extended family. The
molecule found it hard, however, to remain unattached for very long.
Its strong attraction to organic matter drew it to a patch of algae,
rootless plants that floated like a gauzy green veil near the water’s
96
OUR STOLEN FUTURE
surface. When the opportunity presented itself, the molecule grabbed
on to one of the tiny plants and, clinging to its waxy surface, washed
back and forth along the shoreline near the mouth of the Root River,
moving with the vagaries of the wind and waves.
Plant-eaters, such as the water flea, nibbled around the edges of
the green veil, and some of the plants ended up as their salad course,
but the tiny plant PCB-153 was riding managed to escape and live its
full life span—which lasted three weeks. The alga began to yellow
and grow tattered around the edges. The dead plant grew water
logged and sank, carrying PCB-153 with it.
The dead alga settled on the bottom and was quickly covered
by soil washing into the lake from a city dump at the water’s edge.
Accumulating sediment buried the molecule ever deeper in the lake
muds, and with each passing year, its chances of getting back into
circulation seemed to grow slimmer. PCB-153 might be impervious
to the attack of the bacteria that broke down most chemicals, but it
could be entombed.
Persistence is viewed as a virtue in people, in chemicals, it is
the mark of a troublemaker. The synthetic chemical industry helped
bring convenience and comfort to American homes, but at the same
time, it unleashed dozens of chemicals, including PCBs, that be
came notorious for combining the devilish properties of extreme sta
bility, volatility, and a particular affinity for fat.
Besides PCBs, this lot includes the pesticides DDT, chlordane,
lindane, aldrin, dieldrin, endrin, toxaphene, heptachlor, and the ubi
quitous contaminant dioxin, which is produced in many chemical
processes and during the burning of fossil fuels and trash. They ride
through the food web on particles of fat or vanish into vapors that
gallop on the winds to distant lands. In Silent Spring, Rachel Carson
put the persistent pesticides at the top of her most-wanted list. It
didn’t occur to her to include compounds such as PCBs that may not
be particularly poisonous (in the usual sense of causing immediate
death or cancer) but are persistent—a fact scientists did not recog
nize until 1966, four years after Silent Spring was published.
The members of the PCB family that contain fewer chlorine
atoms do have a few enemies, including two bacteria from the Achromobacter genus. But chlorine heavies like PCB-153 are impervious to
*
TO THE ENDS OF THE EARTH
*
99
the back of a station wagon, was heading eastward on the interstate
toward upstate New York. The molecule was moving into new terri
tory on this imaginary journey. The fisherman could hardly wait to
get home and show off the catch of a lifetime to fishing buddies. His
mouth watered at the thought of a truly memorable fish dinner with
his family.
Three days later, however, the fish ended up in the family’s
trash barrel rather than on a platter at the dinner table. At the height
of an August heat wave, the station wagon had broken down, leaving
the family stranded at a gas station in rural Michigan without trans
portation and without ice for the cooler. When the family reached
home and opened the cooler, the fish smelled like old cat food.
A blizzard of gulls swirled around the trash collection truck
when it arrived at a landfill outside Rochester. As the rank fish carrying
the molecule tumbled onto the growing trash mountain, the gulls
dove at it like shoppers at a half-price sale, squawking and jostling
each other to grab a bite. In a matter of minutes, they had picked the
carcass clean.
PCB-153 wound up in the fat of a female gull, which had spent
more than a dozen years feeding on the fish in Lake Ontario, so the
molecule simply added to her already substantial store of contami
nants. In the Great Lakes food chain, the herring gulls occupy a spot
just below the bald eagles, which sometimes nab a herring gull or
two. By the time PCBs have moved this high on the food chain, the
concentrations have multiplied to 25 million times the levels found
in the water.
The following spring, the female herring gull headed for Scotch
Bonnet Island, roughly one hundred miles east of Toronto on the
Canadian shore of Lake Ontario. The gull and her mate quickly set
their stake on a good patch of sand in the middle of the gull colony, a
location considered preferable to the edges, where the chicks might
be more vulnerable to predators. The pair courted and mated. After
ward, the female scraped a hollow in the sand and laid two large
lightly speckled eggs that she dutifully set about incubating.
A tiny beak broke through one shell six weeks later, but the
chick could only muster feeble pecks and it died, seemingly from ex
haustion. The other egg showed no signs of life at all, but the pair
100
OUR STOLEN FUTURE
stayed on the nest for another week. The mother finally abandoned
the nest without fledging a single offspring.
PCB-153 and its relatives had passed from the mother gull into
the yolk of the lifeless egg and had contributed to its death, along
with DDT, dioxin, and other contaminants. A skunk carted off the
rotting egg five days later but then thought better of eating it and
dropped it on a rock near the shore, where it smashed. Some of the
yolk spattered into the water, and PCB-153 was off on another trip
up the food chain, this time via a crayfish—a small bottom-feeding
scavenger that vacuumed up the bits of fatty yolk sloshing in the
shallows near shore.
Before long, the crayfish that had dined on the egg yolk became
dinner for one of the American eels that hunted at night in the weedy
shallows. The eel is something of a contrarian when it comes to spawning. Many species, such as salmon and herring, spend their maturity at
sea and then return upriver to their birthplace to spawn. American
eels, on the other hand, frequent freshwater rivers and lakes most of
their lives before Finally making a long pilgrimage out to the Sargasso
Sea—an area in the Atlantic Ocean between the West Indies and the
Azores—to spawn before dying. Curiously, the eels migrating from the
Great Lakes and other northern waters are all female, while those mi
grating from southern rivers tend to be males.
With the approach of summer, the oldest eels in Lake On
tario, including the sixteen-year-old animal carrying the PCB-153
molecule, began to undergo changes that signal sexual maturity
and preparation for the three-thousand-mile journey to the spawn
ing ground. Their gray green backs began to darken toward silvery
black, their yellow bellies whitened, and their eyes enlarged and
changed to allow better vision in deeper ocean waters. Restless
with the migratory urge, groups of silver eels moved toward the en
trance to the St. Lawrence River waiting apparently for some sign
that the time was right. Then on a stormy night when rain poured
in dense silver sheets out of a black sky, a slithering multitude
suddenly departed down the great river toward the North Atlantic.
The eel carrying PCB-153 swam onward for more than six months
with a mystifying urgency before finally reaching the floating rafts
of sargasso seaweed that give this region of warm, salty waters its
'
TO THE ENDS OF THE EARTH
101
name. There beneath the clear tropical waters east of the Bahamas
and south of Bermuda, a roiling congregation of eels, gathered from
the Gulf Coast to Newfoundland, spawned and then expired from
exhaustion—their long journey ended, their compelling mission
accomplished.
*
The eel’s flesh disintegrated quickly in the warm tropical wa
ters, and PCB-153 sloughed off in a shred of fat that floated up to
the surface of the Sargasso Sea under the intense tropical sun. In the
heat, the molecule suddenly vaporized once more and, carried on
prevailing winds, began hopscotching north. At any cold spot it en
countered, the molecule condensed and settled on any available sur
face, only to be off again as soon as the summer sun warmed the
surface. Alternating between liquid and gas, it rode the winds farther
and farther north. The waters grew colder, making it increasingly dif
ficult for the molecule to become airborne. Instead it hitchhiked on
one of the small floating plants at the bottom of the North Atlantic
food web, sweeping into the Gulf Stream and from then on north
and east toward Iceland.
Two hundred miles east of Iceland, a small shrimplike crea
ture called a copepod finally nabbed the plant and PCB-153 as
it filtered a meal out of the rich waters of the North Atlantic.
Five days later, a cloud of copepods was swept into a swift current
that carried, it quickly north and east like a giant conveyer belt to
ward the edge of the solid pack ice in the Greenland Sea, where a
large school of Arctic cod had gathered to feast on the incoming
bounty.
The gray green water boiled with the feeding cod, one of the
most abundant species in high Arctic waters. As one of the small fish
digested its stomachful of copepods, PCB-153 migrated to the fatty
tissue near its tail, which already had a considerable store of persis
tent chemicals. The Arctic food web, which includes the cod, is
quite simple, but it includes many long-lived animals that accumu
late significant amounts of contamination over a lifetime. For this
reason, the Arctic food web concentrates and magnifies persistent
chemicals to an even greater degree than that of the Great Lakes.
Though far from a top predator, this cod carried PCBs at 48 million
O6
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m2
0UR STOLEN FUTURE
times the concentration found in the surrounding waters. Even so, the
cod are still less contaminated than Great Lakes salmon because the
ocean waters they inhabit are far cleaner.
Arctic cod spend the greater part of their lives feeding beneath
the solid vault of ice that closes over high Arctic waters for most of
the year. That season, the cod carrying PCB-153 followed the shift-,
ing food supply, and on the trail of a particularly abundant crop of
copepods, it gradually swam toward the eastern part of the Greenland
Sea. During the icebound period, ringed seals depend exclusively
upon the schools of cod that wander beneath the ice.
It was only a matter of time before the cod carrying PCB-153
became a meal for a hungry adolescent seal that shot through the
water, propelled by its powerful hind flippers. Like many seals
searching for food, the youngster had wandered along a fracture in
the sea ice west of the Svalbard Islands. The hunting had been good
that winter, and the seal had added significantly to its ample blub
ber, which, despite its short life, contained not only PCB-153 but a
high concentration of chlordane, DDT, toxaphene, and other persis
tent chemicals that were finding their way to the Arctic from all over
the world. A seal eats hundreds of fish, ingesting and storing all the
PCBs that had accumulated in them. For this reason, the PCB levels
in the seals are eight times greater than in the cod, or 384 million
times the concentrations in the ocean water.
Once the sea closes over with ice, the seals breathe through
holes that they keep open by punching through at regular intervals
with their noses. The great white bears can sniff out these holes from
a remarkable distance, and they often hunt by waiting in ambush.
The young seal had just surfaced to breathe when a bear that
had been waiting on its stomach near the breathing hole lunged out
and, in a single continous movement, flipped the 150-pound animal
out of the water and onto the ice. The ringed seal died instantly in
the attack by the five-year-old female bear, who had learned the
hunting technique from her mother before going off on her own two
and a half years earlier.
In thirty minutes, she had consumed the best parts of the seal
its skin and succulent blubber—and acquired PCB-153 along with a
considerable synthetic chemical legacy. The bear was quickly gaining
4
TO THE ENDS OE THE EARTH
1
r
I
■
A
103
weight because of the good hunting, so as she laid on more fat the
molecule moved into her well-insulated rump.
As spring advanced, the young female gradually made her way
toward the land-fast ice around Svalbard, which provides the best
hunting of the year. The seals are particularly vulnerable when they
haul out onto the ice to have their pups, so for bears the living is
easy. Many gather in this polar bear fat city, feasting for days and
consuming huge quantities of seal blubber. Growing visibly rotund,
some animals triple their body weight.
In late April, the young female mated for the first time, with a
large male who had also come to Svalbard to feed on the seals. But as
is the case with all bears, the fertilized eggs did not begin developing
immediately. Instead the female carried them around in her body
until the following November, when she hollowed out a den in the
growing banks of snow on Kongspya Island. As she settled in for the
winter, the fertilized eggs implanted in her womb and began to grow.
In the dead of winter, two tiny pink cubs, weighing only a pound and
a half each, slipped into the world unnoticed by their sleeping
mother. Crawling across her creamy expanse, they found their way to
her nipples and began nursing on her rich, fatty milk.
Throughout the winter, the mother and cubs all lived on the
ample layers of fat she had laid down the previous year. As the fat
melted away, PCB-153 was on the move again, this time into the
breast milk of the female bear. The cubs were nursing greedily and
growing rapidly. As one of the female cubs tugged at the nipple, the
molecule shot into her mouth with a blast of warm, thick milk.
No one yet knows how persistent chemicals like PCBs harm po
lar bears or how much it takes to cause damage. But given experience
with other wildlife species, it seems certain that PCB-153 and other
persistent hormone-disrupting chemicals pose a greater hazard to
the developing cubs than to the mother who ingested the chemicals
from the seal blubber.
The polar bear twins topped twenty pounds by the time the
new mother emerged from her den into the honey light of the Arctic
spring. They would continue to nurse for more than two years and
grow to roughly four hundred pounds each on the rich diet of polar
bear milk. With each meal, they would take in more of the persistent
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chemicals that had traveled thousands of miles to the remote Arctic.
The concentrations of PCBs had multiplied 3 billion times as they
moved up the Arctic food chain to the polar bear, the top predator
and largest land carnivore.
A decade later, one of the twins may have been among the
pregnant females who emerged from a den in Svalbard without any
cubs of her own.
n
IQ
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O
Chemicals manulactuicil on one continent can tia\cl thousands of miles
away. This path traces the journey of a PCB molecule from its point of ori$nn in a factory in Alabama to a refinery in Texas and up the food web in the
Great Lakes ano'North Atlantis region. Tut ooiioenrratioi. oi persisrein
chemicals can be magnified millions of times as they travel to the ends of
the earth.
apt
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10B
DUH STOLEN FUTURE
«
«
*
Like polar bears, humans share the hazards of feeding at the
top of the food web. The persistent synthetic chemicals that have in
vaded the great bear’s world pervade ours as well.
Humans also carry PCBs and other persistent chemicals in their
body fat, and they pass this chemical legacy on to their babies. Virtu
ally anyone willing to put up the $2,000 for the tests will find at least
250 chemical contaminants in his or her body fat, regardless of
whether he or she lives in Gary, Indiana, or on a remote island in the
South Pacific. You cannot escape them. Ironically, some of those liv
ing farthest from industrial centers and sources of pollution have
suffered the greatest contamination: these chemicals travel long dis
tances and build up along the way to high concentrations, especially
in the Arctic, which is becoming a final resting ground. These syn
thetic chemicals move everywhere, even through the placental barrier
and into the womb, exposing the unborn during the most vulnerable
stages of development. When a new mother breast-feeds her baby,
she is giving it more than love and nourishment: she is passing on
high doses of persistent chemicals as well.
It has been three decades since health researchers discovered
that DDT, PCBs, and other persistent chemicals were accumulat
ing in human body fat and breast milk, as well as in every other part
of the environment. The measurements have been the easy part.
Since then, concerned scientists have been trying to understand
their meaning. If we all carry around an alphabet soup of novel
chemicals in our body fat, how is it affecting us? How is it affecting
our children?
While researchers do not have all the answers to these ques
tions, they are convinced that humans carry high enough levels of
synthetic chemicals to endanger their children. Without knowing
exactly how all these chemicals act, separately or together, the re
searchers have linked them not only to damage in wildlife offspring
but in humans as well. We explore these links in later chapters.
While prenatal exposure seems to pose the greatest hazard,
health specialists also worry about the chemicals passed on in breast
milk because some sensitive developmental processes continue in
the weeks immediately after birth. During breast feeding, human in-
*
ID THE ENDS DE THE EARTH
107
fants are exposed to higher concentrations of these chemicals than
at any subsequent time in their lives. In just six months of breast
feeding, a baby in the United States and Europe gets the maximum
recommended lifetime dose of dioxin, which rides through the food
web like PCBs and DDT. The same breast feeding baby gets five
times the allowable daily level of PCBs set by international health
standards for a 150-pound adult.
The contamination of breast milk has been particularly severe
among indigenous people in the high Arctic, where many people still
eat the wild food the land and sea provide. There, researchers have
found that babies take in seven times more PCBs than the typical in
fant in southern Canada or the United States. The PCBs and other
chemicals that contaminate the infants have almost all arrived by
wind and water currents.
Canadian health officials have noted that many children in
Inuit villages are plagued by chronic ear infections. Recent studies
have found abnormalities in the immune systems of these children,
including the discovery that their bodies do not produce the neces
sary antibodies when they are vaccinated for smallpox, measles, polio,
and other diseases. The failure of vaccinations could make these
children much more vulnerable to disease.
The Inuktitut language spoken on Broughton Island in the
Canadian Arctic contains no word for contamination. This has made
it all the harder for the Inuit people living there to grasp the news
brought by Canadian health officials that persistent synthetic chem
icals are polluting the high Arctic and the food they eat. Perhaps,
some villagers suggested, the government officials were telling them
the animals had something called PCBs to scare them, to keep them
from killing any more whales or polar bears. Perhaps they were in ca
hoots with the animal rights crowd.
Broughton Island, which has a village of 450 people, lies off
Baffin Island, west of Greenland, more than sixteen hundred miles
from the smokestacks of southern Ontario, and twenty-four hundred
miles from the industrial centers in Europe, but that distant world
has cast its long shadow over the villagers’ lives, filling them with un
certainty and fear. It threatens their culture, which has endured for
thousands of years.
108
OUR STOLEN FUTURE
As their ancestors have before them, the men of Broughton Is
land fish and hunt to put food on the table. While they may give
chase these days by snowmobile and power boat instead of dogsled
and kayak, they still pursue seals, polar bears, caribou, and narwhals—
small whales with a spiral tusk on their head like the legendary uni
corn. The island does have a store that sells imported food, but the
diet of most islanders still consists largely of wild fish and game.
As the Arctic has become the resting place for volatile per
sistent chemicals, the contamination has passed up the food, web
to humans. Canadian health studies have shown that the people
on Broughton Island have the highest levels of PCBs found in
any human population except those contaminated in industrial
accidents.
The provincial health officials have told the villagers about the
contamination found in their bodies, but they have not been able to
tell them what these high PCB levels mean to their health or to the
health of their children. In the meantime, they have recommended
that the villagers continue to eat the traditional Inuit diet, which is
otherwise far more nutritious than the food imported by bush plane
and sold at a high price in the village store. In any event, with milk
going for $4 a bottle and small turkeys for $40 each, most villagers
have little choice.
Whatever the health effects, the report of high PCB levels,
which was widely covered by the Canadian press, has caused eco
nomic, social, and psychological turmoil for the Broughton Islanders.
Apparently unaware that they are probably carrying high PCB levels
as well, other Baffin Island Inuit communities have begun shunning
the villagers as the “PCB people” and discouraging marriages to
them. A fish dealer in the south, who used to buy and sell Arctic char
caught by the men of Broughton Island as a gourmet specialty, can
celed his contract, thus cutting off one of the major sources of the is
landers’ cash income.
The news that their breast milk contains chemicals has left
some of the women frightened and desperate. One mother decided
to stop nursing in an effort to protect her new baby. After several
weeks of being bottle fed a mixture of water and Coffee-mate, the
baby was hospitalized.
11
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TO THE ENDS OF THE EARTH
109
The Broughton Island people are not a unique case, only the
most extreme example discovered thus far of human contamination
with persistent chemicals. No matter where we live, we share their
fate to some degree. Many chemicals that threaten the next genera
tion have found their way into our bodies. There is no safe, unconta
minated place.
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Out in the wild, Theo Colborn quickly learned, persistent
chemicals were showing up in the most unexpected places. By early
1990, she knew that the problem extended far beyond the Great
Lakes. Her file cabinets contained dozens of papers showing that
scientists had found the same persistent chemicals everywhere
they had bothered to look. The contamination was truly global and
well documented.
There was also little doubt that a surprising number of these
persistent synthetic chemicals can interfere with hormones and dis
rupt development. New ones seemed to be cropping up all the time.
And if there had been any question about human vulnerability, the
work of Howard Bern, John McLachlan, Earl Gray, and others had
clearly demonstrated that DES and other estrogen impostors cause
the same kinds of damage in most mammals. Given the remarkable
similarity in the endocrine system across species, the same was likely
to be true with other kinds of hormone disruptors. It would be pru
dent to assume that whatever happened to animals could also happen
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Taken together, the evidence convinced Colborn that the
hormone-disrupting chemicals that now permeated the environ
ment posed a potential hazard to humans. But were these ubiquitous
chemicals in fact a threat? Were humans exposed to enough to
cause harm?
Toxicologists are fond of the axiom that it is the dose that makes
the poison. The mere presence of a substance doesn’t necessarily pro
duce damage. Even though our body fat and blood testify to our expo
sure to PCBs, DDT, dioxin, chlordane, and a litany of other persistent
chemicals, the amounts we carry are counted in parts per billion or
even parts per trillion. Unimaginably small amounts.
Nevertheless, Colborn knew that Fred vom Saal’s work showed
that even tiny shifts in hormone levels before birth had major conse
quences for mouse pups. Based on his experiments, ten or twenty
parts per trillion of natural estrogen are not inconsequential.
But estrogen is a natural hormone and an extremely potent one
at that. How much of a synthetic chemical does it take to disrupt
hormone levels and do lifelong harm? How much? The question
haunted Colborn. She kept searching through the scientific litera
ture, moving from one paper to another, looking for clues. With the
passion of a pack rat, she collected every sort of relevant evidence
and filed even the smallest tidbit in an ever expanding database on
hormone disruption. She had been at it for three years, already, try
ing to synthesize the far-flung studies from hundreds of researchers
in dozens of disciplines into a coherent picture. It was the kind of
work that almost never gets done by either the government or the
universities because there is no support and no reward for doing it;
nobody ever got tenure for analyzing and assessing other people’s
work. Yet how absurd to spend billions on individual scientific studies
but virtually nothing to figure out what they collectively say about
the state of the Earth.
Colborn herself had only been able to stay on the trail of the
hormone disrupters thanks to a stroke of good luck. As an ecological
scientist, John Peterson Myers had been fascinated by Michael Fry’s
work on DDE and gulls when it came out in the late 1970s, realizing
then that its implications were likely to extend far beyond birds. A
chance encounter with Colborn in 1988 had renewed this interest
112
OUR STOLEN FUTURE
and sparked an effort by Myers and Colborn to collaborate. Then in
1990 he moved to become director of the W. Alton Jones Founda
tion and convinced the board of the private philanthropic trust to es
tablish a senior fellowship for Colborn so that she could focus all her
energies on the issue.
As she tried to keep abreast of the latest science on half a dozen
fronts, she usually had little time to reflect on the implications of
what she was doing. But once in a rare while, alone late at night, she
would sit by her apartment window overlooking the illuminated
dome of the capitol in Washington and think about what all of the
pieces might add up to. The prospects were frightening. What were
the long-term effects of these hormone-disrupting chemicals? Were
we sabotaging our own fertility as well as that of wildlife? Was it pos
sible that we were unknowingly and invisibly undermining the repro
ductive future of our children? The thought seemed on the face of it
preposterous. How could human fertility be in jeopardy when world
population was soaring from five billion toward ten? Maybe she was
chasing phantoms.
A few months later, any lingering doubts vanished. At a meet
ing in Ottawa in the summer of 1990, Colborn happened to hear
Richard Peterson of the University of Wisconsin talk about the sur
prising results his lab had found in new chemical studies. The team
at the School of Pharmacy had given dioxin, a compound even more
notorious than DDT, to pregnant rats to see how it would affect the
development of their male offspring. As they had expected, the dioxin
did damage to the male reproductive system if the pups were ex
posed during a critical period in their prenatal development. What
surprised the scientists was how little dioxin it took to do the dam
age. They hadn’t given a large dose or repeated doses, but they saw
long-term effects on male pups even when the mother rats had in
gested only one dose of an astonishingly tiny amount of dioxin at a
critical moment. It had taken just a single hit.
Unlike many laboratory experiments where animals receive
doses much higher than those found in the environment, these
findings had direct and immediate relevance to the real world. The
lowest doses given to the mother rats had been very near to the
levels of dioxin and related compounds reported in people in in*
k SINGLE HIT
113
dustrialized countries such as the United States, Japan, and those
in Europe.
A.
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In the world of synthetic chemicals, dioxin has enjoyed the rep
utation of being the worst of the troublemakers—the most deadly,
the most feared, and the most elusive to scientists seeking to unravel
the secrets of its toxicity. Lab tests had shown dioxin to be thou
sands of times more deadly than arsenic to guinea pigs, who died
after swallowing only one-millionth of a gram per kilogram of body
weight, and the most potent carcinogen ever tested in a number of
animal species.
Unlike most other hormone-disrupting synthetic chemicals,
however, dioxin was not created intentionally. Although some dioxin
is released by volcanoes and forest fires, the chemical—known to sci
entists as 2,3,7,8-TCDD and to the public as “the most toxic chemi
cal on earth”—is for the most part an inadvertent by-product of
twentieth-century life, a coptaminant created during the manufac
ture of certain chlorine-containing chemicals such as pesticides and
wood preservatives, as well as by bleaching paper with chlorine, in
cinerating trash containing plastics and paper, and burning fossil fu
els. Like DDT and PCBs, dioxin is a fat-loving persistent compound
that accumulates in the body. And like other persistent chemicals, it
has been detected virtually everywhere—in air, water, soil, sediment,
and food.
Although discussion usually focuses on 2,3,7,8-TCDD, it is
important to remember this is only the most toxic and notorious
member of the dioxin family, which contains 74 other problematic
chemicals. Moreover, dioxin is found more often than not in the
company of furans—a related family of contaminants containing 135
chemicals with a structure similar to dioxins and with similar toxic
and biological effects on animals.
The still ongoing Agent Orange controversy centers on this po
tent chemical. From 1962 to 1971, the U.S. military dumped more
than 19 million gallons of synthetic herbicides over 3.6 million acres
in Vietnam in an effort to strip away the rain forest canopy where the
U.S. military command believed enemy forces were hiding.
One of the primary weapons in this operation was Agent Or-
114
OUR STOLEN FUTURE
ange, the military’s name for a mixture that contained the herbicides
2,4-D and 2,4,5-T, the latter a chemical easily contaminated with
dioxin during its manufacture. At the height of the campaign against
Vietnam’s rain forest, enlisted men sprayed Agent Orange not only
from airplanes and helicopters but also from boats, jeeps, trucks, and
on foot using backpack sprayers.
In the years following their return from Vietnam, veterans re
ported a variety of personal and family medical problems ranging
from cancer to handicaps in their children. As they learned that Agent
Orange had been contaminated with dioxin, many became convinced
that their own and their children’s health problems were linked to
this wartime exposure.
After years of debate about whether dioxin was responsible for
the reported illnesses, a panel from the National Academy of Sci
ences at the request of Congress undertook a comprehensive review
of the scientific evidence. In their 1993 report, the group found suffi
cient evidence to link exposure to dioxin-contaminated herbicides to
three cancers: soft-tissue sarcoma, non-Hodgkin’s lymphoma, and
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Hodgkin’s disease.
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In 1979, the U.S. Environmental Protection Agency sus
pended the use of 2,4,5-T for most purposes, but only after the her
bicide had also been used widely on the home front to keep down
weeds and brush in suburban lawns, rice fields, pasturelands, and
coniferous forests, along highway shoulders and railroad tracks, and
under utility power lines. The major nonhousehold uses accounted
for almost 7 million pounds of 2,4,5-T in 1974, according to federal
figures. Numerous other countries have also banned or withdrawn
’ the legal registration of 2,4,5-T, which prevents legal sale or use,
but some nations, such as Australia, have taken no action to restrict
its use.
Dioxin gained further notoriety during two dramatic contami
nation incidents in the United States and Europe.
An explosion at a chemical factory in northern Italy in July
1976 spread a cloud of dioxin over the city of Seveso north of Milan,
contaminating almost nine hundred acres of land and thousands of
people living nearby. Two weeks after the accident, officials finally
decided to evacuate 724 people from the most heavily tainted area.
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The dioxin levels measured in some Seveso residents—up to 56,000
parts per trillion—are the highest ever reported in humans.
Though the accident caused no fatalities, scientists are still de
bating how much it harmed those who were exposed. Shortly after
the incident, at least 183 cases of chloracne, a skin disease linked
specifically to high exposure to dioxin, were confirmed.
Whether the dioxin exposure caused increased miscarriages
and birth defects is unclear. Many pregnant women sought abortions
following the explosion, and under any circumstances, it is extremely
difficult to detect changes in the rate of miscarriages, since many
occur early in pregnancy often without the woman’s knowledge that
she had been pregnant. Health officials could not confirm the belief
that some birth defects had increased after the accident because
Seveso had no registry for birth defects before the incident.
While much of the followup research has focused on the possible
increased risk of cancer among those exposed in the Seveso accident,
insufficient time has passed to fully assess such effects. The prelimi
nary studies examining cancer incidence to date have reported ele
vated rates for some cancers, but these have been controversial, in part
because of the difficulties in accurately determining exposure to those
living at varying distances downwind from the plant.
Until recently, no one had thought to survey the children of
women exposed to high levels of dioxin in the Seveso accident for
any effects save obvious birth defects. Studies are now under way to
determine if there have been delayed effects on their sexual develop
ment and fertility.
In 1982 and early 1983, Times Beach, Missouri, became a ghost
town after the federal government evacuated all 2,240 residents be
cause of dioxin contamination. A company paid to spray the dirt
roads to keep the dust down had used a waste oil tainted with dioxin;
floodwaters had subsequently spread the contamination into homes
and businesses.
Almost a decade earlier, this company, a waste oil hauling oper
ation, experienced a similar incident when it had sprayed the floor of
an indoor horse arena with contaminated waste oil. Shortly after
ward, according to reports, horses began to sicken and die, and birds
that lived in the rafters began dropping to the ground. The owners of
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the arena and two young children also became sick with a flulike ill
ness, but while sixty-two horses eventually died, the stricken humans
survived the contamination.
In the Times Beach case, two small studies have looked at the ef
fects on children born to exposed mothers, finding evidence of im
mune system abnormalities and brain dysfunction, particularly in
the bilateral frontal lobes. The second study focusing on brain effects,
which involved seven boys and girls, found greater dysfunction in the
girls than in the boys, suggesting that the hormonelike activities of
dioxin may have a greater impact on developing females. Researchers
believe that abnormal function in this area of the brain can indirectly
affect thinking processes by altering attention, emotional states, and
motivation.
Few synthetic chemicals have received more scrutiny than
dioxin, in part because of its legendary toxicity. Over the past two
decades, the government and private industry have funded hundreds
of millions of dollars in research to look at everything from how
dioxin acts inside cells to whether workers exposed to high levels on
the job get more cancer. The host of studies have yielded interesting
and sometimes worrisome findings showing that dioxin has a wide
range of effects on the body, such as lowering the sperm count in ex
posed men and suppressing the immune system. Nevertheless, the
heated public debate in the United States about the dangers of
dioxin focused almost exclusively on whether or not it was, in fact, a
potent carcinogen. Based in large part on a reanalysis of a fourteenyear-old study of dioxin-induced liver tumors in rats and creative
interpretations of new scientific and epidemiological findings, the
paper industry kept arguing in the late 1980s that dioxin was less
dangerous than previously believed. In 1991, the U.S. Environmental
Protection Agency reevaluated its position on dioxin.
The EPA's reassessment of the risks of dioxin was already under
way when Richard Peterson’s Wisconsin study hit with the shock of
an unanticipated asteroid. Here was evidence that dioxin could have
dramatic effects at very low doses—at levels close to those routinely
found in humans. In a matter of months, the tide turned and the
dioxin debate shifted from dioxin’s cancer-causing potential to its
developmental and reproductive toxicity. In short order, EPA scien-
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tists repeated the studies giving dioxin to pregnant rats and found
similar effects in female offspring.
This turnaround in scientific thinking was stunning. The studies
suggested that the worst fears about dioxin might, in fact, be justi
fied. Dioxin might after all be more dangerous than anyone had sus
pected, but contrary to what many had thought, its greatest threat
was not cancer. The newly emerging hazard was its power to disrupt
natural hormones.
Dioxin’s bad reputation helped insure a steady flow of funding
to a host of researchers who were probing what this chemical did to
the body and how it did it, but the University of Wisconsin lab
headed by Peterson was one of the few places exploring its effects on
the endocrine system. Robert Moore, one of Peterson’s colleagues at
the School of Pharmacy and the Environmental Toxicology Center,
had set off on this line of research because he believed it held the
greatest potential for explaining the toxic effects of the notorious
2,3,7,8-TCDD.
Dioxin posed a fascinating challenge for toxicologists like Moore
and Peterson because it is not your ordinary poison. Animals given
lethal doses of dioxin don’t keel over quickly; they lose their appetite
and undergo a mysterious wasting before they actually die weeks later.
Dioxin also produces a variety of other nonlethal responses that occa
sionally seem contradictory. It somehow disrupts estrogen responses,
acting sometimes as if it were an estrogen impostor and sometimes as
if it were blocking estrogen, yet studies have shown that dioxin is not a
simple estrogen mimic like DES. It produces apparently estrogenic or
antiestrogenic effects without consorting with the estrogen receptor.
For all the years of research, exactly how dioxin does its harm has re
mained elusive. Peterson and Moore thought the endocrine system
might hold the key to this mystery.
As they had suspected, their experiments with adult male rats
confirmed that dioxin could interfere with hormone levels. When
adult rats were given dioxin, it caused their testosterone levels to
drop and their testicles and accessory sex organs to lose weight. But
it took a lot of dioxin to produce such responses—almost enough to
start killing some of the rats used in the experiments.
120
OUR STOLEN FUTURE
genitals so his equipment does not work properly, making him less
effective at mating. For the moment, the question of whether dioxin
interferes with the development of the brain and thereby disrupts
sexual behavior remains unresolved.
Scientists understand less about dioxin than they do about the
more straightforward hormone mimics or blockers, such as methoxy
chlor and vinclozolin, which cause disruption by binding with estro
gen or androgen receptors. For this reason, Gray explains, he would
be less confident predicting what might happen to humans based
on animal experiments. Recent discoveries are, however, giving sci
entists increasing confidence that the responses in humans and ani
mals are likely to be roughly similar. Researchers have found that
dioxin acts almost exclusively through a receptor—one of the or
phan” receptors whose normal chemical messenger remains unknown.
Although this receptor was Erst identihed in animals, studies have
shown that humans also have a fully functional aryl hydrocarbon, or
Ah, receptor that binds to dioxin. Once dioxin occupies the receptor
in a human cell, researchers have found it binds to DNA in the cell
nucleus, prompting many of the same changes in gene expression
seen in animal experiments. Humans seem no less sensitive to this
effect. But what happens afterward to produce all of dioxin s dis
parate biological effects, including developmental disruption, remains
a mystery.
However it happens, dioxin acts like a powerful and persistent
hormone that is capable of producing lasting effects at very Tow
low
Joses—doses similar to levels found in the human population.
The outstanding irony is that the rats in Moore’s experiments
passed the standard fertility tests with flying colors—tests typically
used by the chemical industry to screen chemicals for safety. Almost
all were able to impregnate females and produce the normal number
of pups. The reason, Moore explains, is that rats are incredibly ro
bust breeders, producing ten times more sperm than they really need
to reproduce. Tests have found that a toxic chemical can knock out
ninety-nine percent of a rat’s sperm and still have no effect on his
ability to reproduce.
Humans, by comparison, are inefficient breeders, who tend to
produce barely the number of sperm required for successful fertiliza-
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In the beginning, Sonnenschein and Soto had been looking for
growth factors, too, but puzzling results in their experiments had led
them to reexamine their assumptions. In tackling the question from
an evolutionary perspective, Sonnenschein and Soto had come to
think the opposite was likely to be true. After all, they reasoned, the
single-cell organisms that first evolved, such as bacteria, do not need
anything to tell them to grow; they reproduce endlessly if the food
and conditions are right. Well-nourished cells only stop continuous
proliferation when they become a part of a multicellular organism,
suggesting that some inhibiting substance keeps them in check.
The question probably wasn’t what makes cells multiply; it’s
what makes them stop. The complex organisms that appeared later
in the history of life cannot survive unless their cells maintain a cer
tain discipline. If these cells start multiplying continuously in the
way bacteria do, the organism will rapidly turn into little more than
one big disorganized tumor. For Soto and Sonnenschein, the goal
was to find such an inhibitor.
They were in hot pursuit of this inhibitor through experiments
with human breast cancer cells—a strain that multiplies in the pres
ence of estrogen. Under normal circumstances, estrogen prompts tissue
growth in the breast and uterus—something Soto and Sonnenschein
think the hormone does by overriding the inhibitor. The hormone has
a similar effect on the estrogen-responsive line of cells that the pair
use in their research. When estrogen is added to these living cells in a
lab dish, the cells will multiply. The pair was confident this cell culture
research could help them track down the inhibitor.
By 1985, Sonnenschein and Soto had found evidence that their
proposed inhibitor really did exist. If they removed the estrogen from
blood serum through a special charcoal filtering process and then
added the serum to estrogen-sensitive breast cancer ceils, the cells
would stop multiplying. Two years later, they were struggling to iso
late and purify the specific substance in the serum that had given the
stop signal.
Working with cells in tissue culture can be a tricky business.
There is only one way of doing things—impeccably. Any lapse in dis
cipline, the least hint of sloppiness, can ruin weeks, months, even
years of work. To eliminate potential problems, Sonnenschein and
124
OUR STOLEN FUTURE
Soto ran the lab with very few people and followed carefully dehned
procedures to maintain maximum control. They kept the hormones
used in the experiments locked in a tackle box in a different lab. Any
work with the cells, they did themselves. Their system of elaborate
precautions bordering on paranoia had paid off. They had never had
a problem—until that final week in 1987.
Four days earlier, Sonnenschein had prepared a series of multi
welled plastic plates, placing breast cancer cells in the twelve small
cups and then adding varying levels of estrogen and of the estrogenfree serum to each of the tiny cell colonies. Now Sonnenschein and
Soto were returning to see how the cells had fared. Over the years,
they had done variations of this experiment hundreds of times. Ac
cording to the routine, they would examine the cells under the micro
scope before transferring the cells from the plates to special counting
vials, so the cells could be tallied by an electronic particle counter.
Somehow the plate didn’t look right, so Sonnenschein adjusted
the microscope and looked again. His eyes were not playing tricks.
The whole plate—every single colony growing in a specially modified
blood serum—was as crowded as a subway train at rush hour. Re
gardless of whether they had added estrogen or not, the breast can
cer cells had been multiplying like crazy.
In all their years of cell work, they had never seen anything like
it. At first, they felt stunned. They didn’t know what to think except
that something had gone seriously wrong.
It had to be some sort of estrogen contamination, they pre
sumed. They could see that immediately because Carlos was working
with other cells as well and these were behaving as expected. The only
cells multiplying wildly were the estrogen-sensitive breast cancer cells.
They carefully prepared another batch of plates with breast
cancer cells, and once again, they saw the same galloping prolifera
tion. It wasn’t a fleeting event. The mysterious contamination was
still somewhere in the lab.
Soto and Sonnenschein spent the New Year’s holiday fighting
depression and going over their lab procedures again and again,
searching for changes or possible slipups that might account for the
runaway proliferation. Since they did all the cell work themselves,
there was no one else to blame. But what could they possibly have
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happened?
Maybe the breast cancer cells had somehow changed or been
contaminated by foreign cells.
No, they quickly ruled that out by comparing the cells with frozen
samples of the same cell line and with other estrogen-responsive cells.
When tested, all showed the same mysterious proliferation without
exposure to estrogen.
They considered every possible explanation from carelessness
to sabotage. Had somebody unthinkingly entered the lab with an
open bottle of estradiol, the form of estrogen used in their experi
ments? The hormone is so powerful they keep only one gram on
hand for their research—less than a teaspoon. A stray speck could
contaminate a lab. That’s why it was locked away in another lab.
Given the tight controls, such an accident seemed highly unlikely.
Could someone have derailed their experiments intentionally?
That thought crossed their minds when they failed to come up with
more mundane explanations. Sabotage of experiments by jealous
colleagues was not unheard of in science. Their work was breaking
new ground and upsetting long-held notions. But there had to be a
more reasonable explanation.
In the end, the cause proved beyond their wildest imaginings,
something even stranger and more unsettling than human sabotage. It
would be four long, frustrating months before they finally tracked
down the “phantom estrogen” and two whole years before they were
able to put a name to the chemical that was mimicking the hormone.
Their discovery shook even veteran investigators of hormonedisrupting chemicals. For years, the ongoing discussion about possi
ble human health risks from synthetic chemicals had been based on
the assumption that most human exposure comes from chemical
residues, primarily pesticides, in food and water. Now Soto and Sonnenschein had discovered hormone-disrupting chemicals where you
would least expect them—in ubiquitous products considered benign
and inert. Here was glaring evidence of our vast ignorance about hor
mone-disrupting chemicals in the environment and how we might
be exposed to them.
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search? Could they in good conscience ignore the implications of
their accidental discovery?
Giving up would have been not only irresponsible but also out
of character. As a woman from a Latin country in a profess.on dom
inated by men, Soto had not gotten as far as she had by taking no
for an answer. Such a refusal simply brought out her terrier le
tenacity. Although Cados might appear more easygoing he shared a
similar stubborn streak. It was evident in their research. Taking on
the establishment in one’s field requires a certain independence an
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another, they agreed, they would find out what the chemical was
that was leaching out of the plastic and causing rampant prolitera
tion in their breast cancer cells.
Soto wondered what effect tubes of this same composition
would have if they were used in diagnostic tests in laboratories. Sonnenschein thought about all the plastics used to package food, even in
baby bottles. Sonnenschein worried that kids might be taking m estro
genic substances with their milk. As physicians and researchers who
had spent decades studying hormone effects, they held the strong con
viction that increasing estrogen exposure is risky and unwise
It took months to purify the compound in the plastic that caused
the estrogenlike effect in their experiments and do a preliminary i entification using mass spectrometry analysis. Finally, they were.ready, o
send a sample of the substance across the river to chemists at the
Massachusetts Institute of Technology for final identification.
At the end of 1989—two years after their detective work had
started—thev had a definitive answer: p-nonylphenol.
Through further investigation, Soto and Sonnenschein learned
that p-nonylphenol is one of a family of synthetic chemicals known as
alkylphenols. Manufacturers add nonylphenols to polystyrene an
polyvinyl chloride, known commonly as PVC, as an antioxidant o
make these plastics more stable and less breakable^ The plastic cen
trifuge tubes in which they stored blood serum had been of polystyrene—a plastic that, depending on the manufacturer, may or may
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In a search of the scientific literature, they found bits and pieces
of information that only heightened their concern. One study had
found that the food processing and packaging industry used PVCs
that contained alkylphenols. Another reported finding nonylphenol
contamination in water that had passed through PVC tubing. Soto
and Sonnenschein even discovered that nonylphenol is used to syn
thesize a compound found in contraceptive creams—nonoxynol-9. In
studies with rats, researchers had found that the nonoxynol-9 breaks
down once inside the animal’s body, creating nonylphenol.
They also learned that the breakdown of chemicals found in in
dustrial detergents, pesticides, and personal care products can like
wise give rise to nonylphenol. The United States and other countries
use vast quantities of these chemicals called alkylphenol polyethoxy
lates—450 million pounds in 1990 in the United States alone and
more than 600 million pounds globally. Although the products pur
chased by the consumer, such as detergents, are not themselves es
trogenic, studies have found that bacteria in animals’ bodies, in the
environment, or in sewage treatment plants degrade these alkylphe
nol polyethoxylates, creating nonylphenol and other chemicals that
do mimic estrogens.
In follow-up work, Soto and Sonnenschein took the chemical
they had found in their lab tubes and injected it into rats to verify that
it acted like estrogen in living animals as well as in cells in a lab dish. In
tests with female rats without ovaries, they found that p-nonylphenol
would cause the lining of the uterus to proliferate as if the rats had
been given estrogen. Because the synthetic chemical is less potent
than natural estrogen, it took higher doses to produce an effect.
Alkylphenol polyethoxylates have been widely used since the
1940s, but in the past decade they have come under increasing
scrutiny because of their toxicity to aquatic life, particularly as they
break down. By the late 1980s, several European countries had al
ready banned the use in household cleaners of nonylphenol ethoxy
lates, the compound in this group most commonly used in cleaning
products, and similar restrictions are under consideration in other
countries as well. While many still allow their use, however, in clean
ers prepared for industrial purposes, fourteen European and Scandi
navian countries agreed in 1992 to phase out this use by 2000.
130
OUR STOLEN FUTURE
When Soto and Sonnenschein published their findings in
1991, they added a new concern to the growing list. This was the first
report that these widely used and reasonably well studied chemicals
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might also act to disrupt hormones.
By strange coincidence, while Soto and Sonnenschein were
chasing contamination in their lab, a similar drama was unfolding at
the opposite end of the country at Stanford University School of
Medicine in Palo Alto, California. In this case, too, the mystery es
trogen was traced to plastic lab equipment but not to polystyrene
products or to nonylphenol. The Stanford team found another estro
gen mimic, bisphenol-A, which was leaching from an entirely differ
ent kind of plastic, polycarbonate. This plastic is used for lab flasks
and for many consumer products such as the giant jugs used to bot
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Here again, the discovery was accidental and one that occurred
only because the scientists were conducting research with estrogen
sensitive cells. David Feldman, a professor of medicine, and his col
leagues in the endocrinology division had initially discovered a
protein in yeast that binds with estrogen, which they thought might
be a primitive estrogen receptor, and if yeast had such an estrogen
receptor, then there must be a yeast hormone. The team was hunt
ing for such a hormone when they saw that some substance was in
deed binding to the yeast receptor. But the researchers soon realized
the estrogenic effect was due to a contaminant rather than a hor
mone. They determined that the contaminant was bisphenol-A and
that the source of the contamination was the polycarbonate lab
flasks used to sterilize the water used in the experiments.
In a 1993 paper, the Stanford team reported their discovery and
their discussions with the manufacturer of polycarbonate, GE Plas
tics Company. Apparently aware that polycarbonate will leach, par
ticularly if exposed to high temperatures and caustic cleaners, the
company had developed a special washing regimen that they thought
had eliminated the problem. In working with the company, however
the researchers discovered that GE could not detect bisphenol-A
in samples sent by the Stanford lab—samples that were causing pro
liferation in estrogen-icsponsive breast cancer cells. The pro em
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proved to be the detection limit in GE’s chemical assay—a limit of
ten parts per billion. The Stanford team found that two to five parts
per billion of bisphenol-A was enough to prompt an estrogenic re
sponse in cells in the lab.
Though bisphenol-A is two thousand times less potent than es
trogen, notes Feldman, “it still has activity in the parts per billion
range.” Feldman is cautious, however, about making people alarmed
about plastics. “We don’t know enough yet to make this into a public
health crisis.” He adds, however, that the accidental discovery about
polycarbonate raises a host of questions that need to be answered.
The Stanford paper shows that bisphenol-A prompts an estrogen re
sponse in cells in a lab. The next logical question, he says, is whether
it prompts the same response when given in water to an animal.
Unfortunately, such questions remain unanswered at this time
because researchers like Sonnenschein and Soto have been unable to
secure the funding to further investigate biologically active plastics
and other hormone-disrupting synthetic chemicals. The problem
seems to stem largely from the inertia of institutions and ideas.
Those seeking to do this research complain that grant reviewers tend
to be locked into older ideas, -which focus on the damage done by
toxic chemicals to DNA. As a consequence, they often don’t fully
grasp or appreciate the importance of this new line of research and
tend to have a narrow view of the types of studies that should receive
federal funds. To make matters worse, few if any grant-making in
stitutions are receptive to or prepared to review proposals for the
kind of interdisciplinary research that is needed to investigate these
questions.
In this same period, John Sumpter, a scientist in a very differ
ent field, had been enlisted to help solve another mystery on the
other side of the Atlantic—the case of the sexually confused fish.
Sumpter is a biologist from Brunel University in Uxbridge, who has
studied the role of hormones in fish reproduction.
Anglers fishing in English rivers had been reporting that some
thing strange was happening to the fish, particularly in the lagoons
just below the discharges from sewage treatment plants. The prob
lem was not the usual fish kills that can occur because of pesticides
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or low oxygen levels. Nor did the fish appear to have any obvious dis
ease. But many looked quite bizarre. Even experienced fishermen
could often not tell if a fish was male or female, for they showed
male and female sexual characteristics at the same time. They
seemed perfect examples of the condition scientists refer to as “in
tersex,” where an individual is stranded between sexes.
The government fisheries staff approached Sumpter because
they suspected that something in the water—either hormones or a
substance that mimics hormones—was causing the sexual confusion.
So they put this question to him: is there anything to measure in a
fish that will indicate whether it is being exposed to hormones?
It depends on the hormone, Sumpter replied. If thfe water con
tained anything that acted like estrogen, he was sure there would be
a telltale sign in males. They would respond to the estrogen by mak
ing a special egg-yolk protein normally produced only by females. In
the females, the liver produces this protein, vitellogenin, in response
to an estrogen signal from the ovaries. Once the liver synthesizes
vitellogenin, the blood carries it back to the ovaries, where it is taken
up and incorporated into the eggs as the female prepares for repro
duction. Although males do not produce eggs, their livers will never
theless produce vitellogenin if they are exposed to elevated levels of
estrogen. Since this response is extremely dependent on estrogen,
vitellogenin levels found in male fish provide a good indication of
estrogen exposure.
The initial question—whether the sewage treatment plants were
releasing something that acted like estrogen—proved the easiest to
answer. The fish bore unequivocal testimony that this was the case.
Within a week after the research team placed cages of rainbow
trout bred in captivity in the water flowing from a sewage treatment
plant on the River Lea fifty miles north of London, the vitellogenin
levels measured in the blood of the fish soared. The caged fish were
producing five hundred times more vitellogenin than trout main
tained in clean water elsewhere. In three weeks, levels of Sumpter’s
telltale estrogen marker climbed even higher, to more than one
thousandfold.
A nationwide survey followed in the summer of 1988 involving
twenty-eight sites in England and Wales. Although low oxygen lev-
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els and plant malfunctions killed off some of the caged fish, the
researchers still obtained results from fifteen of these sites, finding
dramatic increases in vitellogenin levels in each and every case.
Some of the increases were truly staggering: in one fish vitellogenin
reached one hundred thousandfold above normal. Whatever this
estrogenic substance was, the survey showed it was a national, not a
local problem.
The findings raised troubling questions about possible human
exposure through drinking water, which is taken for the most part
from these rivers. In summer, up to fifty percent of the water in
rivers can be effluent from sewage treatment plants, and in a dry
summer, the proportion of effluent can rise to as much as ninety per
cent. Tests with caged fish at eight water reservoirs on rivers, how
ever, found no vitellogenin effects in fish. While this is somewhat
reassuring, it shows only that there is not enough of the estrogenic
substance present to produce a response in adult fish. They did not
test fish during sensitive developmental stages, nor did they look for
other, non-estrogen-based hormone disruption. It does not rule out
the presence of estrogenic chemicals in drinking water. British water
companies are not required by law to test routinely for these chemi
cals. Even if tests are conducted there is no requirement that they
disclose results to the public.
But where the estrogenic substance was coming from proved
harder to answer. The first thought was birth control pills. Sumpter
and his colleagues theorized that women taking oral contraceptives,
which contained a form of estrogen called ethynylestradiol, would
excrete it in their urine, so the hormone would eventually end up at
the treatment plant and ultimately in the rivers. In laboratory exper
iments, they established that this form of estrogen does produce ef
fects in fish at concentrations of one-billionth of a gram per liter of
water. As hard as they looked, however, the British scientists could
not detect this chemical in the water released from sewage treat
ment plants.
Sumpter and his colleagues then considered other estroge
nic substances, such as plant estrogens and pesticides. While these
certainly might contribute to some overall estrogenic effect, they
thought it unlikely that there was enough coming out of treatment
134
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ina then d.scovery of nonylphenol in polystyrene plast.c anc1 o h
praxis He learned from it that detergents can contain mgredients
ths* --zrade into estrogenic chemicals. Here was a new suspect
' Vie researchers developed a new round of tests to. see whot, .er
thn theory was indeed plausible. First, were the alky phenols est
ger ■- ‘o fish as well as to the human breast cancer cells u ed by the
Tutt; researchers? And second, is there enough of the substancemn
the environment to produce an effect in fish? The answer, o both
onions proved to be yes. The frsh d.d respond, and the level
f'o -/ m river water were high enough to cause male fish to produce
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that all contribute to the effect.
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The initial discoveries of hormone-disrupting chermcals
some unexpected places has inevitably led to others.
Sourred by the Tufts researchers’ report of biologically act
plastics, Spanish scientists at the University of Granada^decided to
Investigate the plastic coatings that manufacturers us tohneunet
cans. These often inconspicuous coatings had been added. becauseo
concerns that metals might contaminatethe.food or impart am
lie taste Such plastic linings are reportedly found in eighty
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cent of the food cans in the United States and about forty percent of
those sold in Spain.
The brother and sister team of Fatima Olea, a food toxicolo
gist, and Nicolas Olea, a physician specializing in endocrine cancers,
had visited the United States and worked at the Tufts Medical
School lab with Soto and Sonnenschein. Their time in Boston had
alerted them to the potential hazards from plastics.
Their suspicions proved well-founded. In a study analyzing
twenty brands of canned foods purchased in the United States and in
Spain, they not only discovered bisphenol-A, the same chemical that
Stanford researchers had found leaching from polycarbonate lab
flasks, they also found stunningly high concentrations in such prod
ucts as corn, artichokes, and peas. Bisphenol-A contamination was
detected in about half the canned foods they analyzed. In some in
stances, the cans contained as much as eighty parts per billion—
twenty-seven times more than the amount that the Stanford team
reported was enough to make breast cancer cells proliferate. At such
levels, a synthetic estrogen mimic might contribute significantly to a
person’s exposure regardless of whether it is a “weak” estrogen or not.
Biologically active plastics were leaching from cans, containers
where one would not expect to find plastic at all.
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All the incidents discussed in this chapter involve synthetic
chemicals that mimic estrogen, but the synthetic chemicals that dis
rupt hormones do not all act like estrogens. Other hormones in the
body are vulnerable as well. Recall, for example, that some fungicides
interfere with the action of male hormones. Moreover, in ongoing
studies at the U.S. Environmental Protection Agency lab in Research
Triangle Park, North Carolina, Earl Gray has discovered that even
the classic estrogen mimics have far broader effects than scientists
in this field had hitherto recognized. Some of these “estrogenic” syn
thetic chemicals, it turns out, also take a direct toll on males by block
ing the androgen receptors that respond to male hormones.
The question of exposure lies at the heart of the debate about
whether hormone-disrupting chemicals pose a hazard or not.
Some skeptics dismiss such concerns, arguing that the hormone
effects of synthetic chemicals are far weaker than those of natural
........ A-'n i
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hormones and that humans are not being exposed to enough to pose
a hazard.
Such assertions are not supported by the evidence. When one
surveys the available information and scientific literature, one quickly
discovers that there are far too many blank spaces and missing pieces
to provide even a rough picture of how much humans might be tak
ing in or to allow for definitive conclusions. Often the needed in
formation simply does not exist or it is unavailable. Manufacturers
frequently withhold information about the ingredients in their prod
ucts using the claim of proprietary information or trade secrets—a
principle that is far more rigorously protected by legal precedent and
the courts than is the public’s right to know. Even the federal Free
dom of Information Act, which is supposed to give U.S. citizens ac
cess to information held by the government, contains an exemption
for trade secrets or confidential business information. It is anybody’s
guess how many of the plastic consumer goods on the market con
tain hormone-disrupting chemicals. Even in the case of pesticides,
where governments maintain closer oversight, it is impossible to ob
tain coherent data on the production of specific pesticides. The gov
ernment figures available in the United States and elsewhere are
limited and disjointed at best.
The information in the scientific literature about the bio
logical activity of and human exposure to chemicals of concern is
equally fragmentary and unsatisfactory. In some instances, there
are isolated studies reporting on concentrations of one chemical or
another in human blood or body fat, describing various sources
of exposure, or detailing how a hormone-disrupting chemical affects
the liver, the cells, the nervous system, the brain, or some other part
of the body.
Oftentimes, the studies show trends that differ from place to
place or among chemicals. This is not surprising. The industrialized
countries that controlled persistent chemicals such as DDT wit
nessed a dramatic drop in DDT concentrations in the late 1970s. Al
though the rates of DDT reduction in human tissue have slowed
markedly since then, this is nevertheless an encouraging sign that
government action can lower the level of exposure. In developing
countries in Latin America. Africa, and tropical Asia, where heavy
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use of DDT and lindane continues, human tissue still shows signifi
cant concentrations of these persistent chemicals.
PCBs are another story altogether. The concentrations in hu
man tissue have remained steady in recent years even though most
industrial countries stopped PCB production more than a decade
ago. This no doubt reflects the fact that exposure continues despite
the ban, because two-thirds of the PCBs ever produced are still in
use in transformers or other electrical equipment and therefore sub
ject to accidental release.
One is left with isolated snapshots of one aspect of the problem
or another. But in the end, we do not know how to tally these discon
nected facts. We do not know what they collectively mean. If any
thing, it is becoming even harder to assess exposure as persistent
chemicals have been phased out in industrial countries and replaced
by less persistent compounds such as methoxychlor. Like DDT,
methoxychlor disrupts hormones, but unlike its predecessors, it does
not leave telltale signs of exposure in body tissue. And the troubling
question looms of how many more hormone-disrupting chemicals
remain to be discovered.
Although synthetic chemicals now seem an inextricable part of
the fabric of modem life, they have come into common use relatively
recently. The synthetic chemical industry first developed in the second
half of the nineteenth century, after chemists learned to synthesize tex
tile dyes in the laboratory and manufacturing of these man-made dyes
began on a large scale. But the “chemical age” that has transformed
daily life did not dawn until around World War II, when new discover
ies and new techniques revolutionized the industry and led to an era of
explosive expansion in the production of synthetic chemicals. Between
1940 and 1982, production of synthetic materials increased roughly 350
times, and billions of pounds of man-made chemicals poured into the
environment, exposing humans, wildlife, and the planetary system to
countless compounds never before encountered.
Consider a few figures that sketch the magnitude of this global
experiment that has been ongoing for half a century now.
U.S. production of carbon-based synthetic chemicals, which
represent the lion’s share of synthetic chemicals, topped 435 billion
pounds in 1992, or 1,600 pounds per capita. Global production is
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estimated to be roughly four times greater, but actual figures are im
possible to come by.
Around the world, one hundred thousand synthetic chemicals
are now on the market. Each year one thousand new substances are
introduced, most of them without adequate testing and review. At
best, existing testing facilities worldwide can test only five hundred
substances a year. In reality, only a fraction of this number actually
do get tested.
The world market in pesticides amounted to 5 billion pounds
in 1989 and included sixteen hundred chemicals. Worldwide use is
still increasing. Pesticides are a special class of chemicals in that they
are biologically active by design and intentionally dispersed into the
environment.
Today the United States uses thirty times more synthetic pesti
cides than in 1945. In this same period, the killing power per pound
of the chemicals used by 900,000 farms and 69 million households
has increased tenfold. Pesticide use in the United States alone
amounts to 2.2 billion pounds a year, roughly 8.8 pounds per capita.
Thirty-five percent of the food consumed in the United States
has detectable pesticide residues. U.S. analytical methods, however,
detect only one-third of the more than six hundred pesticides in use.
Pesticide contamination of food is often much higher in developing
nations. In Egypt, most milk samples surveyed in one study con
tained high residue levels of fifteen pesticides.
The world trade in chemicals includes fifteen thousand syn
thetic chlorinated compounds—a category of chemicals that has
come under attack because of their persistence and a record of caus
ing health and environmental problems. Although most industrial
countries imposed restrictions in the 1970s on the most notorious
chemicals in this class, in developing countries, where'they are used
to control pests that threaten public health and crops, their use is
increasing.
In 1991, the United States exported at least 4.1 million pounds
of pesticides that had been banned, canceled, or voluntarily sus
pended for use in the United States, including 96 tons of DDT.
These exports included 40 million pounds of compounds known to
be endocrine disruptors.
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The amounts of potentially harmful chemical compounds pro
duced each year are truly staggering—thousands upon thousands of
chemicals and billions of pounds. Five billion pounds of pesticides
alone are spread far and wide not only on agricultural fields but in
parks, schools, restaurants, supermarkets, homes, and gardens.
At best, a few hundred of these chemicals have been studied in
any depth or detail—among them the persistent compounds such as
DDT, PCBs, dioxin, and lindane. But even here, it appears that our
ignorance far exceeds our knowledge. Despite the billions of dollars
that have been invested in dioxin research, the recent findings at the
University of Wisconsin—showing that very low doses can have pro
found long-term effects on the reproductive system of those exposed
in the womb—took most by surprise, including the scientists con
ducting the experiment.
Few if any safety data exist for many of these chemicals. The
safety data that do exist are typically limited to whether the chemical
may cause cancer or gross birth defects. Possible effects on the en
docrine system or transgenerational effects are rarely, if ever, examined.
The existing information may not allow any reliable estimates
regarding human exposure to hormone-disrupting chemicals and the
magnitude of the hazard, but there is enough evidence to raise pro
found and troubling questions. As scientists have begun to explore
the possible threat, new discoveries have only heightened concern.
Just as leading researchers had predicted, more endocrine-disrupting
chemicals have been discovered as the first systematic investigations
have gotten under way. And more are expected.
Contrary to assertions by critics, the hormonal activity of syn
thetic chemicals is not always “weak.” In recent studies, Earl Gray
has found that p'p-DDE, a degraded form of DDT that is ubiquitous
in human body fat, is a potent androgen blocker and equal in power
to flutamide, a drug designed to block the receptors for male hor
mones that is used in treating prostate cancer.
The discovery that hormone-disrupting chemicals may lurk in
unexpected places, including products considered biologically inert
such as plastics, has challenged traditional notions about exposure
and suggests that humans may be exposed to far more than previ
ously believed.
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140
OUR STOLEN FUTURE
Even more worrisome, scientists are now finding evidence that
hormone-disrupting chemicals can act together and that small, seem
ingly insignificant quantities of individual chemicals can have a ma
jor cumulative effect. Ana Soto and Carlos Sonnenschein have now
demonstrated this with breast cancer cells in culture. When they
exposed the estrogen-sensitive breast cancer cells individually to
small quantities of ten chemicals known to be estrogen mimics, they
found no significant growth in the cells. But the cells showed pro
nounced proliferation when these same small quantities of the same
ten chemicals were given together. Sumpter is finding evidence of
additive effects as well.
Scientists have also been exploring the critical question of
whether special blood proteins bind to synthetic estrogen mimics in
the way they do to estrogen. In pregnant women, this binding action
ties up most of the estrogen circulating in the blood and acts to pro
tect fetuses from excessive hormone exposure in the womb. As stud
ies proceed, scientists are finding increasing evidence that the blood
proteins do not bind to synthetic chemicals just as they do not bind
to DES. If all of a synthetic mimic is free and unbound, this would
greatly increase the potential disruption and increase concern about
relatively small doses of so-called weak estrogens or other hormone
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daily lives.
In truth, no one yet knows how much it takes of these synthetic
hormone-disrupting chemicals to pose a hazard to humans. All evi
dence suggests that it may take very little if the exposure occurs
before birth. In the case of dioxin at least, the recent studies have
shown that human exposure is sufficient to be of concern.
Despite our vast ignorance, we should not lose sight of some
important things we do know.
Most of us carry several hundred persistent chemicals in our body,
eluding many that have been identified as hormone disruptors.
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Each and every discovery discussed in this chapter has added to
scientific knowledge about endocrine-disrupting chemicals, but iron
ically, these discoveries have also underscored our astonishing igno
rance about the man-made chemicals that we have spread liberally
across the face of the Earth and incorporated into every part of our
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Moreover, we carry them at concentrations several thousand times
higher than the natural levels of free estrogen—the estrogen that is not
bound up by blood proteins and is therefore biologically active.
As Fred vom Saal has discovered, vanishingly small amounts of
free estrogen are capable of altering the course of development in
the womb—as little as one-tenth of a part per trillion. Given this ex
quisite sensitivity, even small amounts of a weak estrogen mimic—a
chemical that is one thousand times less potent than the estradiol
made by the body itself—may nevertheless spell big trouble.
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The hydraulic crane groaned as it hoisted its pale burden out
of the water. For a brief moment, the one-ton beluga whale seemed
to swim in the air as the crane swung toward the long, thin trailer
waiting on the dock at Mont-Joli, on the south bank of the St.
Lawrence River in Quebec. It deposited the whale with a dull thud.
Earlier that day, May 31, 1989, a fisherman had found the ani
mal floating belly up offshore and had towed it to the jetty at Pointeaux-Cenelles. Out on the river, belugas are dazzling creatures—all
magic and grace when one catches sight of them slipping through the
waves like watery angels. Yanked from their element, they look dif
ferent indeed. If it resembled anything, the thirteen-foot-long whale
carcass parked on the trailer looked like a huge bloated sausage, ex
cept that it was strikingly white. Like porcelain.
“Another entry for the Book of the Dead, Pierre Beland
thought as he turned and climbed into the cab of the high-powered
diesel Ford pickup to start the long drive back toward Montreal.
Over the past seven years, Beland, a scientist and founder of the St.
Lawrence National Institute of Ecotoxicology, had logged thousands
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of kilometers driving back and forth along both banks of the St.
Lawrence to fetch dead belugas and bring them back to the vete
rinary school at the University of Montreal. In six hours or so, he
would be back in the autopsy room with his colleagues, veterina
rian Sylvain De Guise and technician Richard Plante, digging into
the bowels of another whale in the middle of the night. The find
ings would add to their growing record on St. Lawrence belugas—
Beland’s Book of the Dead, a chronicle of loss as well as a valuable
body of scientific data.
By now, Beland and his colleagues figured they had seen just
about every kind of abnormality, but the whale hurtling down the
highway behind him would prove no routine case. This beluga har
bored a freakish secret that would earn it a special place in the annals
of science.
For years, scientists had offered theories about why the St.
Lawrence beluga population had continued to decline even after
large-scale commercial whaling had ceased in the 1950s, blaming
the dwindling numbers on overexploitation and a subsequent loss of
habitat through dredging and hydroelectric projects. If the pollu
tion in the St. Lawrence was mentioned at all, it was treated as a mi
nor factor. Whaling, without question, had taken a devastating toll.
The population had plummeted from an estimated five thousand
at the turn of the century to twelve hundred in the early 1960s. But
in the three decades since then, beluga numbers had continued
downward to a current population of about five hundred.
Beland entered the debate and the field of whale research quite
by accident. Although trained as a biologist, he had spent more time
with computers than with animals in the field, earning his Ph.D.
in mathematical ecology, which seeks to probe the dynamics of an
ecosystem through mathematical models and equations. In Septem
ber 1982, he was working in the marine ecosystems branch of a new
federal Fisheries and Oceans research center in Rimouski on the
south shore of the St. Lawrence when a beluga washed up nearby.
Out of curiosity, he had gone out with a young veterinarian, Daniel
Martineau, to take a look at the beluga, an animal he had seen only
at a distance as a dancing white flash in the broad expanse of blue
gray water. As the two men were standing there on the beach. Mar-
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tineau, who was far more interested in the whales he saw on the river
than in the cows he routinely treated, suddenly suggested they cut it
open to try to find out why it had died.
Even that first encounter suggested that synthetic chemicals
might be a greater factor in the beluga decline than anyone had rec
ognized. The Fisheries and Oceans lab in Montreal, where Beland
had sent a sample of the whale’s tissue, reported that the animal was
highly contaminated with toxic chemicals, including DDT, PCBs,
and mercury. When two more belugas washed up that fall, Beland
and Martineau examined them as well and found a variety of abnor
malities and lesions never before reported in whales.
In the intervening years, Beland, working with Martineau and
De Guise, had taken part in dozens of whale autopsies and compiled
an astonishing list of afflictions, most of them never seen in beluga
populations inhabiting less polluted waters. The St. Lawrence whales
had malignant tumors, benign tumors, breast tumors, and abdomi
nal masses. One had bladder cancer like many of the workers at the
aluminum plant on the Saguenay River, a tributary where some of
the whales spend a good deal of time. They suffered from ulcers of
the mouth, esophagus, stomach, and intestines. Most had severe
gum disease and missing teeth. Many had pneumonia or widespread
viral or bacterial infections. A large number also suffered from en
docrine disorders, including enlargement of and cysts in the thyroid
gland. More than half the females examined showed signs of severe
breast infections that would have made it difficult, if not impossible,
to nurse properly, and nursing mothers had pus mixed with their milk.
Some had twisted spines and other skeletal disorders. It was a litany
worthy of a cetacean Job.
Shortly after Beland pulled into the vet school with the latest
casualty, they began examining the animal—a normal-looking adult
male with a healed-over scar on its left side that looked like five cir
cular indentations. The distinctive mark identified him unmistak
ably as DL-26 (for the belugas’ Latin name Delphinapterus leucas),
one of the previously identified and photographed individuals in the
institute’s files.
Beland had a sinking feeling when he realized this was Body,
one of the first whales to find a sponsor in the institute’s new Adopt-
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A-Beluga program, which had been established as a way to raise
money for the research program. Just six months earlier, the father of
a whale-loving boy in Toronto had sent a check for $5,000; the boy
had chosen to christen his adopted beluga Booly.
The autopsy continued into the early hours of the morning and
proceeded according to the usual routine—missing teeth, emphy
sema, extensive stomach ulcers—until they hit the abdominal cav
ity. Inside, they found two small testicles and normal-looking male
plumbing such as the epididymis and vas deferens. But, to their
astonishment, Booly had a uterus and ovaries as well—a complete
female reproductive tract save for a vagina. All the firsts they had al
ready reported in the St. Lawrence beluga population paled by com
parison to this finding. They had discovered the rarest of biological
curiosities: a true hermaphrodite. This is a phenomenon seldom
seen in wildlife and never before reported in a whale. Even more un
usual, Booly had two testes and two ovaries, which previously had
been reported scientifically in only two rabbits and a pig. Something
had happened to Booly in the womb to derail the normal course of
sexual development.
Was Booly an accident of nature or was he a victim of pollu
tion-induced hormone havoc? There is no way to answer this ques
tion decades after Body’s birth, but the autopsy report noted: “One
cannot rule out that pollutants present in the mother’s diet had in
terfered with hormonal processes” guiding the “normal evolution of
the sexual organs of her fetus.” Based on the rings of enamel in his
teeth, which scientists count like tree rings to estimate a whale’s age,
the team concluded that Booly was twenty-six years old when he
died. He had been born in the early 1960s—a time when the pollu
tion in the St. Lawrence was likely at its peak. •
Although pollution levels in the river have dropped markedly
since then, the belugas still show high levels of contamination, es
pecially the young. Some of the most contaminated individuals
have been under two years of age, and high levels are found even
in prematurely born animals who failed to survive, indicating that
the contamination had been transferred from the mother across
the placenta. After birth, the transfer of contaminants to the off
spring continues through the rich, fatty breast milk. While nursing,
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a mammalian mother (including humans) draws down her fat stores,
dumping not only the fat but also the persistent toxic chemicals she
has accumulated in her body fat over the years into her milk. In this
way, a load of contaminants that it has taken the mother decades
to accumulate is passed on to her baby in a very short time. By
the time a baby beluga stops nursing at two years of age, it will have
acquired a toxic load that, relative to its size, far exceeds that of
its mother.
Beland and his associates found one young whale that had over
five hundred parts per million of PCBs in its body—ten times more
than the level necessary to qualify as hazardous waste under Cana
dian law. Ships on the St. Lawrence carrying waste with more than
fifty parts per million required a special permit.
Whatever the cause of Booly’s unique abnormality, the studies
by Beland and his associates suggest there may be widespread hor
mone disruption among the St. Lawrence belugas, undermining their
reproduction and preventing the recovery of the population. The fe
males in the St. Lawrence now have underactive ovaries and a lower
rate of pregnancy than Arctic belugas. And based on surveys of
younger animals, who have gray skin until they assume the snow
white mantle of adulthood at around six years of age, they are pro
ducing fewer young than their northern relatives. In the Arctic,
young animals make up over forty percent of the population, while
the percentage of young animals in the St. Lawrence hovers around
thirty, indicating that the reproductive rate is down by twenty-five
percent compared to belugas elsewhere.
Such reproductive problems are not surprising. The St. Law
rence belugas carry substantial loads of several synthetic chemicals
that are known to disrupt hormones and to interfere with normal re
productive cycles. In a study conducted in the Netherlands, Dutch
researchers found impaired reproduction in seals fed contaminated
fish from the Baltic, but no problems in a second group fed with
cleaner North Atlantic fish. The synthetic chemical contaminants in
the Baltic fish are similar to those found in the St. Lawrence fish that
the belugas eat.
Besides showing low reproduction, the St. Lawrence beluga popu
lation is also experiencing higher than expected mortality among
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adults in their prime—deaths that the researchers in Quebec think
stem partly from the toll that toxic chemicals are taking on their im
mune systems. There is growing evidence in the scientific literature
that both prenatal exposure to hormone-disrupting chemicals and
direct adult exposure to toxic compounds can weaken immunity.
As with humans suffering from AIDS, the deficient immune systems
make the whales more vulnerable to pneumonia, skin diseases, a va
riety of infections, and cancer. The team is now investigating the
beluga immune system and undertaking a comparative study of
the St. Lawrence and Arctic populations in an effort to characterize
the nature of the immune system damage.
One way or another, Beland says, pollution is killing the whales.
But it is not the acute poisoning commonly associated with toxic
chemical spills, which causes the quick death of fish and animals
caught in the wake. This death is slow, invisible, and indirect.
The discoveries made by Beland, Martineau, and De Guise dur
ing their investigation of the St. Lawrence belugas raise broader
questions relevant to animal populations everywhere.
As was the case in the St. Lawrence, researchers have com
monly blamed the decline and disappearance of wildlife populations
on human disruption of their habitat, excessive hunting, fishing, and
trapping, or on the introduction of aggressive foreign species that
overwhelm native competitors. All these forces are unquestionably at
work in the global loss of animal species, but biologists find that they
do not explain all the declines.
In light of the growing evidence that many synthetic chemi
cals disrupt hormones, impair reproduction, interfere with develop
ment, and undermine the immune system, we must now ask to what
degree contaminants are responsible for dwindling animal popula
tions. Could hormone disruptors account wholly or in part for some
losses that have been blamed on classically invoked factors such as
habitat loss or overexploitation? Have overexploited species failed to
rebound after protection because synthetic chemicals are impairing
reproduction?
Asking these questions has already prompted surprising reassess
ments, even regarding one of the most closely monitored animal
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populations in the United States—the critically endangered Florida
panther. The decline of the big cat, which has come to symbolize the
effort to restore the much abused Everglades, had been blamed on
reproductive problems caused by inbreeding, human encroachment,
road kills, and mercury contamination. Seeking to halt the panther’s
slide toward extinction, state and federal officials constructed a se
ries of specially designed wildlife underpasses along Alligator Alley, a
highway running across the Everglades where a number of panthers
have been killed.
The panthers’ range in southern Florida, which includes Ever
glades National Park and the Big Cypress swamp, lies downstream
from major agricultural areas and consequently suffers from pesti
cide and fertilizer pollution. But until quite recently, no one had
considered synthetic chemicals a factor in the panthers’ plight.
The first clue came in 1989. Prompted by the death of an ap
parently healthy female in Everglades National Park, federal and
state wildlife agencies began a study of the remaining panthers,
which number no more than fifty. Wildlife specialists concluded
that the female had died from mercury poisoning, which they attrib
uted to the fact that Florida panthers prey heavily on raccoons and
are therefore linked through the raccoon to the aquatic food web
where mercury and other contaminants accumulate. But the study
showed the panthers had a host of other problems as well. These
included apparent sterility in some males and females, an extra
ordinary level of sperm abnormalities, low sperm count, evidence of
impaired immune response, and malfunctioning thyroid glands.
Thirteen out of seventeen males had undescended testicles, and
records on the population showed that the incidence of this problem
had increased dramatically in male cubs since 1975. Those investi
gating the panthers attributed their poor reproduction and related
symptoms to lack of genetic diversity resulting from inbreeding in
the tiny population.
But as U.S. Fish and Wildlife Service contaminant specialist
Charles Facemire became aware of the emerging information on hor
mone-disrupting synthetic chemicals, he began to question whether
bad genes were really the problem. In his research, he had found
that the panthers are not particularly inbred compared to other
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large felines and that their genetic diversity is, in fact, slightly above
average. At the same time, he was learning that undescended testi
cles are a known consequence of prenatal hormone disruption.
If the panthers had suffered hormone disruption in the womb,
he learned, it might be evident in the hormone ratios in their
blood—specifically in the relative levels of testosterone, the typi
cally male hormone, and estrogen, the typically female hormone.
One would expect males to have far higher levels of testosterone,
but an analysis of the panthers’ blood found ratios that seemed pe
culiar indeed and suggested that many of the males had been “fem
inized.” Two males had far more estradiol, a form of estrogen, in
their blood than testosterone. In several others, estradiol was pre
sent at nearly equal levels to testosterone. Although such ratios ap
pear highly abnormal, no definitive conclusion is possible until
further work determines normal hormone ratios in other popula
tions of these cats.
The hormone disruption theory took on even more power
when Facemire reviewed archived data on contaminants in the ani
mals, for these records showed that the panthers carry high levels
of several synthetic chemicals that are known to disrupt hormones.
Besides lethal levels of mercury, the fat of the female found dead
in 1989 contained 57.6 parts per million of DDE, a breakdown
product of the pesticide DDT, as well as 27 parts per million of
PCBs, a persistent industrial chemical. At the same time, new find
ings by Environmental Protection Agency reproductive toxicologist
Earl Gray indicate why DDE may be affecting the development of
male panther cubs. DDE has long been described as a weak es
trogen, but Gray’s studies have demonstrated that it is also a po
tent blocker of male hormones. If something blocks testosterone
messages while a male is developing in the womb, Facemire notes,
undescended testicles might be one of the consequences, for tes
tosterone cues their descent from the abdomen into the scrotum
late in gestation.
Despite the uncertainties about the cause of the panthers’
predicament, wildlife managers are nevertheless proceeding with an
expensive translocation program that will bring panthers from
healthier out-of-state populations to Florida. The hope is that these
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imported cats will mate with local panthers and reduce the reproduc
tive problems that some still attribute to inbreeding.
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It may take several years to settle the question of what has
brought the Florida panther to the brink of extinction, but with this
pmhmmX work, hormone disruption caused by contammants ha
mddZ emerged as the most compelling theory to explam the r
reproductive problems. In a number of other species, however, scien
tists have already established persuasive evidence linking or
d^ denials to reproductive failures, and in many of these
eases the losses had been blamed m.tially on other factors.
One of the best examples is the work done by biologists fro
the Unhersit of Flor,da, the U.S. Fish and Wildlife Service, and the
Pl >1 Came and Freshwater Fish Commission on the alhg
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on the shore of Lake Apopka more than a decade earlier, the sy p
toms in the wildlrfe began to make sense only when he discovered
that synthetic chemicals could act like hormones.
kat revelation came, Guillette recalls, on a lazy Fnday^afto-
noon in the spring of 1992, when his longtime mentor,
a comparative endocrinologist and professor e
versify of California at Berkeley, gave an informal lecture du ng
visit to the Gainesville campus. In that talk, Bern
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about how contaminants might affect alligators and other organisms
and a whole new set of questions. “We knew it was contamination,”
he says, “but we didn’t realize it was a hormone effect.”
With this insight, Guillette could now imagine how the unusual
problems seen in the alligators might be connected to the 1980 chem
ical spill, an event that placed the area on the federal Superfund list of
the nation’s most serious hazardous waste sites. The chemical released
in the spill was dicofol, a close pesticide relative of DDT and a com
pound that also interferes with hormones. Since then, Guillette, along
with Timothy Gross of the University of Florida, Franklin Percival of
the U.S. Fish and Wildlife Service, and Allan Woodward of the
Florida Game and Freshwater Fish Commission, have been gathering
the data that support such a connection.
After the issue first broke into the news in early 1994, a parade
of journalists began trooping down to Lake Apopka to record the
plight of its alligators and photograph their tiny members, which are
only one-third to one-half normal size. The problem is more severe
in those living near the site of the chemical spill than in those living
in the northern part of the lake five to ten miles away, Guillette and
his colleagues have found. But regardless of where they live on the
lake, the Apopka males as a whole have smaller penises than males
hatched on a relatively clean lake. More recent studies also show that
this problem extends beyond Lake Apopka, although the symptoms
are less severe in lakes with no history of industrial chemical spills.
Researchers are now exploring the possibility that agricultural con
tamination is responsible.
Even if these males had normal-size penises, the Apopka alli
gators would still be having reproductive difficulties because both
sexes suffer from profound but less visible disruption in their inter
nal reproductive organs. The ovaries in the female alligators display
abnormalities in their eggs and in the follicles, where the eggs ma
ture before ovulation, that are remarkably similar to abnormalities
reported in humans and lab animals exposed to DES early in devel
opment. The males’ testicles showed structural defects as well.
The Apopka alligators also have skewed hormone ratios, with
males showing a profile that looks typical of a normal female. These
males have elevated levels of estrogen and greatly reduced levels of
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OUR STOLEN FUTURE
testosterone in their blood—only one-fourth the level found in
males from the relatively uncontaminated Lake Woodruff. The fe
males from Apopka also have elevated estrogen levels and an estrogen-to-testosterone ratio that is twice as high as normal. These
significantly aberrant hormone levels in males and females suggest
their sex organs may function poorly or not at all.
To Guillette’s surprise, the contamination on Apopka has also
taken a devastating toll on its red-eared turtle population. Unlike the
carnivorous alligators, which are top predators and therefore exposed
to higher levels of contaminants that have become more concen
trated in the journey up the food web, the red-eared turtles also eat
plants—a dietary habit that should expose them to less pollution.
Nevertheless, they, too, are having reproductive difficulties. In their
case, however, the problem is not unhatched eggs but an absence of
males. Researchers find females in the lake and many turtles that are
neither male nor female. Because of hormone disruption during sex
ual development, the animals that would have become males end up
stranded in the gender-bending state called intersex. There are few
normal males to be found.
In turtles, sex is determined by temperature rather than by a
gene, leading some to suggest that this intersex condition could be a
natural abnormality caused by temperature fluctuations during the
incubation of the eggs. But subsequent research by David Crewes of
the University of Texas at Austin has shown that such aberrations do
not show up even when turtle eggs are incubated at a borderline
temperature for producing one sex or the other. Something more
than temperature fluctuation is needed to produce sexually confused
animals. In laboratory experiments, researchers have been able to
produce intersex animals by incubating turtle eggs at a male temper
ature and exposing them at the same time to estrogen or estrogenic
synthetic chemicals such as some of the RGBs.
While the effects of the contaminants on the alligators and tur
tles are obvious, the team has not yet determined which chemical
or chemicals are responsible. The leading suspect is the DDT break
down product DDE, the contaminant found in the highest con
centrations in the alligator eggs and one that could originate from
the spilled dicofol, but other endocrine-disrupting contaminants
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153
are present as well, including dieldrin and chlordane. In tests in
which researchers painted alligator eggs with DDE, as little as one
part per million was enough to produce greater than expected rates
of ambiguous development in the sex organs—aberrations resem
bling those reported in contaminated birds by University of Califor
nia researcher Michael Fry. Chemical analyses of Apopka alligator
hatchlings have found that they contain four to five parts per million
of DDE.
Given these severe reproductive problems, one would expect to
find few if any alligators, but that is far from the case. Researchers
believe the immigration of healthy alligators from cleaner lakes
to Apopka has prevented their disappearance. It is not unusual
for Florida alligators to move among lakes looking perhaps for
better habitat and for better hunting, so a lake such as Apopka—
with prime habitat and a depleted native alligator population—would
be bound to attract migrants. This constant replenishment from out
side has totally masked the lake’s severe problems. Indeed, Apopka’s
dire condition might have gone undiscovered if wildlife officials hadn’t
become interested in supplying wild alligator eggs for commercial
alligator ranches. Faced with the question of how many eggs could
be collected from the wild without jeopardizing the once endan
gered species, Guillette’s colleagues surveyed several Florida lakes in
cluding Apopka. In this way-, they found that most of the eggs in
Apopka nests were not hatching.
Lake Apopka vividly illustrates how appearances can be totally
at odds with reality. The lake appears to be a healthy, relatively
unspoiled place, and the surrounding swamps seem to be rich in
wildlife, including turtles and alligators. By ordinary water quality
measures, the 1980 spill is ancient history and the lake is again clean.
But even years later the poisons from the accident have not truly dis
appeared. Though absent from the water, they are still circulating in
Apopka’s food web and causing havoc. Only with closer scrutiny does
the profound disruption of its wildlife become evident.
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clean areas constantly move into contaminated habitats and settle—
is also hiding continuing problems in other wildlife species in the
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OUR STOLEN FUTURE
United States, including the bald eagle. After the federal govern
ment restricted use of DDT and dieldrin in the early 1970s, eggshell
thinning diminished, and by the 1980s, the bird began making a re
markable recovery across the country. By 1994, the U.S. Fish and
Wildlife Service proposed removing the bird from the federal endan
gered species list. Nevertheless, some of the nation s bald eagle pop
ulations remain troubled.
In the Great Lakes, bald eagle numbers climbed from 26 to
134 pairs between 1977 and 1993, but this recovery may be more ap
parent than real. U.S. Fish and Wildlife Service biologists believe
that the growth of the Great Lakes population depends largely on
immigration of eagles hatched in cleaner areas. These recruits from
inland areas of Michigan, Minnesota, and Wisconsin often breed
well at first but become less successful as contaminants from the
lakes accumulate in their bodies and impair their fertility. Studies
have found that the birds take in the contaminants through their
prey and that the higher the levels of DDE and PCBs, the lower
their breeding success.
An eagle’s diet determines how quickly it acquires sufficient
levels of contaminants to impair reproduction. Although Lake Supe
rior is less polluted than the other Great Lakes, its eagles accumulate
an appreciable amount of contamination because of their eating
habits. Rather than preying directly on fish, Lake Superior eagles fre
quently prey on fish-eating birds such as gulls—one step higher in
the food web. Because of this taste for gulls, they accumulate con
centrations of contaminants that are twenty times greater than they
would have if they had eaten only fish.
Poor reproduction among bald eagles continues to be a prob
lem in several other areas of the country as well, affecting popula
tions in the lower Columbia River in the Pacific Northwest, in an
area near Yellowstone National Park, and in Maine’s coastal areas,
where eagle populations may prey more heavily upon birds.
Impaired reproduction in adults was just one of the problems
that emerged in the Great Lakes. In eagles and other fish-eating
birds, field biologists began to see severe birth defects such as miss
ing eyes, clubbed feet, and crossed bills and a bizarre wasting syn
drome that would suddenly strike an apparently healthy chick and
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cause it to wither and die. Here again, low genetic diversity was ini
tially invoked to explain the problems. Those offering this explana
tion reasoned that DDT had almost totally wiped out some species
in the region, so the animals in the rebounding populations were all
likely to be descendants of the small number of animals that had
survived the crash and hence inbred.
Based on environmental detective work and sophisticated toxi
cology, scientists now have evidence that this, too, is a case of con
tamination rather than inbreeding. For several decades, researchers
believe, DDT-induced eggshell thinning masked the effects of other
contaminants by killing the embryo. With reduced use of DDT,
eggshell thinning abated and chicks began to survive, allowing other
physical and behavioral abnormalities to emerge. Some of these
problems have been linked to dioxins along with furans, and cer
tain PCBs that act through the same mechanism. As described in
Chapter 7, all these chemicals behave in a dioxinlike manner and
bind to an orphan receptor, whose normal function in the body re
mains unknown.
In 1993, the bald eagles nesting along the Great Lakes produced
four deformed chicks—three with crossed bills and one with mal
formed feet—but such problems are not limited to the Great Lakes.
In the summer of 1994, the U.S. Fish and Wildlife Service began in
vestigating a cluster of similar deformities among birds in Oregon,
where nine birds in the Rogue Valley, including red-tailed hawks,
kestrels, an osprey, a Brewer’s blackbird, and a robin, were found with
crossed bills, missing eyes, or both. Wildlife specialists say that a
crossed bill is a developmental deformity analogous to a cleft palate
in mammals.
As many of these cases indicate, adult animals can tolerate lev
els of pollution that devastate their offspring. But in the most sensi
tive species, such as the mink, pollution levels in the Great Lakes
appear to be still too great even for adult survival. Although records
are sparse, it appears that mink began disappearing from the shore
line of the Great Lakes in the mid-1950s, and even with the restric
tions on DDT, PCBs, and other persistent chemicals they have not
yet returned. Some have blamed their disappearance on the destruc
tion of habitat and human disturbance, but wildlife specialists doubt
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156
part because of the abundance of
this is an adequate explanation, in
and muskrats prefer similar habimuskrats at the water’s edge. Mink
. one should be suitable to the other
tats, so conditions hospitable to
muskrats 'thrive and m.nk are absent is likely related
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to t--- on the food web, and those inhabitmg the shorehne
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dence indicates that PCBs, acting alone or in concert with other con
taminants such as mercury, had a significant role in their disappear
ance. Studies on the threatened otter populations in Oregon and
Sweden have found a similar association with PCBs.
Some fish species also appear to be extremely sensitive to cer
tain synthetic chemicals, though fisheries specialists have been slow
to recognize their role in collapsing fisheries. The lake trout was ex
tinct in Lake Ontario by the early 1950s and crashed during this
same period elsewhere in the other Great Lakes as well. Today, this
native top predator reproduces naturally only in Lake Superior and
parts of Lake Huron, so the presence of the species is maintained
largely through artificial stocking programs.
The demise of the native lake trout has been attributed to a
combination of overfishing, habitat destruction, and predation by
the sea lamprey, an exotic parasite that attaches itself to other fish
and sucks their body fluids, but recent studies are now challenging
this explanation. Although the contaminant levels found in the lakes
do not kill adult fish, experiments have shown that trout eggs are ex
tremely sensitive to dioxin and other chemicals, such as some PCBs,
that share the same toxic mechanism. They appear to be the most
sensitive species ever tested. When exposed to doses of as little as
forty parts per trillion of dioxin or 2,3,7,8-TCDD (or its toxic equiva
lent), trout eggs or newly hatched fish begin to show significant mor
tality. By one hundred parts per trillion, all the eggs die. Based on
core samples taken of the lake sediment, EPA toxicologists are re
constructing the history of dioxin exposure in the lake using com
puter models. This work indicates that dioxin reached sufficient
levels by the 1940s in Lake Ontario to begin killing trout eggs and se
riously undermining their reproduction.
Growing evidence that dioxin and dioxinlike PCBs are in part
or wholly responsible for the loss of the lake trout raises additional
questions about whether contamination has claimed other species
as well. The lake trout fed on the deep-water sculpin, a species that
was never commercially harvested, but it, too, has vanished. DDT,
dioxin, and PCBs bind most effectively to the smallest organic parti
cles, which are constantly sorted and resorted by currents within the
lakes until they are finally deposited in the muds of the deepest wa-
I
158
OUR STOLEN FUTURE
ter, where the deep-water sculpin lived. As a result, that species was
exposed to much higher levels than other fish.
Egg mortality is not the only factor undermining the survival
among Great Lakes fish. In the 1960s, fish and game agencies intro
duced several species of salmon from the Pacific Northwest, which
are now stocked annually from fish hatcheries and provide the basis
for a multibillion-dollar sport fishing industry in the region. Today,
all the salmon in the Great Lakes have severely enlarged thyroid
glands, a symptom of inadequate levels of thyroid hormone, a chem
ical messenger that plays a role in reproduction and in the develop
ment of healthy offspring. Salmon eggs normally contain high levels
of thyroid hormone, but studies have found that Great Lakes salmon
eggs have lower thyroid hormone levels than eggs from Pacific
salmon in less contaminated areas. Although iodine deficiency can
cause such symptoms, researchers have ruled it out as the cause. Re
searchers have found that Great Lakes herring gulls, which prey on
fish, also suffer from thyroid enlargement. All evidence indicates
that these thyroid problems stem from contamination, and studies
have shown that many of the chemicals found in the lakes can block
the action of thyroid hormones, but the specific chemicals responsi
. .I
ble have not been identified.
The salmon in Lake Erie also show a variety of reproductive and
developmental problems, most notably precocious sexual develop
ment and a loss of typically male secondary sexual characteristics
such as heavy protruding jaws and red coloration on the flanks. Al
though secondary and sexual characteristics have been known to di
minish in hatchery fish because of the absence of natural selection,
John Leatherland, a fish specialist at the University of Guelph in On
tario, Canada, does not believe that the evolutionary phenomenon
known as "genetic drift" is sufficient to explain the significant loss of
visible sex differences in these fish, as some have suggested. Genetic
drift is an evolutionary process that occurs in very small populations
where chance begins to play a much larger part in determining which
genetic characteristics appear in the next generation. In this case, it
becomes an alternative to natural selection, the evolutionary process
at work in large populations. But efforts to explore whether endocrinedisrupting chemicals are responsible for the changes seen in the
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salmon have been stymied by ignorance about basic physiology in
this family of fish and about the processes that determine the ex
pression of secondary sexual characteristics.
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Many animals show reproductive problems that have been
linked to contaminants, but marine mammals such as whales, dol
phins, seals, and polar bears may face the greatest jeopardy, par
ticularly over the long term. As illustrated by the journey of the
PCB molecule in Chapter 6, persistent chemicals accumulate and
concentrate greatly in the marine food web, exposing the long-lived
predators to high levels of contamination. These marine animals
are especially vulnerable to persistent chemicals because they carry
heavy layers of fat that serve both as insulation against cold wa
ters and reserve fuel for times when food is in short supply. With
time, the vast quantities of persistent chemicals released over the
past half century on land, such as PCBs, will gradually make their
way into the oceans and increase already threatening levels of con
tamination.
In Europe and Scandinavia, researchers have done a series of
studies, beginning in the early 1970s, on declining populations of
harbor, ringed, and gray seals in the Baltic and on harbor seals in
the Wadden Zee, a large extension of the North Sea off the coasts
of Holland, Germany, and Denmark. Like the belugas m the St.
Lawrence, the harbor seal population off the Dutch coast dropped
from about 1,540 to 550 between 1965 and 1975 even though hunt
ing had stopped.
Taken together, these studies show significantly decreased
reproduction among seals living in contaminated areas, which is
strongly correlated with their levels of PCBs. In the Baltic, high body
burdens of PCBs are linked to a higher incidence of abnormalities
in female ringed seals, including tumors and other obstructions in
the uterus that can result in the death of their offspring. Studies on
Dutch harbor seals have also found a strong correlation between the
decrease in reproductive success and high levels of PCBs in their tis
sue. In follow-up experimental studies mentioned earlier in this
chapter, Dutch researcher Peter J. H. Reijnders fed two groups of fe
male common seals fish from two sources—the contaminated Dutch
160'
OUR STOLEN FUTURE
Wadden Zee and the cleaner northeast Atlantic. In breeding season,
the females from both groups consorted with three males who had
been eating uncontaminated Atlantic fish. The difference in the
pregnancy rate between the two groups was remarkable. Ten out of
the twelve females eating cleaner Atlantic fish became pregnant, but
only four in the second group that had eaten Wadden Zee fish.
Then in the late ’80s, a series of dramatic marine epidemics be
gan to kill off thousands of seals, dolphins, and porpoises, hitting
populations in the Baltic and North Seas, the Mediterranean, the
Gulf of Mexico, the North Atlantic, the eastern coast of Australia,
and even seals in Lake Baikal in Siberia. The losses devastated several
populations:
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■ In 1987, a distemper virus claimed an estimated ten thousand
seals in Lake Baikal.
■ That same year the Atlantic coast from New Jersey to Florida
witnessed a die-off of bottlenose dolphins that extended into
1988 and claimed more than 700 victims—a loss of more than
half of that migratory coastal population.
■ In 1988, twenty thousand harbor seals, up to 60 percent of
some local populations, perished in a matter of months in the
North Sea.
■ Between 1990 and 1993, more than a thousand striped dol
phins washed up on the shores of the Mediterranean.
Are all these die-offs a bizarre coincidence or evidence of some
serious and pervasive problem among marine mammals?
In three cases, the animals had succumbed to infections caused
by distemperlike viruses. In others, bacteria or fungi were implicated
as the “causative agents.” But even if the immediate cause of death
seemed clear, this does not answer the deeper question of why so
many animals in different places have become so vulnerable. The
autopsies on the victims did, however, yield some suggestive clues.
The dead animals showed weakened immune systems, and those ex
amined carried high levels of contaminants such as PCBs, synthetic
chemicals that have been shown to suppress immune response in
numerous animal studies.
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Distemper virus itself certainly contributed to immune system
suppression among the victims of these outbreaks of virus. But two
recent studies have suggested that contaminant-induced immune
suppression may also have been involved.
Virologist Albert Osterhaus and a team of Dutch researchers
at the National Institute of Public Health and Environmental Pro
tection undertook another feeding study with two groups of seals
to see whether eating contaminated fish had any effect on the ani
mals’ immune response. As in the earlier study looking at reproduc
tion, half of the twenty-two seals in the study ate relatively clean
North Atlantic fish; the other half ate fish from the heavily pol
luted Baltic, which contained roughly ten times more dioxinlike
organochlorines and similar-acting compounds than the Atlantic
herring. Osterhaus has noted in press interviews that all the fish
fed to both groups had come from commercial catches destined for
human consumption.
The seals that dined on Baltic herring for nearly two years
quickly showed several signs of depressed immune function and
weakened ability to fight off viral infections. The action of their nat
ural killer cells, which act as a first line of defense against viral infec
tions, was twenty to fifty percent below normal and the response of
T cells, which direct the immune defense, dropped by twenty-five to
sixty percent. T lymphocytes play a crucial role in clearing viral infec
tions, especially in the case of distemperlike viruses.
A second study done in the United States by immunologist
Caret Lahvis looked at the relationship between immune response
and pollutant levels in relatively healthy dolphins, whose blood was
taken after they were encircled by nets in shallow water off the coast
of Florida. Using lymphocyte assays similar to those used to detect
early signs of immune impairment in humans infected with the
AIDS virus, Lahvis found evidence that immune response in dol
phins dropped as levels of PCBs and DDT increased in their blood.
This provides added evidence that highly contaminated animals
were already likely to be suffering from weakened immune systems
before they were attacked by the distemperlike viruses implicated in
some of the marine epidemics.
Like the reproductive system, the immune system is especially
162
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vulnerable to damage from hormone-disrupting chemicals during
prenatal development. As we've seen, animal studies and evidence
from DES-exposed humans show that such exposure can alter the
development of the immune system and have a lifelong impact. The
growing evidence of the links between synthetic chemicals and im
mune system impairment has particularly serious implications for
marine mammals. These species carry high levels of contamination,
making it likely their offspring enter the world with already impaired
immune systems. The chronic exposure to toxic chemicals afterward
during a lifetime in polluted waters simply adds insult to injury. Be
cause of their prenatal exposure, the offspring may be less able to
fight off disease than their parents, whose exposure to chemicals was
limited to their adulthood.
If synthetic chemicals have weakened marine mammal im
mune systems and contributed to the rash of epidemics, one might
wonder why the outbreaks didn't occur earlier. Part of the reason
may be that these are long-lived species, so it would take some time
for this second-generation double whammy to emerge. There is also
a lag time between the release of contaminants on land and their ac
cumulation in the sea. These two factors may explain in part why
these major marine epidemics did not show up until recently.
Even less is known about the cause of the dramatic and myste
rious frog declines that have been reported in many parts of the
world. The loss of frogs in urban areas of the United States where de
velopment has gobbled up wetlands seems no mystery, but why are
frogs vanishing in undisturbed forest in Costa Rica and in remote
areas of Australia? One of the world's leading amphibian experts,
Robert Stebbins, believes that hormone-disrupting chemicals are
likely suspects in declines that do not have obvious causes such as
habitat disruption or drought. Speaking at an international gathering
of herpetologists in Australia in December 1993, Stebbins, professor
emeritus of zoology at the University of California at Berkeley, urged
his colleagues to give the possible role of hormone-disrupting chemi
cals high priority in their search for a cause.
During his research on amphibians, Stebbins has reviewed the
reports of frog declines and found a synchronous pattern in many
that suggests a widespread cause such as wind-borne contaminants.
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Based on his review, it appears that many populations declined
rapidly or vanished altogether between the mid-1970s and early
1980s. Populations living at high altitudes have been particularly
hard hit, leading some to suggest that the thinning ozone layer
might be playing a role by exposing them to increased levels of dam
aging ultraviolet-B radiation. While depleted ozone may be under
mining some frog populations, Stebbins has not found this theory
adequate to explain losses such as the golden toad of Costa Rica, a
species that lives deep in the rain forest and is well protected from
UVB radiation by the trees.
High-altitude areas are not only more vulnerable to ozone loss,
they are also more vulnerable to pollution that arrives on the winds.
As our hypothetical journey of the PCB molecule illustrated, many
persistent synthetic chemicals evaporate and travel around until they
hit a cooler spot, such as a mountain, where they recondense and
come to rest. As scientists have studied the role of long-distance pol
lution in acid rain, they have found all kinds of contaminants on
seemingly remote mountainsides.
Stebbins sees other symptoms that seem to implicate chemical
contamination as well. Like the dolphins, some of the disappearing
frogs seem to be showing signs of weakened immune systems, as in
dicated by outbreaks of “red leg.” This sometimes lethal infection,
which causes inflammation on the underside of the legs, is caused by
a common bacterium that is found in freshwater around the world.
“If a population is healthy,” Stebbins says, “the frogs can han
dle this bacterium quite well. But in a lot of places where there are
declines, animals are showing up with red leg.” Because of the appar
ent relationship to a weakened immune system, Stebbins has de
scribed the phenomenon as “AIDS-like.”
Finally, Stebbins notes, the frog’s unique physiology and life
history make it highly vulnerable to the assault of hormone-disrupting
chemicals. Endowed with permeable skin that can breathe and take
in water, frogs absorb the chemicals they encounter more readily
than most other animals. They also experience a dramatic passage
called metamorphosis that transforms them from creatures that
breathe in water to creatures that breathe in air. As tadpoles become
frogs, a profound reorganization of their structure and physiology
164
OUR STOLEN FUTURE
takes place—a process driven by hormones and therefore vulnerable
to synthetic chemicals that disrupt hormone messages. By their na
ture, frogs are prime candidates for hormone havoc.
And many other creatures may be as well. Scientists are just
beginning to explore the possible impacts of pesticides and other
synthetic chemicals on the migration of birds, a complex and awe
inspiring phenomenon that is still not fully understood. Some small
birds fly as high as airplanes; some make ninety-hour nonstop flights
from Massachusetts to South America. Two-thirds of the bird species
in North America are migratory, and many of the long-distance mi
grants have shown alarming declines.
In the mid-1980s, Pete Myers, then a young scientist studying
shorebirds, began to wonder about the possible impact of pesticides
as he contemplated the plunging numbers of shorebirds, a family
that includes such species as sandpipers and plovers. Shorebirds per
form some of the greatest migratory feats in the avian world, with
some species traveling well over fifteen thousand miles in a single
year, from breeding sites in the Arctic to wintering grounds in far
southern South America. Data from the Manomet Bird Observatory
in Plymouth, Massachusetts, suggested that the population of sanderlings moving south along the East Coast of the United States in au
tumn had declined eighty percent over a fifteen-year period. Much
of this population, Myers had recently discovered in his research,
wintered on the west coast of South America in Peru and Chile,
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What was happening to them and why? The birds cover so
much ground in the course of a year hopscotching their way back
and forth across the equator, depending not only on breeding and
wintering grounds but on important stopover sites along the way
where they feed and build up energy for the next leg of their journey.
The destruction of just one of these key feeding areas along the way
might derail their marathon migrations and doom the birds.
The sanderling decline did not appear to be caused by a loss in
winter habitat, for there was an abundance of sandy beaches where
the birds could feed and rest. Perhaps something had gone wrong
in the breeding grounds in the Arctic in Alaska and Canada or in one
of the key feeding sites such as Delaware Bay or the coast of Massa-
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chusetts. Myers and his colleagues began to tackle these habitat
questions, working to identify the precise migratory routes the birds
were traveling and the critical way stations in their journey.
But Myers suspected that there might be another factor to con
sider as well. Every day he watched the birds congregate to feed and
bathe at the mouths of the rivers and streams that emptied intensely
cultivated river valleys in the otherwise harsh Peruvian desert. Virtu
ally every rivulet and stream, no matter how small, reeked of pesti
cides used in the cotton and rice fields packed tightly into verdant
river valleys. As the birds put on weight in preparation for heading
north again, it appeared likely they were taking on a load of contami
nants carried in their food. Where did those pesticides go when the
birds suddenly burned off that fat during a marathon flight from
South America to Cape Cod? As the stored fat is converted to energy
for their flight, the contaminants would be liberated into the blood
and most likely move to either the sex organs or the brain, both of
which contain major fat deposits. If that was happening, the pesti
cides might be interfering with migration, disrupting reproduction,
or even killing the birds. Would a contaminated brain steer a bird off
course? If they reached their breeding grounds, would they be able to
reproduce? And what would happen to the offspring of young born
to contaminated adults? Would their behavior and ability to orient
in migration be impaired? Science was not prepared to answer, and
even today, it is unknown whether pesticides played a role in the de
cline of the sanderlings and other migratory species over the past
four decades.
With the growing amount of evidence and theories that link
wildlife problems to hormone disruption, there is now good reason
to regard endocrine-disrupting chemicals as a major long-term threat
to the world’s biodiversity and perhaps an immediate threat to cer
tain endangered species, such as the St. Lawrence belugas and the
Florida panthers. In searching for the causes of loss, scientists must
look for functional changes, such as impaired reproduction and al
tered behavior, along with more evident disruptions, such as vanish
ing habitat and changing climate. As many of the cases discussed in
this chapter demonstrate, it is important to look beyond appear
ances. Animals that appear normal and healthy may. in fact, show
166
OUR STOLEN FUTURE
skewed hormone ratios, scrambled sex organs, or physical changes in
their brains when one takes a closer look. Diminished and impaired
by invisible damage, such animals lose the edge honed by millions of
years of natural selection. They may lose their ability to withstand
otherwise tolerable stresses or to rebound after natural disasters. For
no apparent reason, they may suddenly disappear or slowly, imper
ceptibly slip into extinction.
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“Our fate is connected with the animals,” Rachel Carson wrote
more than three decades ago in Silent Spring, a now classic indict
ment of synthetic pesticides and human hubris that helped launch
the modern environmental movement. This has long been a guiding
belief among environmentalists, wildlife biologists, and others who
recognize two fundamental realities—our shared evolutionary inher
itance and our shared environment. What is happening to the ani
mals in Florida, English rivers, the Baltic, the high Arctic, the Great
Lakes, and Lake Baikal in Siberia has immediate relevance to hu
mans. The damage seen in lab animals and in wildlife has ominously
foreshadowed symptoms that appear to be increasing in the human
population.
As noted in earlier chapters, basic physiological processes such
as those governed by the endocrine system have persisted relatively
unchanged through hundreds of millions of years of evolution. Evolu
tionary narratives tend to highlight the innovations of natural selec
tion, ignoring the stubborn conservative streak that has marked the
history' of life on Earth. At the same time that evolution experimented
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OUR STOLEN FUTURE
greatly with form, shaping the vessels in various and wondrous ways, it
has strayed surprisingly little from an ancient recipe for life’s biochem
ical brew. In examining our place in the evolutionary lineage, humans
tend to focus inordinately on those characteristics that make us
unique. But these differences are small, indeed, when compared to
how much we share not only with other primates such as chim
panzees and gorillas, but with mice, alligators, turtles, and other ver
tebrates. Though turtles and humans bear little physical similarity,
our kinship is unmistakable. The estrogen circulating in the painted
turtle seen basking on logs during lazy summer afternoons is exactly
the same as the estrogen rushing through the human bloodstream.
Humans and animals share a common environment as well as a
common evolutionary legacy. Living in a man-made landscape, we
easily forget that our well-being is rooted in natural systems. Yet all
human enterprise rests on the foundation of natural systems that
provide a myriad of invisible life-support services. Our connections
to these natural systems may be less direct and obvious than those of
an eagle or an otter, but we are no less deeply implicated in life’s
web. No one has stated this fundamental ecological principle more
simply than the early twentieth-century American environmental
philosopher, John Muir. “When we try to pick out anything by itself,
we find that it is bound by a thousand invisible cords ... to every
thing in the universe.”
Our regrettable experience with persistent chemicals over the
past half century has demonstrated the reality of this deep and com
plex interconnection. Whether we live in Tokyo, New York, or a re
mote Inuit village in the Arctic thousands of miles from farm fields
or sources of industrial pollution, all of us have accumulated a store
of persistent synthetic chemicals in our body fat. Through this web
of inescapable connection, these chemicals have found their way to
each and every one of us just as they have found their way to the
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birds, seals, alligators, panthers, whales, and polar bears. With this
shared biology and shared contamination, there is little reason to
expect that humans will in the long term have a separate fate.
Yet, some skeptics question whether animal studies provide a
useful tool for forecasting threats to humans. The refrain that “mice
are not little people” has been heard frequently in the ongoing de-
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ALTERED DESTINIES
169
bate about whether animal testing accurately predicts whether a
chemical poses a cancer risk to humans. Critics have also attacked
testing procedures for using unrealistically high doses, arguing, for
example, that mice tested to discover if DDT caused cancer were fed
more than eight hundred times the average amount humans would
take in eating a typical diet.
Whatever the merits of these criticisms regarding cancer test
ing, they have little relevance to the use of animals to predict the ef
fects of hormone-disrupting chemicals. Because scientists have only
an incomplete understanding of the basic mechanisms that induce
cancer, extrapolating from one species to another has admitted un
certainties. In contrast, scientists have a good grasp of the mecha
nisms and actions of hormones. They understand how chemical
messages are sent and received and how some synthetic chemicals
disrupt this communication. They know that hormones guide devel
opment in basically the same way in all mammals, and if there was
any doubt, the DES experience has verified the similarity of disrup
tion across many species, including humans. Time after time, the
abnormalities first seen in laboratory experiments with DES later
showed up in the children of women who had taken this drug during
pregnancy.
The relevance of the DES experience to the threat from envi
ronmental endocrine disruptors has also been questioned because of
the very high doses given to pregnant women and to laboratory ani
mals in experiments. While most of the early experiments did in
deed use high doses, recent studies using much lower doses have
produced no less alarming results. In fact, in some cases a high dose
may paradoxically cause less damage than a lower dose. In exploring
the effects of much lower doses of DES, Fred vom Saal has found
that the response increases with dose for a time and then, with even
higher doses, begins to dimmish.
Vom Saal’s dose response curve looks like an inverted U. Its
shape is profoundly important to the interaction between the en
docrine system and synthetic contaminants. Neither linear nor always
moving in the same direction, the inverted U seems characteristic
of hormone systems and it means that they do not conform to the
assumptions that underlie classical toxicology—that a biological rc-
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spouse always increases with dose. It means that testing with very high
doses will miss some effects that would show up if the animals were
given lower doses. The inverted U is another example of how the ac
tion of endocrine disruptors challenges prevailing notions about toxic
chemicals. Extrapolation from high-dose tests to lower doses may in
some cases seriously underestimate risks rather than exaggerate them.
Because the endocrine disruption question has surfaced so re
cently, the scientific case on the extent of the threat is still far from
complete. Nevertheless, if one looks broadly at a wide array of exist
ing studies from various branches of science and medicine, the
weight of the evidence indicates that humans are in jeopardy and are
perhaps already affected in major ways. Taken together, the pieces of
this scientific patchwork quilt have, despite admitted gaps, a cumu
lative power that is compelling and urgent.
This was the lesson from the historic meeting on endocrine dis
ruption that took place in July 1991 at the Wingspread Conference
Center in Racine, Wisconsin. Over the years, dozens of scientists have
explored isolated pieces of the puzzle of hormone disruption, but the
larger picture did not emerge until Theo Colborn and Pete Myers fi
nally brought twenty-one of the key researchers together. At this
unique gathering, specialists from diverse disciplines ranging from an
thropology to zoology shared what they knew about the role of hor
mones in normal development and about the devastating impacts of
hormone-disrupting chemicals on wildlife, laboratory animals, and hu
mans. For the first time, Ana Soto, Frederick vom Saal, Michael Fry,
Howard Bern, John McLachlan, Earl Gray, Richard Peterson, Peter
Reijnders, Pat Whitten, Melissa Hines, and others explored the excit
ing connections between their work and the ominous implications
that arose from this exercise. As the evidence was laid out, the parallels
proved remarkable and deeply disturbing. The conclusion seemed in
escapable: the hormone disruptors threatening the survival of animal
populations are also jeopardizing the human future.
At the end of the session, the scientists issued the Wingspread
Statement, an urgent warning that humans in many parts of the
world are being exposed to chemicals that have disrupted develop
ment in wildlife and laboratory animals, and that unless these chem
icals are controlled, we face the danger of widespread disruption in
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171
human embryonic development and the prospect of damage that
will last a lifetime.
The pressing question is whether humans are already suffering
damage from half a century of exposure to endocrine-disrupting syn
thetic chemicals. Have these man-made chemicals already altered
individual destinies by scrambling the chemical messages that guide
development?
Many of those familiar with the scientific case believe the
answer is yes. Given human exposure to dioxinlike chemicals, for
example, it is probable that some humans, especially the most sensi
tive individuals, are suffering some effects. But whether hormonedisrupting chemicals are now having a broad impact across the
human population is difficult to assess and even harder to prove.
This is inescapable in light of the nature of the contamination, the
transgenerational effects, the often long lag time before damage be
comes evident, and the invisible nature of much of this damage.
Those trying to document whether perceived increases in specific
problems reflect genuine trends in human health find themselves
thwarted by a dearth of reliable medical data. Few disease registries
exist for anything except cancers. A number of pediatricians from
various parts of the United States have expressed their concern
about an increasing frequency of genital abnormalities in children
such as undescended testicles, extremely small penises, and hy
pospadias, a defect in which the urethra that carries urine does not
extend to the end of the penis, but it is virtually impossible to docu
ment these anecdotal reports. Unfortunately, the problems caused
by endocrine disruption may have to reach crisis proportion before
we have a clear sign that something serious is happening.
In the face of these difficulties, the animal studies provide a
touchstone for identifying and investigating what might be happen
ing in humans. They can alert us to the probable kinds of disruptions
and help focus research efforts. They can also provide early warnings
about the hazards of current levels of contamination. Because of the
diversity of life, some animals are bound to be more readily exposed
to contaminants than humans. Transgenerational effects, such as
changes in behavior and diminished fertility, are also likely to show
up faster in wildlife because most animals mature and reproduce
172
OUR STOLEN FUTURE
more quickly than humans. Experimental work with animals adds
another equally invaluable dimension. As the history of DES demon
strates, laboratory experiments with rats and mice accurately fore
casted damage that later showed up in humans. The tragedy is that
we ignored the warnings.
Based on the warnings from wildlife and lab animals, what
kinds of problems should we expect? Earlier chapters explored how
hormonally active synthetic chemicals can damage the reproductive
system, alter the nervous system and brain, and impair the immune
system. Animals contaminated by these chemicals show various be
havioral effects, including aberrant mating behavior and increased
parental neglect of nests. Synthetic chemicals can derail the normal
expression of sexual characteristics of animals, in some cases mas
culinizing females and feminizing males. Some animal studies indi
cate that exposure to hormonally active chemicals prenatally or in
adulthood increases vulnerability to hormone-responsive cancers,
such as malignancies in the breast, prostate, ovary, and uterus.
Is there evidence of such problems in humans? Are these
problems increasing? In some instances, it appears that this is in
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fact the case.
Laboratory experiments, wildlife studies, and the human DES
experience link hormone disruption with a variety of male and fe
male reproductive problems that appear to be on the rise in the gen
eral human population—problems ranging from testicular cancer to
endometriosis, a condition in which tissue that normally lines the
uterus mysteriously migrates to the abdomen, ovaries, bladder, or
bowel, resulting in growths that cause pain, severe bleeding, infertil
ity, and other problems.
The most dramatic and troubling sign that hormone disruptors
may already have taken a major toll comes from reports that human
male sperm counts have plummeted over the past half century, a blink
of the eye in the history of the human species. The initial study, done
by a Danish team headed by Dr. Niels Skakkebaek and published in the
British Medical Journal in September 1992, systematically reviewed the
international scientific literature on semen analysis performed on nor
mal men since 1938 and based its findings on sixty-one studies involv
ing almost fifteen thousand men from twenty countries in North
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America, Europe, South America, Asia, Africa, and Australia. The study
excluded men sampled at fertility clinics, who might have particularly
low sperm counts, or men who were diseased, and it used only those
studies that counted sperm in the same way using light microscopes.
The Danish researchers found that the average male sperm
count had dropped forty-five percent, from an average of 113 million
per milliliter of semen in 1940 to just 66 million per milliliter in
1990. At the same time, the volume of the semen ejaculated had
dropped by twenty-five percent, making the effective sperm decline
equivalent to fifty percent. During this period, the number of men
with extremely low sperm counts in the range of 20 million per milli
liter had tripled, increasing from six percent to eighteen percent,
while the percentage with high sperm counts over 100 million per
milliliter had decreased.
The study is still meeting with a skeptical response in parts of
the medical community. This skepticism recalls similar disbelief at
the first news in 1985 that a dramatic hole had developed in the
Earth’s protective ozone layer over Antarctica. Some scientists then
doubted the reports and were even more skeptical that man-made
chlorofluorocarbons, known as CFCs, might be responsible. The
NASA satellite monitoring network had failed to pick up the ozone
loss, which was discovered by British researchers doing measure
ments from the ground, because those who had programmed thecomputers receiving the satellite data assumed such large ozone
losses were impossible. Similarly, many medical researchers had been
incredulous at the first reports of sperm count decline, regarding such
a large drop in sperm count across the human population as next to
impossible.
Skakkebaek, a specialist in male reproduction and chief of the
Department of Growth and Reproduction at the University Hospital
in Copenhagen, had been a skeptic himself. Although he had been
seeing increasing abnormalities in the male reproductive system, in
cluding rising rates of testicular cancer in young men, he had doubted
earlier reports of declining human sperm counts over the past two
decades. He suspected that they stemmed largely from a bias in the
samples, such as the inclusion of men from fertility clinics, and did
not, therefore, truly reflect sperm counts among normal men.
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His team’s own broad review of dozens of sperm count studies
from around the world convinced him that a precipitous drop in
sperm counts had, indeed, occurred over just two generations—a sig
nificant change that is likely, in his view, to have a “negative influ
ence on male fertility.” Since such a rapid decline could not be a
consequence of genetic changes, the cause must lie in changed living
habits or environmental factors.
As these sperm count findings came under scrutiny, critics
claimed that flaws in the data made it impossible to draw definitive
conclusions. For example, they erroneously criticized Skakkebaek’s
team for excluding men with abnormally low sperm counts and fur
ther objected that the definition of “abnormal” had changed over
time. In fact, Skakkebaek and his colleagues made no such exclusion
other than to exclude all data from fertility clinics. At the same time,
critics offered no data to refute Skakkebaek’s conclusion; they simply
maintained that he hadn’t proven his case beyond doubt.
This debate stimulated other studies, and subsequently at least
three independent analyses, undertaken in one instance by another
skeptic, have confirmed that sperm counts have dropped. Based on
semen samples from 5,440 men, these new studies carried out in
France, Belgium, and Scotland have provided additional evidence
that the cause is probably environmental.
The new results reveal a striking inverse correlation between
the year of birth and the health of men’s sperm. The more recently a
man was born, the lower the average sperm numbers and the greater
the number of sperm abnormalities. For example, the Scottish study
conducted by the Medical Research Council’s Reproductive Biology
Unit in Edinburgh on a sample of 3,729 men found a median sperm
count of 128 million per milliliter in semen donors bom in 1940 but
a median count of only 75 million in those bom in 1969.
Belgian researchers, comparing sperm samples from 360 men
donated between 1990 and 1993 to earlier samples from 1977 to
1980, found an alarming increase in unhealthy sperm over this sixteen-year period. The percentage of well-formed sperm had declined
from 39.6 percent to 27.8 percent, while the percentage of sperm
showing normal swimming ability, or motility, dropped from 53.4
percent to 32.8 percent. The authors’ conclusion was unusually di-
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rect for scientists, who tend toward qualification and understate
ment: the decline, they warned, “threatens male fertilizing ability.”
Most recently, a team of French scientists led by Jacques Auger
published a study examining sperm count trends in Paris from 1973
to 1992. Auger had embarked on the analysis because he simply
didn’t believe the Danish study. To Auger’s surprise, his team’s
analysis lent strong support to the conclusion that male sperm counts
have dropped steadily over the twenty-year period.
The French findings are particularly persuasive because the data
allowed the researchers to correct for two important confounding vari
ables that might call sperm count results into question: age and absti
nence. A man’s sperm count generally declines as he gets older, and it
drops immediately after sex, recovering within a few days.
The French team was, therefore, able to compare the average
sperm counts of thirty-year-old men born in 1945 with thirty-yearolds born seventeen years later in 1962. For those born in 1945 and
measured in 1975, sperm counts averaged 102 million per milliliter
of semen. The men born in 1962 and measured in 1992 had counts
that were only half that number—51 million sperm per milliliter on
average.
If this downward trend were to continue, the thirty-year-old
man in 2005, who was born in 1975, would have a sperm count of
roughly 32 million sperm per milliliter—about one-fourth the count
of the average male born in 1925.
Declining sperm counts are just one of many signs of trouble.
Over the past half century, Skakkebaek noticed, the incidence of tes
ticular cancer and other reproductive abnormalities in men has risen
sharply. In Denmark, testicular cancer, a disease of young men, has
tripled, and other industrial countries have seen similar trends. “The
frightening thing,” Skakkebaek notes, “is that the incidence is still
increasing in Denmark.”
British researchers report a doubling in the number of cases of
undescended testicles in England and Wales between 1962 and
1981, and similar increases have been reported in Sweden and Hun
gary. Men with undescended testicles have a higher risk of testicular
cancer and typically have lower sperm counts and more abnormal
well as younger men. The fact that the sperm counts are lower in
younger men and correlate inversely with date of birth argues that
the damage was done in the womb.
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sperm. There also appears to be an increasing incidence of the genitai defect hypospadia.
In his earlier work, Skakkebaek had slowly accumulated evi-
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members of the cabbage family, indole-3-carbinol, reduces cancer
risk by pushing estrogen metabolism toward the good pathway.
In recent studies, however, the Cornell researchers report that
hormonally active chemicals have the opposite effect—they push es
trogen metabolism toward the bad pathway and increase cancer risk.
The experiments, which exposed breast cancer cells in test tubes to
synthetic chemicals including DDT, PCBs, endosulfan, kepone, and
atrazine, found that all these chemicals have a “profound effect” and
greatly increase the production of a bad form of estrogen.
“Our data show that a wide variety of pesticides and related
compounds clearly have effects on estrogen metabolism that would
act in the direction of increasing breast cancer and endometrial can
cer risks,” Bradlow says.
Researchers have been exploring possible links in other ways as
well, including analyzing body concentrations of synthetic chemicals
in women who develop breast cancer. A Canadian study involving a
small number of women found significantly higher levels of DDE, a
DDT breakdown product, in women with estrogen-responsive tumors,
supporting the hypothesis that exposure to hormonally active chemi
cals may affect the incidence of hormone-responsive breast cancer.
Two other studies collected and stored blood samples from large
numbers of healthy women without any signs of cancer. When some
of the women later developed cancer, researchers analyzed the blood
looking for differences in exposure to DDT and PCBs between those
who developed cancer and those who did not. The New York Uni
versity Women’s Health Study, whose study group was composed
primarily of Caucasian women, found that those with the highest
levels of DDE had a fourfold greater risk than those with the lowest
levels. But the second study done in California with a larger group of
women, which included Caucasian, African-American, and Asian
women, found no link between breast cancer and DDE levels overall.
Whatever the design, the studies to date have several short
comings that make such inconsistent results not at all surprising.
The contribution of synthetic chemicals to estrogen exposure may
come from many different chemicals, some of them exceedingly per
sistent, such as PCBs, and others that are not persistent and leave no
telltale evidence of exposure in blood or body fat. The studies to
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185
date have looked only at a handful of well-known persistent com
pounds such as DDE and PCBs.
Also, studies have usually treated all 209 chemicals in the PCB
family as one, even though various members of this chemical family
have completely different and in some cases opposite biological ef
fects. Some are estrogen mimics, while the dioxinlike compounds can
act as estrogen blockers. Moreover, the mix of PCBs found in humans
varies from individual to individual, depending on their diet and other
exposure. Teasing out any correlation between PCBs and breast can
cer is going to require treating the PCBs as individual chemicals.
The discovery that estrogenic chemicals lurk in plastics, canned
goods, and detergent breakdown products also suggests that signifi
cant exposure may result from chemicals other than the usual sus
pects. Studies have not screened human tissue for less well-known
estrogen mimics such as bisphenol-A or nonylphenol, even though
they could conceivably be contributing in a major way to estrogen
exposure from synthetic chemicals. Some researchers, including Ana
Soto and Carlos Sonnenschein, are now exploring ways to separate
out the natural estrogen found in women’s blood from foreign estro
gens in an effort to determine how much overall estrogen exposure
comes from synthetic chemicals.
Because of our poor understanding of what causes breast cancer
and significant uncertainties about exposure, it may take some time to
satisfactorily test the hypothesis and discover whether synthetic chem
icals are contributing to rising breast cancer rates. In part because
of political pressure from breast cancer advocacy groups on the U.S.
Congress, federal funding agencies are now directing more money
toward exploring this important question. The National Cancer Insti
tute is currently funding a 6-miIlion-dollar four-year study to in
vestigate the connection between breast cancer and environmental
exposure to several hormonally active synthetic chemicals. This effort,
known as the Northeast/Mid-Atlantic Study, is focusing particularly
on the possible connection between synthetic pollutants and the ele
vated breast cancer risk faced by women living in this region.
Among cancer victims in the United States, breast and prostate
cancer are two of the four biggest killers. Hormones play a major role
m both these cancers, and the rates of incidence of both continue to
186
OUR STOLEN FUTURE
climb upward not only in the United States but in most other coun
tries as well. The highest rates of breast cancer deaths are in Western
Europe, followed by the United States, but the fastest increase in
deaths from the disease is now occurring in Eastern Europe and East
Asia. For prostate cancer, the highest death rates occur in the Nordic
countries, while East Asia, which has a very low incidence, is seeing
the greatest increase. The quest to discover the role of hormonedisrupting chemicals in these cancers deserves higher priority than the
quest for hereditary breast and prostate cancer genes because research
aimed at environmental factors offers the hope of finding ways to pre
vent these devastating diseases in the vast majority of victims.
Our fears about toxic chemicals have typically centered around
cancer and other physical illnesses. But as one surveys the scientific
literature, it becomes quickly apparent that physical disease or visi
ble birth defects may not be the most immediate danger. Long be
fore concentrations of synthetic chemicals reach sufficient levels to
cause obvious physical illness or abnormalities, they can impair
learning ability and cause dramatic, permanent changes in behavior,
such as hyperactivity. Save for a few compounds such as PCBs, we
know virtually nothing about the hazards posed to thinking and be
havior by the thousands of synthetic chemicals in commerce.
What little we do know about those few chemicals that have been
studied has alarming implications. Both animal experiments and hu
man studies report behavioral disorders and learning disabilities similar
to those reported with increasing frequency among school children
across the nation. In the United States, an estimated five to ten percent
of school-age children suffer from a suite of symptoms related to hyper
activity and attention deficit that make it difficult for them to pay at
tention and learn. Countless others experience learning problems
ranging from difficulties with memory to impaired fine motor skills
that make it harder to hold a pen and learn how to write.
Scientists still do not have a complete understanding of how
PCBs impair neurological development in the womb and early in
life, but emerging evidence suggests that the ability of PCBs to cause
brain damage stems in part from disruption to another component
of the endocrine system, thyroid hormones.
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Extensive research on the developing brain and nervous system
has found that thyroid hormones help orchestrate the elaborate stepby-step process that is required for normal brain development. As
touched on in Chapter 3, these hormones stimulate the proliferation
of nerve cells and later guide the orderly migration of nerve cells to ap
propriate areas of the brain. The brain and nervous system, like other
parts of the body, pass through critical periods during their develop
ment both in the womb and in the first two years of life. When thyroid
levels are too high or too low, this development process will go awry
and permanent damage will result, which can range from mental retar
dation to more subtle behavioral disorders and learning disabilities.
The precise nature of the damage done by abnormal thyroid levels will
depend on the timing and the extent of the disruption.
It has long been recognized that acute thyroid deficiency dur
ing pregnancy can cause profound mental retardation, but thyroid
researcher Susan Porterfield, an endocrinologist at the Medical Col
lege of Georgia, notes that few have considered the more subtle ef
fects of less severe thyroid disruption during the development of the
brain and nervous system—disruption that can occur naturally or be
the result of hormone-disrupting chemicals in the environment.
PCBs and dioxin affect the thyroid system in diverse, complex,
and as yet incompletely understood ways. Some analyses indicate
they may mimic or block normal hormone action perhaps by binding
to the thyroid receptor. Other data suggest they may even increase
the number of receptors present to receive the hormone signals.
They also seem to act particularly on T4, the form of thyroid hor
mone that is critical to prenatal brain development. Researchers
Daniel Ness and Susan Schantz of the University of Illinois have
established that two PCBs commonly found in human tissue and
breast milk—PCB-118 and PCB-153—reduce T4 levels in rats ex
posed prenatally. These compounds also compete more powerfully
than natural hormones for binding to a carrier protein called trans
thyretin, which transports T4 to brain cells.
In a June 1994 article in the journal Environmental Health Per
spectives, Porterfield outlined her theory that “very low levels” of
PCBs and dioxins—levels well below those generally recognized as
toxic—can alter thyroid function in the mother and the unborn baby
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OUR STOLEN FUTURE
and thereby impair neurological development. Like Sharpe and Skakkebaek, Porterfield cites evidence showing that skewed hormone lev
els in the womb can cause permanent damage—in this case, learning
disabilities, attention problems, and hyperactivity.
The emerging evidence linking PCBs to thyroid disruption and
neurological damage is especially worrisome because PCBs are a persis
tent, ubiquitous contaminant whose levels had dropped initially in hu
man tissue but have held steady in recent years, even though most of
the industrial countries stopped making them more than a decade ago.
In the former Soviet Union, production of PCBs did not stop until 1990.
Based on the concentrations in breast milk fat of PCBs, some
have estimated that at least five percent of babies in the United
States are exposed to sufficient levels of contaminants to cause neu
rological impairment. But while the most extensive data on neuro
logical effects concern PCBs, it is important to stress that PCBs are
not by any means the only culprit. Many other synthetic chemicals
act on thyroid hormones as well, adding to the concern. The thyroid
system is one of the most frequent targets for synthetic chemicals,
according to Linda Birnbaum, who heads the environmental toxicol
ogy division at the U.S. Environmental Protection Agency’s Health
Effects Research Laboratory. With the possibility for multipl e assaults on the thyroid system, the hazards to the developingg brain
may be considerable.
Laboratory animals exposed to PCBs in the womb and early in
life commonly show behavioral abnormalities as adults. The off
spring of some mice fed relatively low doses of PCBs develop a “spin
ning syndrome” in which they constantly circle their cage. Other
exposed mice, while showing no overt behavioral abnormalities, have
depressed reflexes and learning deficits. Rats exposed in the womb
make more errors in running a maze and have greater difficulty
learning how to swim, perhaps reflecting motor impairment. In rhe
sus monkeys, researchers also find that exposure to PCBs in the womb
and through breast milk causes motor impairment as well as deficits
in memory and learning. The greater the PCB exposure, the greater
the number of errors the monkeys made in learning tasks designed to
test their cognitive skills.
But the most obvious and thus most reported behavioral sign of
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neurological damage found in laboratory animals exposed to PCBs in
the womb and early life is hyperactivity, which has shown up in rats,
mice, and monkeys. Although one might expect that extrapolation
from animal studies to humans would be less reliable when consider
ing questions of behavior and cognition, some striking parallels be
tween animal and human effects appear in these neurological studies
as well. In her paper, Porterfield notes that this problem occurs at
higher frequency in the children born to women who had abnormally
low levels of thyroid hormones during pregnancy.
Much of our knowledge about the impact on humans comes
from studying those individuals exposed in accidents. One major
long-term study involves the children born to women in Taiwan who
in 1979 consumed cooking oil accidentally contaminated with high
levels of PCBs and furans. Some of the 128 children studied were in
the womb during the time their mothers actually consumed the con
taminated oil. Others were conceived and born after the period of
contamination had ended, so their exposure came from residual con
tamination within their mothers. In a series of examinations and
tests conducted on these children between 1985 and 1992, a team
headed by Yue-Liang L. Guo of Taiwan’s Department of Occupa
tional and Environmental Health found that the children suffer
from an array of problems—physical and neurological—that had
been predicted from animal studies.
As some of these children approached puberty, researchers noted
abnormal sexual development in the males, paralleling one of the
most striking effects recorded in wildlife literature. Like the alligators
in Lake Apopka, these boys have significantly shorter penises than
unexposed boys of the same age.
These Taiwanese children also show permanent impairment in
their motor and mental abilities and behavior problems including
higher than normal levels of activity. Tests have repeatedly found
signs of retarded development, and the children scored five points
lower on intelligence tests than similar unexposed children. Guo and
his colleagues believe that these children score lower in IQ tests be
cause they suffer from attention deficits and are unable to think as
quickly as their unexposed peers.
Fortunately, few people are exposed to the intense contamina-
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OUR STOLEN FUTURE
tion suffered by victims of this unfortunate accident in Taiwan. Two
studies done in the United States have attempted to discover
whether children suffer neurological damage when exposed through
their mothers to the normal range of contamination encountered in
the environment. Both reported signs of impaired neurological de
velopment, which might not be evident to the parents but could be
detected through specialized tests.
The first study, done in the early 1980s by psychologists Sandra
and Josepn Jacobson of Wayne State University, enlisted new moth
ers in Michigan who had eaten Great Lakes fish, which contain sig
nificant levels of PCBs and numerous other chemical contaminants.
Despite the contamination levels, state fish and game agencies in
the Great Lakes region continue to stock salmon, lake trout, and
other game fish, and sport fishing remains a 3- to 4-billion-dollar
industry. Signs posted by state health officials at some fishing areas
warn that eating salmon and lake trout may be hazardous to health,
but many fishermen and their families continue to eat what they
catch. The women in the fish-eating group in this study had all eaten
two or three fish meals a month in the six years before becoming
pregnant, although some had eaten no fish during pregnancy. Since
PCBs are persistent, these women accumulated them in their body
fat and then passed the PCBs on to their babies through the pla
centa and through breast milk
Differences between the children of fish-eaters and nonfish
eaters were evident immediately at birth. The higher the mother’s
consumption of Lake Michigan fish, the lower the birth weight and
the smaller the head circumference of her baby. A series of tests
done at birth and at intervals afterward also found persistent evi
dence of neurological impairment. The Jacobsons cannot be certain,
however, that PCBs are solely responsible for the effects seen in the
children born to these women because their mothers were exposed
to so many other chemicals as well.
Among the more than three hundred children tested in this
study, those whose mothers had eaten greater quantities of fish
showed subtle signs of damage, including weak reflexes and more
jerky, unbalanced movements as newborns. In later testing at seven
months of age, the Jacobsons found signs of impaired cognitive func-
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Lion based on a test in which a child is shown two identical pictures
of human faces posted on a board. After a period of time, the re
searcher will remove the board, replace one of the pictures with a
new face, and show the display to the child again. A child normally
recognizes the new face and spends more time looking at it rather
than the face the child had seen before. T he higher the PCB levels in
the mother, the less time an infant spent looking at the new picture.
Children with lower scores on this test tend to perform more poorly
on intelligence tests during childhood. When the children were tested
again at four years of age, the children of women with the highest
PCB levels had lower scores in verbal and memory tests.
The second study done in North Carolina involved neurological
tests on 866 infants and compared their performance to the levels of
PCBs detected in their mother’s breast milk—an indication of their
prenatal exposure as well as their exposure after birth. The more
highly exposed infants showed weaker reflexes, and in follow-up
studies done at six and twelve months of age, they still showed poor
performance on tests for gross and fine motor coordination. This
study did not include tests to assess thinking and memory skills.
At the State University of New York at Oswego, which sits on
the shore overlooking Lake Ontario, a team made up of psychologists
and a physician is now extending the groundbreaking research done
by the Jacobsons into differences between children of those who do
and do not eat Lake Ontario fish. The effort includes a human study
on the children of fish-eating women and parallel laboratory research
with rats who are being fed Lake Ontario fish. If the human and rat
studies find the same changes in behavior, it will indicate that the re
sults of rat studies can be generalized to humans. Since the rat studies
done by psychologist Helen Daly are showing evidence of behavioral
changes in adult rats, the research team, which also includes Edward
Lonky, Thomas Darvill, Jacqueline Reihman, and Joseph Mather, Sr.,
is testing the parents in the human study as well as the children. A
similar epidemiological effort is also underway in the Netherlands,
where researchers are exploring the link between PCB exposure, thy
roid levels at birth, and later behavioral and cognitive problems in
the children of mothers with high PCB levels.
Daly’s studies with rats fed Lake Ontario salmon have added
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another dimension to the growing literature on the impact of syn
thetic chemicals on thinking and behavior and new questions about
possible effects on humans. Her early work had focused on learning
in normal rats, particularly the role of frustration in the learning
process. But in the early ’80s, she and her colleagues began to won
der about the possible effect of eating contaminated fish. The ques
tion was literally inescapable in Oswego, for as the state began to
stock game fish, the city at the mouth of the Oswego River on Lake
Ontario became a booming sports-Rshing center. In autumn, fisher
men, who often come from great distances, line up shoulder to
shoulder along the riverbank angling for one of the huge salmon
heading up the river to spawn. The town has even built special clean
ing stations where fishermen can have their fish dressed for a small
fee. In conversations with fishermen and their wives, Daly and her
colleagues learned that many families were filling their freezers with
fish and eating significant amounts through the winter.
A number of researchers at the university began to feed labora
tory rats with Lake Ontario fish to see if it affected them in any way.
One of Daly’s colleagues, David Hertzler, found signs of changed
behavior in rats after twenty days on a diet that was thirty percent
salmon. When put through a standard test, the rats showed de
creased activity. The finding was intriguing, but since many factors
can cause decreased activity, it did not give much insight into how
the contamination was affecting the animals. Daly then embarked
on a series of learning experiments to try to discover why they were
becoming less active.
“We thought that toxic chemicals should make them dum
mies,” she recalls. “That’s what you would expect.”
What she found was totally contrary to her expectations. There
was no evidence of severe learning deficits, but there was a dramatic
change in their behavior. In the years since then, Daly has conducted
a series of different experiments trying to pinpoint and characterize
the nature of this change. The studies all compare the behavior of
rats fed on Lake Ontario salmon to rats fed with Pacific Ocean salmon
that contain much lower levels of contamination or to a second con
trol group that is not fed salmon. Over and over again, she has seen a
consistent pattern in the results.
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The two groups of rats show no difference in behavior as long as
life is pleasant and uneventful, but as soon as they are confronted by
any sort of negative event, great differences are apparent. In every in
stance, the rats who have eaten Lake Ontario salmon show a much
greater reaction than those who have dined on Pacific salmon or rat
chow. Daly describes them as “hyper-reactive” even to mildly nega
tive situations.
If the contaminants have similar effects on humans as on rats,
Daly says, “every little stress will be magnified.” She thinks that
some of the children in the Jacobsons’ study showed reactions simi
lar to those she has seen in the rats. When the children were tested
at four years of age, seventeen of them refused to cooperate during
at least one test, all of them children of mothers with the highest lev
els of PCBs in their milk. She thinks this is probably an overreaction
to the mildly frustrating experience of taking such tests.
Daly’s findings are unusual in other respects, for she saw this
behavioral change, not only in those exposed during critical develop
ment stages in the womb but also in adult rats fed Lake Ontario
salmon. She also found such changes in the offspring of these adults
and in the second generation as well. In studying these transgenerational effects, Daly fed the fish only to the grandmothers before and
during their pregnancies and while they were feeding their pups. The
offspring got the contaminants only through the mother’s placenta
and through breast milk. Daly fed none of the female offspring fish
at any point in their lives, yet she still saw behavioral changes in the
pups they produced. Her studies suggest that contaminants taken in
by a mother can somehow have effects that reach across two genera
tions and affect grandchildren as well as immediate offspring. Other
researchers are beginning to repeat Daly’s experiments, carefully fol
lowing the same procedures to see whether they get the same results.
In May 1995, the Oswego team announced the initial results
from their ongoing human study, reporting behavioral and neuro
logical differences in the children of women who had eaten Lake
Ontario fish. In this new study, babies whose mothers had eaten
surprisingly modest amounts of Lake Ontario fish—the equivalent
of forty pounds or more of salmon over a lifetime, not just during
pregnancy—showed a larger number of abnormal reflexes, express-
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OUR STOLEN FUTURE
ing greater immaturity in a lower autonomic response score, and
poor habituation to repeated disturbances.
The habituation assessment, which was not a part of the Jacob
son study, looked at a sleeping baby’s response to awakening by a
bell, a rattle, or a light shining in its eyes. Such stimulation initially
startles the baby, but if he or she is awakened repeatedly, the startle
response should diminish and eventually disappear. The babies of
women who had eaten no Lake Ontario fish grew accustomed, or ha
bituated, to the disturbance most quickly. In contrast, children of
heavy fish-eaters habituated poorly, reacting much more negatively
to repeated disturbances.
This follows beautifully,” Daly said, speaking of the similari
ties emerging between the human studies and her earlier work with
rats. Like the human infants, she notes, “my rats [fed on Lake On
tario salmon] are also more reactive to unpleasant events.” The find
ings from this first large-scale replication of the Jacobsons’ study are
also consistent with behavioral differences noted in that earlier ef
fort, although this study did not find the physical differences re
ported by the Jacobsons such as smaller head circumference and
lighter birth weight in babies of heavy fish-eaters. Daly and her col
leagues believe this is evidence that contaminants will affect be
havior before they reach levels high enough to have a measurable
physical impact on a baby. Daly is encouraged by evidence that ro
dent studies can provide an early warning about possible behavioral
effects in humans.
Although the Jacobson study found correlations between neuro
logical symptoms and PCBs, Daly doubts that they are the only chem
ical involved in the changes the Oswego team is seeing. Estimates for
the number of toxic chemicals released in the Great Lakes basin range
as high as twenty-eight hundred, flow many of them find their way
into the salmon and the people who eat them is anybody’s guess. In
such a toxic stew, she says, it would not be surprising if a number of
chemicals are acting in an additive or synergistic fashion.
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Reports linking wildlife contamination with such unexpected
behaviors as females sharing nests and feminized males inevitably
raise questions about human parenting and sexual choice. Could
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hormone disruption alter these human attributes? The science on
this is slender indeed. While emerging evidence suggests that varia
tions in sexual preference may stem from differences in biology,
scientists have only a dim understanding of the factors involved.
In 1991, Dr. Simon LeVay published data in Science on his dis
covery of differences in the brain structure of homosexual and hetero
sexual men. LeVay’s work, including his recent book, The Sexual Brain,
supports the theory that sexual behavior is biologically based and
strongly influenced by exposure to hormones during the period when
the fetal brain undergoes sexual differentiation.
Other scientists’ work supports this interpretation. For example,
some studies in DES daughters find that they have higher rates of
homosexuality and bisexuality than do their sisters who were not ex
posed to this synthetic estrogen before birth. Unfortunately, no credi
ble studies exist on the effects of this synthetic estrogen on DES sons.
This body of work would indicate, in principle, that chemicals
interfering with hormonal messages at crucial times in fetal devel
opment could alter sexual choice. Current science tells us little more.
Studies have shown that disrupting hormone levels can sometimes
masculinize and sometimes feminize. Thus if endocrine disruption
does influence sexual choice, it could conceivably cut both ways, caus
ing a person who might by nature have been homosexual to develop as
heterosexual, or causing some who were destined to be heterosexual to
become homosexual. One must also remember that diversity in sexual
choice has been part of the human experience for millennia, since long
before chemical contaminants became widespread. There is no indica
tion that patterns of human sexual choice have changed since syn
thetic endocrine-disrupting chemicals entered into commerce. While
gays and lesbians have become more visible thanks to social trends
that have enabled them to participate as full members of society, the
best studies available indicate the proportion of homosexuals and
heterosexuals in the population has remained constant.
Human sexual orientation is no doubt a complex phenome
non, just as is most human behavior. We doubt any single factor—
nature, endocrine disruption, or nurture—will prove to be its sole
determinant.
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OUR STOLEN FUTURE
At the moment, there are more questions than answers about
the impact of hormone-disrupting chemicals on humans.
Even if damage is apparent and documented, however, it will
never be possible to establish a definitive cause-and-effect connec
tion with contaminants in the environment. Although we know that
every mother in the past half century has carried a load of synthetic
chemicals and exposed her children in the womb, we do not know
what combination of chemicals any individual child was exposed to,
or at what levels, or whether he or she was hit during critical periods
in their development when relatively low levels might have signifi
cant lifelong effects. This is a common and inescapable dilemma in
trying to assess the delayed effects of environmental contamination.
We also face the problem of having no genuine control group of un
exposed individuals for comparative scientific studies. The contami
nation is ubiquitous. Everyone is exposed to some degree. One of
the sad ironies is that researchers discovered the high levels of conta
mination among people in remote Inuit villages while looking for a
less exposed control group.
For these reasons, those who demand such definitive “proof”
before reaching a judgment are certain to be waiting an eternity. In
the real world, where humans and animals are exposed to contami
nation by dozens of chemicals that may be working jointly or some
times in opposition to each other and where timing may be as
important as dose, neat cause-and-effect links will remain elusive.
The tobacco industry disingenously used arguments about the
lack of a proven cause-and-effect link between smoking and lung
cancer in humans, knowing full well it is impossible to obtain such
evidence in humans without subjecting them to controlled labora
tory experiments. But after delays, health officials have moved ahead
with warnings on cigarettes, limits on cigarette advertising, and ef
forts to stop exposure to cigarette smoke in public places. They have
done so based on evidence of a correlation between smoking and
lung cancer in humans backed up by controlled laboratory experi
ments with animals that do have the ability to demonstrate such a
cause-and-effect relationship.
It will take a similar approach to tackle the problem of hormone
disruptors, but it will be vastly more difficult than untangling the
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web of cause and effect for tobacco. Given the nature of the contam
ination, it is important to recognize at the outset that those respon
sible for safeguarding human health will have to act on information
that is less than perfect.
As we wrestle with the question of how much chemical contami
nants are contributing to the trends and societal patterns we see—in
breast cancer, prostate disease, infertility, and learning disabilities—it
is important to keep one thing in mind. Scientists keep Ending signifi
cant, often permanent effects at surprisingly low doses. The danger we
face is not simply death and disease. By disrupting hormones and de
velopment, these synthetic chemicals may be changing who we be
come. They may be altering our destinies.
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Early in her detective work, Theo Colborn stumbled onto a
long-forgotten study published in the Proceedings of the Society of
Experimental Biology and Medicine in 1950—the first warning in the
scientific literature that synthetic chemicals could have the inadver
tent effect of disrupting hormones. The paper by two Syracuse Uni
versity zoologists, Verlus Frank Lindeman and his graduate student
Howard Burlington, described how doses of DDT prevented young
roosters from developing into normal males and even suggested that
the pesticide was acting as a hormone. So the first bizarre, frighten
ing evidence of hormone havoc had surfaced soon after the chemical
age swept into American life at the end of World War II like a
tsunami. Colborn posted the Burlington and Lindeman paper above
her desk—a reminder of the slow acceptance of new ideas.
How did we miss so many warning signs, and for so long?
Colborn’s own experience with the Great Lakes provides part of
the answer. Our obsession with cancer blinds us to other dangers.
There is a strong tendency, seen again and again in this story, to
overlook or ignore important new evidence that does not fit into
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reigning concepts about how things work and what is important—a
strong tendency to turn a deaf ear.
If Burlington and Lindeman’s study sank into oblivion, it cer
tainly wasn’t because their findings were subtle or hard to under
stand. The Syracuse team decided to explore the effects of long-term
poisoning from DDT by injecting the pesticide into forty young
roosters for a period of two to three months. As they watched what
happened to the white leghorns, they must have puzzled about this
most peculiar poison. The daily doses of DDT didn’t kill the roosters
or even make them sick. But it certainly did make them weird. The
treated birds didn’t look like roosters at all; they looked like hens.
As young cockerels mature, tall red combs blossom on their
heads and luxurious cherry-colored skin folds called wattles burgeon at
their necks—hallmarks of rooster masculinity. The birds dosed with
DDT, however, failed to develop in the expected way. Even as adults,
their combs and wattles remained pale and stunted, measuring just
one-third the size of those displayed by untreated roosters raised in
the zoology lab for the purpose of comparison. When the researchers
examined the birds’ testicles, the findings were even more startling.
The sex organs had grown to only eighteen percent of normal size.
From all appearances, the birds had suffered chemical castration.
Decades would pass before scientists would begin to understand
exactly how DDT had altered the sexual destiny of the young roosters.
But in discussing the “interesting effects” of their experiment, the
Syracuse team teased out the ominous implications with a remarkable
prescience. They suggested—in 1950—that DDT may be exerting an
“estrogenlike action,” that it was acting like a hormone.
The study provided alarming evidence of the power of a syn
thetic chemical to derail sexual development, but this warning went
unheeded. Such findings simply did not fit into prevailing views
about pesticide hazards, which had been shaped by the previous gen
eration of poisons—many of them acutely toxic arsenic-based com
pounds that left dangerous residues on fruits and vegetables that had
sometimes killed people outright. Based on this prewar experience,
public health officials in 1950 thought in terms of classical poisoning
and judged chemicals safe if they did not cause death or obvious dis
ease in those exposed to high concentrations, such as farmers.
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OUR STOLEN FUTURE
By this measure, DDT, which came onto the civilian American
market in 1946, was a remarkably safe product. Within a year, this
“miracle” pesticide was in widespread agricultural use in the United
States. Between 1947 and 1949, chemical companies had poured
$3.8 billion into production facilities aimed at a vast new market for
synthetic pesticides. Sales of DDT alone, which totaled $10 million
in 1944, soared to more than $110 million by 1951. On farms, in
homes and gardens, and along suburban streets as a part of mosquito
control efforts, DDT was spread and sprayed with a casual abandon
that is now hard to imagine.
By the 1960s, new fears about the health effects of pesticides
were coming to the fore—fears about cancer that would dominate
the public debate about toxic chemicals, scientific research, and gov
ernment regulation for the next three decades. Reflecting this shift
in public consciousness, Rachel Carson focused on cancer in her
chapter on pesticides and human health in Silent Spring, even
though she had found ample evidence of other hazards in her explo
ration of the scientific literature. The “Fable for Tomorrow” that
opens the book paints a chilling picture of reproductive failures. “On
the farms the hens brooded, but no chicks hatched. The farmers
complained that they were unable to raise any pigs—the litters were
small and the young survived only a few days.”
Carson evidently read the Burlington and Lindeman study be
cause she refers to their results, but without citation or mention of
their names. Although it is now clear that their hypothesis about
DDT’s hormone actions sheds light on some of the wildlife symp
toms detailed in the opening chapters of Silent Spring, Carson never
pursued the clues that pesticides might impair reproduction by dis
rupting hormones. This is particularly intriguing, since she clearly
recognized that “something more sinister” than straightforward poi
soning was occurring—“the actual destruction of the bird’s ability
to reproduce. Somehow this thread was lost, perhaps because of
the state of scientific understanding about the endocrine system at
the time, perhaps because Carson, who was herself suffering from
breast cancer, was as preoccupied with the dreaded disease as her
readers. In the later chapters of Silent Spring, the reproductive
theme so prominent early in the book disappears as Carson turns her
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full attention to concerns that synthetic pesticides cause genetic
mutations and cancer.
It is only in this context that Carson touches on the idea that peshades might somehow interfere with hormone levels and thereby abet
cancers of the reproductive system. This might occur indirectly, she ar
gues, through damage to the liver, which is easily harmed by synthetic
chlorinated compounds. The liver plays a key role in maintaining hor
mone balance by breaking down estrogen and other steroid hormones
to allow for their excretion. If impaired liver function slowed this break
down process, she speculated, it could lead to “abnormally high estro
gen levels. Carson was correct, medicine now acknowledges, in linking
overall estrogen exposure to these cancers and in recognizing that syn
thetic chemicals can disrupt hormones by impeding normal liver
processes. Now, thirty years later, the inquiry into the role of DDT and
other synthetic chemicals in breast cancer has been renewed following
the discovery in breast tumors of DDT, of its breakdown product
DDE, of PCBs, and of other synthetic chemicals and the recogni
tion that some synthetic chemicals are indeed hormonally active, as
Burlington and Lindeman first suggested more than four decades ago.
Cancer holds a special dread in our culture. If Rachel Carson
helped publicize suspected links between rising cancer rates and in
creasing use of synthetic pesticides, other forces added momentum
to the emerging cancer paradigm. In June 1969, the National Cancer
Institute completed animal tests prompted by Silent Spring and did
find a higher incidence of liver tumors in mice exposed over a long
period to low levels of DDT. Within a week, President Richard
Nixon received a petition from seventeen congressmen who asked
for a ban on DDT on the grounds that it caused cancer. In 1971,
President Nixon declared an all-out War on Cancer. Given the tem
per of the time and new evidence that pesticides like DDT might
cause cancer, environmentalists seeking to ban DDT began to frame
the battle around human health risks rather than the wildlife and
environmental concerns put forward in earlier phrases of the long
campaign. In his 1972 decision to restrict most uses of DDT, U.S.
Environmental Protection Agency Administrator William Ruckelshaus gave equal prominence to possible human cancer risks and to
the adverse impacts on fish and wildlife.
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Just as cancer holds a special place in our fears, it also com
mands a special place in federal regulation. It has defined and driven
the EPA’s regulatory process for toxic chemicals for more than two
decades, mainly because the agency uses different assumptions for
assessing cancer risk than it does when considering other risks. For
noncancer hazards such as reproductive and developmental damage,
the agency assumes that a chemical may pose no hazard in low con
centrations beneath some threshold level. But when it is a question
of cancer, the EPA turns to a linear model, which assumes that no
level is safe. Even the tiniest dose of a chemical is presumed capable
of causing cancer.
The federal appeals court had reinforced such a regulatory bias
by a series of rulings on pesticides in the early 1970s, beginning with a
1970 case concerning federal tolerance levels for DDT residues on
food. The Environmental Defense Fund, which brought the action,
based its case on the Delaney clause, a 1958 amendment to the Fed
eral Food, Drug, and Cosmetic Act, which prohibits the use of any
food additive that has been shown to cause cancer in laboratory ani
mals. In its opinion, the court decided that this law applies to pesti
cide residues as well and that the carcinogenicity of these residues has
to be considered in setting tolerance limits. The court also required
the responsible cabinet secretary to explain the basis for deciding any
level of DDT residues to be safe if he proposed continuing to allow
residues in food commodities. The ruling in effect endorsed the strict
attention to carcinogens that the Delaney clause mandates. By the
mid-1970s, “cancer-causing” had become inextricably wedded to the
words “toxic chemical” in the popular culture.
With cancer as the ultimate measure of our fears, it was widely
assumed that setting levels based on cancer risk would protect hu
mans as well as fish and wildlife from all other hazards as well. So
over the past two decades, pesticide manufacturers and federal regu
lators looked mainly for cancer and obvious hazards such as lethal
toxicity and gross birth defects in screening chemicals for safety.
Cancer has also dominated the scientific research program exploring
possible human health effects from chemical contaminants in the
environment. This preoccupation with cancer has blinded us to evi
dence signaling other dangers. It has thwarted investigation of other
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risks that may prove equally important not only to the health of indi
viduals but also to the well-being of society.
If this book contains a single prescriptive message, it is this: we
must move beyond the cancer paradigm. Until we do, it will be im
possible to grapple with the challenges of hormone-disrupting chem
icals and the threat they pose to the human prospect. This is not
simply an argument for broadening our horizons to recognize addi
tional risks. We need to bring new concepts to our consideration of
toxic chemicals. The assumptions about toxicity and disease that
have framed our thinking for the past three decades are inappropri
ate and act as obstacles to understanding a different kind of damage.
Hormone-disrupting chemicals are not classical poisons or typi
cal carcinogens. They play by different rules. They defy the linear logic
of current testing protocols built on the assumption that higher doses
do more damage. For this reason, contrary to our long-held assump
tion, screening chemicals for cancer risk has not always protected us
from other kinds of harm. Some hormonally active chemicals appear
to pose little if any risk of cancer. And as Lindeman and Burlington
discovered, such chemicals are typically not poisons in the normal
sense. Until we recognize this, we will be looking in the wrong places,
asking the wrong questions, and talking at cross-purposes.
Up to now, our concept of injury from toxic chemicals has fo
cused primarily on two things: whether a chemical damages and
kills cells as poisons do or whether it attacks the DNA, our genetic
blueprint, and permanently alters it by causing a mutation as car
cinogens do. With poisoning, the consequences can be illness
illness or
death for the affected human or animal. Mutations can eventually
give rise to cancer.
At levels typically found in the environment, hormone-disrupting
chemicals do not kill cells nor do they attack DNA. Their target is
hormones, the chemical messengers that move about constantly
within the body’s communications network. Hormonally active syn
thetic chemicals are thugs on the biological information highway
that sabotage vital communication. They mug the messengers or im
personate them. They jam signals. They scramble messages. They
sow disinformation. They wreak all manner of havoc. Because hor
mone messages orchestrate many critical aspects of development,
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OUR STOLEN FUTURE
from sexual differentiation to brain organization, hormone-disrupting
chemicals pose a particular hazard before birth and early in life. As
previous chapters have recounted, relatively low levels of contami
nants that have no observable impact on adults can have devastating
impacts on the unborn. The process that unfolds in the womb and
creates a normal, healthy baby depends on getting the right hormone
message to the fetus at the right time. The key concept in thinking
about this kind of toxic assault is chemical messages. Not poisons,
not carcinogens, but chemical messages.
The scientific preoccupation with mapping the human genome
and ferreting out the genes responsible for inherited diseases such as
cystic fibrosis has created the popular impression that the root of al
most all that ails us will be found in our genes. But as must be clear
from the scientific work explored in this book, the inherited genetic
blueprint is just one factor shaping a baby before birth. Imagine
what would happen if somebody disrupted communications during
the construction of a large building, so the plumbers did not get the
message to install the pipes in half the bathrooms before the carpen
ters closed the walls. Imagine that the wrong instructions arrived
when the program for the climate control system was being set up,
and the building thermostat was fixed at eighty-five degrees rather
than sixty-eight. Imagine what it would mean if, through a commu
nications mix-up, the high-rise ended up with only one elevator in
stead of eight.
The construction of a building is as important as the blueprint.
A baby’s intelligence depends as much on the levels of thyroid hor
mone reaching the brain during critical periods of development as
on inheriting smart genes. A young man may develop testicular can
cer because of abnormal hormone levels in his mother’s womb rather
than because of an inherited cancer gene. As the scientific evidence
laid out in this book indicates, synthetic chemicals can obstruct the
hormone messages during prenatal development and permanently
alter the outcome.
Since hormone-disrupting chemicals do not play by the same
rules as classical poisons and carcinogens, efforts to apply conven
tional toxicological and epidemiological approaches to this problem
have typically led to more confusion than enlightenment.
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Some critics of EPA regulation have, for example, been arguing
that the body can tolerate low levels of contaminants because it has
evolved mechanisms that provide a defense against environmental
assaults. Operating from the cancer paradigm, they cite the body’s
ability to repair damaged DNA. As far as we know, however, the body
has no analogous repair mechanisms to cope with the hormonedisrupting effects of chemicals. Why? Cells are primed to receive
hormone messages, and as we have seen, they readily accept syn
thetic impostors that mimic natural hormones. The body responds
to the impostors as legitimate messengers and allows them to bind
to hormone receptors; it does not recognize their action as damage
that needs to be repaired.
Hormone systems do not behave according to the classical
dose-response model that informs our thinking about biological re
sponses to perturbations. The practice of toxicology and epidemiol
ogy rests on the principle first articulated in the sixteenth century by
Paracelsus, a Swiss physician who is considered by some to be the fa
ther of toxicology. He observed that things that are not poisonous in
small quantities can be lethal in larger doses, hence his axiom: the
dose makes the poison. Implicit in this axiom is the notion of the
classical dose-response curve, where the biological response to a for
eign substance increases as the dose becomes greater. This is the op
erating assumption in epidemiological studies that seek to identify
the toxic effects of synthetic chemicals by studying factory workers,
who are exposed to higher-than-average levels of contamination.
Such an approach may prove fruitful for toxic substances that
act as classical poisons or as carcinogens, though it is also controversial
whether the assumption of linearity holds even for carcinogens. In the
case of hormonally active chemicals, any study that assumes linearity
is bound to yield confusing results because the response does not nec
essarily continue to increase as doses increase. As described in Chap
ter 10, high doses may, in fact, produce less of an effect than lower
doses. Such dose-response curves are not unusual in hormone systems,
where the response will increase with escalating doses at first, but
then it typically peaks and decreases as the doses climb still higher.
Those studying the endocrine system do not fully understand
why this happens. The reason may lie in the basic ways that hormones
206
work through receptors and in the complexity of feedback loops that
characterize the endocrine system as a whole. Thus a natural hormone
or a chemical impostor can produce effects at low levels because very
few receptors are needed to trigger a response. In the case of estro
gen, the hormone needs to bind to only one percent of the receptors
contained in a cell to stimulate cell proliferation. But as the level of
hormones or hormone mimics rises higher and higher, the system
eventually responds as if to an overload by shutting down and showing
little or no response. With high doses, the cells actually lose receptors,
so the cells can no longer respond until hormone levels again drop to
low levels long enough for the receptor system to recover.
As EPA toxicologist Linda Birnbaum has noted, most epidemio
logical studies have focused on adults, typically adult men. This bias is
particularly problematic in regard to endocrine-disrupting chemicals.
Health studies often look for harmful effects among workers exposed
to high levels of toxic chemicals in factories and chemical plants, but
these high levels may produce less damage in adults than much lower
levels in individuals exposed second hand in the womb. Timing, as we
have seen, may be more important than dose, and one may find more
telling results by studying the second generation exposed in the womb
than by studying those who were exposed only as adults. A major
study following the chemical factory accident in Seveso, Italy, focused
primarily on the question of whether the high-level dioxin exposure
has increased cancer rates among accident victims. Although one
study did look for obvious birth defects, this investigation did not
consider damage invisible at birth, such as delayed effects on the en
docrine, immune, and nervous systems. As evidence has emerged
about dioxin’s powerful impact on the unborn, researchers are looking
again at the Seveso population and exploring other possible conse
quences of the accident that took place almost two decades ago.
The cancer paradigm also hampers the recognition of the effects
of endocrine disruption because it characterizes the threat as dis
ease. Hormone-disrupting chemicals can diminish individuals with
out making them sick. For this reason, there is an urgent need to
look for “impaired function” as well as for disorders that fit the clas
sic notions of disease. For example, having a poor short-term mem
ory or difficulty in paying attention because of exposure to PCBs is
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very different from having a brain tumor. The former are deficits,
not diseases, but they can nevertheless have serious consequences
over a lifetime and for a society. They erode human potential and
undermine the quality of human life. They undermine the ways in
which humans interact with one another and thereby threaten the
social order of modern civilization.
Exposure to a hormone-disrupting chemical before birth does
not produce just a single clear-cut effect, and in this way, too, the re
sults defy our prevailing notions of chemically induced disease. De
pending on the dose and the timing, a foreign chemical can derail
development in a variety of ways that will become evident at differ
ent times. For example, a boy exposed before birth to chemicals that
mimic estrogen may have undescended testicles at birth, a low
sperm count at puberty, or testicular cancer in middle age because of
this prenatal hormone disruption. These are effects that manifest
themselves in many shades of gray rather than in the black-andwhite distinctions made between health and illness.
To screen for chemicals that can rob human potential before
birth, it will be necessary to look for developmental effects across three
generations—those individuals exposed only as adults and their chil
dren and grandchildren who inherit hand-me-down poisons. Although
this book focuses largely on threats to the middle generation—the first
generation to be exposed in. the womb—the hormone disruption ex
perienced by these individuals could potentially affect the next gener
ation as well. Those exposed prenatally to endocrine-disrupting
chemicals may have abnormal hormone levels as adults, and they
could also pass on persistent chemicals they themselves have inher
ited—both factors that could influence the development of their
own children. It will be necessary to invest in more multidisciplinary
studies to better diagnose and understand the effects of hormone
disruption. Despite alarming signs, such as the report of dropping
male sperm count, the lion’s share of research money for investigat
ing the effects of environmental contamination of human health still
goes into cancer studies. Leading researchers investigating hormonedisrupting chemicals frequently find it impossible to get funding to
pursue their work, even though they have already produced landmark
studies pointing to profound risks for wildlife and humans.
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If we are to come to grips with this threat, we must also shift to
a different way of making judgments about environmental contami
nants. There is little chance of showing a simple cause-and-effect
link between any one or selected groups of hormone-disrupting syn
thetic chemicals and problems such as the drop in human sperm
count that we have already witnessed. Risk assessment in the real
world must respond to real problems in real time.
To address this need, some in the environmental held have be
gun developing an assessment method known as eco-epidemiology.
This method, which was pioneered by Glen Fox, Canadian Wildlife
Service, and Michael Gilbertson at the International Joint Commis
sion, the advisory body to the United States and Canadian govern
ments on Great Lakes policy, draws together information from a
variety of sources, including wildlife data, laboratory studies, and re
search on the mechanisms of hormone action or toxicity, and makes
pragmatic judgments based on the entire body of evidence. In this
approach, one assesses the totality of the information in the light of
epidemiological criteria for causality, such as whether the exposure
precedes the effect, whether there is a consistent association be
tween a contaminant and damage, and whether the association is
plausible in light of the current understanding of biological mecha
nisms. But this real-world environmental detective work comes to
judgment based on “the weight of the evidence” rather than on sci
entific ideals of proof that are more appropriate to controlled labora
tory experiments and the practice of science than to problem solving
and protecting public health in the real world. As some have noted,
it is akin to the decision-making process a physician uses to diagnose
a case of appendicitis—where failing to act has grave consequences.
In the same way that accumulating evidence and common-sense in
ferences led to the conclusion that smoking causes lung cancer, it
may soon be possible to conclude, if not prove, based on the weight
of the evidence, that hormone-disrupting chemicals are linked to
testicular cancer, falling sperm counts, and learning disabilities and
attention deficits in children.
Cancer is a dramatic disease with devastating effects on victims
and their families. It poses little threat, however, to the survival of
animal and human populations as a whole. While cancer is tragic on
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a personal level, healthy populations can quickly replace individuals
lost to the disease.
Because hormone-disrupting chemicals act broadly and insidi
ously to sabotage fertility and development, they can jeopardize the
survival of entire species—perhaps in the long run, even humans.
This might be hard to imagine in a world facing soaring human
numbers, but the sperm count studies suggest environmental conta
minants are already having an impact on the human population as a
whole, not just on individuals. In their assault on development, these
chemicals have the power to erode human potential. In their assault
on reproduction, they not only undermine the health and happiness
of individuals suffering from infertility, they attack a fragile biologi
cal system that over billions of years of evolution has allowed life to
miraculously recreate life.
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The threat explored in this book may seem overwhelming, especially to those confronting it for the Erst 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 well
being is as yet unclear. It would likewise be dangerous to retreat into
denial, which can be a strong temptation in the face of large, insidi
ous 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 pesti
cides 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 easv. Much of the concern about hormonally active
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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 pro
duction 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 pro
duction, and unexpected new sources of exposure continue to come
to light. Most disturbing of all, many of us already carry contamina
tion 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; re
design of chemicals, manufacturing processes, and products by com
panies; 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 evi
dent 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 dam
age 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 mes
sages 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, pes
ticides, 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
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much longer vigilance—over years and decades—because the dose
reaching the womb depends not only on what the mother takes in dur
ing 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 dur
ing 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 gen
erations. The food we ourselves eat may help safeguard our children.
The way we raise and feed our daughters may help protect our grand
children.
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 assump
tions 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 risks to take. Tell your water offi-
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cials 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 un
der 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 chemi
cals are chlorine-containing compounds, the treatment of drinking
water with chlorine is unlikely to contribute to the hazards of hor
mone 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 sullies may
wish to distill their drinking water as they work to improve the qual
ity of their public water supply. Home distilling units are available.
But distillation is only a radical, short-term step. It is wholly imprac
tical 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 advi-
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series 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. Chil
dren 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 warn
ings 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 dimin
ish d head size at birth. Helen Daly found the offspring of female rats
ft l ,ake Ontario salmon to be less tolerant of stress, and parallel bu
ns m 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
the^move upward to the top predators such as polar bears and hu
mans. 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 re
duce exposure to hormone-disrupting chemicals. Again, it is particu
larly 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 cont
amination. 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 chil
dren 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 residue.” Ask your grocer if the grocery chain
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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.
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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, cau
tion 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 benehts
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, breast
feeding exposes infants to disturbing levels of chemical contaminants,
including a number of known hormone disruptors. According to vari
ous 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 benehts of
breast-feeding balance against the risks of transferring hormonally ac
tive 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 hu
man 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-
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sistent chemicals than first-time mothers who are twenty. Though
cow’s milk lacks some of the specific benefits of human milk, it con
tains only one-fifth the concentration of persistent contaminants be
cause 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 contami
nants when weighing the merits of breast-feeding against alternatives
such as bottle feeding with a formula based on cow’s milk.
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Wash your hands frequently. Studies show that many synthetic chem
icals 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 contami
nants in buildings by wiping surfaces with special equipment. Devel
oping the habit of handwashing, 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 hu
mans 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 ani
mals 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 pesti
cides 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
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away. Organize within your neighborhood to set strict standards for
chemical treatment of lawns. Lawn care services sometimes try to reas
sure 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 regis
tration is no measure of safety. In fact, chemical companies register
with the EPA precisely because a product is potentially harmful. La
beling 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 alter
natives. 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 extermi
nator. 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 se
crets” provisions allow them to avoid disclosure to consumers. So you
cannot tell by looking at a product label whether a pesticide contains
an endocrine-disrupting ingredient.
Make a concerted effort to control fleas on pets without insecti
cides. 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. Fre
quent grooming, use of a flea comb, and regular baths with a nomnsecticidal 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 sprin
kling diatomaceous earth, a natural inert product found on the shelf
in garden stores, in your pet’s favorite areas to discourage fleas.
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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
they 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 ef
forts 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 na
tions should move quickly to implement comprehensive interna-
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tional 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 chemi
cals 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 hor
mones. 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 ac
tive chemicals should be used to identify those posing the great
est 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 al
lowed 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 keep
ing untested chemicals off the market and eliminating the most
worrisome compounds in an orderly, timely fashion.
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® 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 irre
versible, 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.
22 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 chemi
cals. There is never just 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.
b 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 drink
ing water or pesticide residues on food. This type of approacn
often fails to consider how the exposure from all the different
sources—air, water, food, dust, etc.—adds up. Although expo
sure 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
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■ 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 con
sumer goods and other potential sources of exposure, to monitor
their products for contamination. This should begin in the gro
cery store. Grocers should be able to tell you, when you want to
know, whether your food is contaminant-free. The current test
ing system, implemented by the Food and Drug Administra
tion, 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 power
ful 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-
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tent releases during manufacturing. Companies should, there
fore, be required to report the quantity of known endocrinedisrupting compounds incorporated into products sold or
transferred from each facility.
■ Require notice and full disclosure when pesticides are used in set
tings 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 information 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 under
take 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 comprehen
sive data. Until this kind of scientific data are available, it will be
impossible to determine whether important changes are occur
ring 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:
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■ How much are we exposed?
■ How is the human body really responding to these chemicals?
■ What is the impact on ecosystems?
H When and how should the government act?
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forensic research
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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 in
fertility, and more children with learning disabilities such as hyperac
tivity 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 particu
larly 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 ex
posed 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 diffi
cult 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 contami
nation 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 un
der what circumstances are biologically active compounds leaching
from plastics into food and beverages? Is this contamination suffi
cient 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 com-
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pounds 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 understand
ing 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 con
sider 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 mam
mals, and other notable biological disruptions. Some classic wildlife
crashes should be revisited to ask whether hormone disruptors con
tributed to the declines or perhaps are impairing recovery. The dra
matic 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?
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cals. Are there permissable exposures? Do they vary from one com
pound 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, effi
cient, 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 11. 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 implica
tions for toxicological testing and regulation. Industry representa
tives 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 chem
icals 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 in
escapable 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 per
sonal choice and through government action, but such after-the-fact
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OUR STOLEN FUTURE
remedies are inevitably disruptive, difficult, and incapable of elimi
nating 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 prob
lem. Here and there, efforts that move in this direction are already
under way. Two advocates for fundamental rethinking and re
design—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.
e 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 exposure or their fate in the environment.
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■ Restrict production to only products that have a completely defined
chemical makeup and stop production of products containing un
predictable 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.
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Braungart and McDonough also advocate a major change in
the way we use synthetic chemicals in products and industrial
processes, guided by the axiom that there should be “no such thing
as 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 an
other. One can see this principle at work in the backyard compost
pile where worms, insects, and bacteria transform leaves, grass clip
pings, 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 materi
als 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 pro
found impact on the automobile industry worldwide. Spurred in part
by proposals in Europe to require manufacturers to take back what
ever they make, a new trend—products designed for disassembly, or
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OUR STOLEN FUTURE
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 recy
cling 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 ma
terials 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 Biaungart have helped design a line of upholstery fab
ric so 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, muta
genic, 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 rethink
ing 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 sanita
tion. During this period, farm operations have moved into areas
where pest problems had previously made farming infeasible.
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■ Consumers, food processors, wholesalers, and supermarkets in
creasingly 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 cos
metic 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 wa
tering, 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 chemi
cal 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 sparinglv 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 evolution-
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OUR STOLEN FUTURE
ary struggle. Within a few years of DDT’s introduction, new super
bugs 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 pesti
cides we need to control disease-carrying insects may no longer
be effective. Resistance has become so widespread that we may
soon End 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.
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Any reader who has come with us this far, who has followed
the path from the gull colonies on Lake Ontario and the swamps of
Florida to university laboratories and then to the doctor’s office,
must have paused at some point to wonder whether these symptoms
have anything to do with the ills of modern human society. Such
questions inevitably leap to mind when one learns that gulls in con
taminated colonies neglect their nests, or that male mice born to
mothers fed with pesticides are much more territorial and poten
tially aggressive as adults than those who did not have this prenatal
exposure. At the moment, there are many provocative questions and
few definitive answers, but the potential disruption to individuals
and society is so serious that these questions bear exploration.
Declining sperm counts loom ominously over this discus
sion, for these reports harbor implications that extend beyond the
question of male fertility. Animal experiments indicate that con
tamination levels sufficient to impair sperm production may affect
brain development and behavior as well. Thus, it is likely that sperm
counts are just one concrete, measurable signal of much broader
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OUR STOLEN FUIURE
effects on aspects of human health and well-being that are not so
easily quantihed. What is at stake is not simply a matter of some in
dividual destinies or impacts on the most sensitive among us but a
widespread erosion of human potential over the past half century.
The evidence taken as a whole makes it difficult to avoid questions
about the significance of this chemical assault for society at large.
Wildlife data, laboratory experiments, the DES experience,
and a handful of human studies support the possibility of physical,
mental, and behavioral disruption in humans that could affect fer
tility, learning ability, aggression, and conceivably even parenting
and mating behavior. To what extent have scrambled messages con
tributed to what we see happening around us—the reproductive
problems seen among family and friends, the rash of learning prob
lems showing up in our schools, the disintegration of the family and
the neglect and abuse of children, and the increasing violence in our
society? If hormone-disrupting chemicals undermine the immune
system, could they be increasing our vulnerability to disease and,
thus, contributing to rising health-care costs? Most fundamentally,
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what does this mean for the human prospect?
If these effects are occurring broadly, hormone disruption may
well be contributing to aberrant and unhealthy tendencies in our so
ciety. On the other hand, it is doubtful these chemicals are causing
all the social dysfunction we see around us. Those seeking a single,
simple explanation for such complicated phenomena are bound to
be frustrated and disappointed.
Even in the case of relatively straightforward physical problems,
such as sperm count declines, we understand far too little about the
hormone-disrupting chemicals unleashed in the environment to as
sess the prospects with confidence. The four studies reported to date
show a precipitous drop in human male sperm counts in recent
decades—a loss on average of one million sperm per milliliter of se
men a year. Such a sharp downward trend is truly alarming. Even
more alarming is the fact that this decline continued for almost a
half a century before medical researchers recognized what was hap
pening. Will this stunning rate of loss continue? Where will it end?
If currently regulated persistent chemicals are largely responsi
ble for the decline, sperm counts could begin rebounding around
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2030. As noted in Chapter 10, the studies find a correlation between
the quantity and quality of sperm and the date of a man’s birth, with
the youngest men showing the lowest sperm counts and the greatest
number of malformed sperm—a pattern that strongly supports the
theory that the decline is the result of damage before birth or early in
life. There is inevitably a long delay, however, before damage be
comes evident through a sperm count analysis. The youngest men in
the recently reported sperm count studies were born in the early
1970s, just at the time that the United States and other industrial
ized countries began to restrict the use of highly persistent organochlorine chemicals such as DDT, dieldrin, lindane, and PCBs. So
their low sperm counts could reflect the high exposure of their
mothers to persistent chemicals in the 1960s and 1970s before gov
ernments imposed restrictions. Since then, the concentrations in
human tissue of DDT, the DDT breakdown product, DDE, and lin
dane, for example, have dropped considerably in countries where
their use is restricted. If prenatal exposure to endocrine-disrupting
pesticides has played a major role in sperm count reductions, one
would expect to see an upswing in sperm numbers over the next
decade, at least in developed countries, as males born in the 1980s
reach maturity. In countries such as India, however, just two persis
tent pesticides, DDT and lindane, make up at least sixty percent of
the pesticides, and their use is still increasing, according to pesticide
experts.
Falling sperm counts could be an unfortunate historical epi
sode—an unforeseen consequence of the midcentury experiment
with persistent chemicals, which many countries have now wisely
discontinued. The threat could now be essentially behind us, even
though it may take decades to play out the effects. Unfortunately, the
worrisome new discoveries described in previous chapters indicate the
hazard from synthetic chemicals has probably not abated. As human
exposure to DDT and other persistent compounds has diminished in
countries like the United States, exposure to other hormone-disrupting
chemicals has rapidly increased. Consider the extent to which plastic
has replaced glass and paper in packaging over the past two decades.
A series of accidental discoveries has demonstrated that plastics are
not inert as was commonly assumed and that some of the chemicals
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OUR STOLEN FUTURE
leaching from plastics are hormonally active. Plastics have found their
way into every corner of our lives, creating the potential for signifi
cant chronic exposure to hormone disruptors. They carry everything
from soda to cooking oil, they line metal cans and are the preferred
material for children’s toys. It is unlikely that all plastics are haz
ardous, but because of manufacturers’ claims of trade secrets, there
is no way to know the chemical composition of any given plastic con
tainer or to judge how much of the plastic in use might be shedding
hormone-disrupting chemicals. Scientists also warn that hormonedisrupting chemicals may lurk in ointments, cosmetics, shampoos,
and other common products.
It would be comforting to know that hormonally active chemi
cals are not casting a shadow on the next generation, but the evidence
provides no such assurance. As the list of hormone-disrupting chemi
cals continues to expand, each new addition argues against the likeli
hood that male sperm count levels will fully recover in the years ahead.
So we find ourselves at an unsettling juncture—uncertain
whether the dire trend in human male sperm count will soon bottom
out or whether it will continue downward. It is encouraging that
some of the most notorious persistent chemicals have been restricted
in developing countries and that human body burdens in at least
some of these countries have declined as a result. At the same time,
surprising discoveries of hormonally active chemicals in unexpected
places such as plastics raise new concerns about chronic widespread
exposure.
There is always a temptation to extrapolate worrisome trends
into apocalyptic, worst-case scenarios, but it is hard to imagine that
sperm counts will fall inexorably downward and reach a point that
poses an imminent threat to human survival. Even so, humans do
appear to be gambling with their ability to reproduce over the long
term, which should be of grave concern.
What we fear most immediately is not extinction, but the in
sidious erosion of the human species. We worry about an invisible
loss of human potential. We worry about the power of hormonedisrupting chemicals to undermine and alter the characteristics that
make us uniquely human—our behavior, intelligence, and capacity
for social organization. The scientific evidence about the impact of
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hormone disruptors on brain development and behavior may shed
new light on some of the troubling trends we are witnessing.
Why did the Scholastic Aptitude Test scores of high school se
niors seeking college admission begin to fall sharply from their high
point in 1963 and continue downward for almost two decades? Is it
solely the result of demographic and social factors, such as changes
in the pool of college aspirants or reduced motivation on the part of
students, as studies have suggested? What about the problems in
our schools? Why can’t many children read? Is it because they watch
too much TV or spend all their time playing video games, because of
a lack of family support for schools, or because they were exposed to
PCBs or other thyroid-disrupting chemicals before birth?
While any connection is still speculative, the human and ani
mal studies reporting learning difficulties and hyperactivity in those
exposed prenatally to PCBs suggest to us that synthetic chemicals
may indeed be increasing the burden on our schools. This seems par
ticularly probable in light of data discussed earlier showing that five
percent of the babies in the United States are exposed to sufficient
quantities of PCBs in breast milk to affect their neurological devel
opment. Moreover, this figure does not take into account the large
number of other synthetic chemicals that can also disrupt the thy
roid hormones that are vital to brain development. It is difficult to
tease this contamination factor out from all the other stresses con
fronting children in our society—disintegrating families, neglect,
abuse, and increasing violence on the streets and even within schools.
But save for lead and mercury, educators, physicians, and others have
been slow to recognize that the chemical environment may un
dermine educational efforts as well as the social environment. The
hitherto unrecognized hazards of endocrine disruptors need serious
investigation, because such disruption could be a major factor in
learning and behavioral problems and one that could be reduced in
the future through preventive measures.
If such invisible losses are already taking place, they will have
greater impact on the society as a whole than on any individuals.
Some human studies have suggested that contaminants at levels cur
rently found in the human population could impair mental develop
ment enough to cause a five-point loss in measurable IQ If this
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OUR STOLEN FUTURE
global. With that transformation, we have been altering the funda
mental systems that support life. These alterations amount to a great
global experiment—with humanity and all life on Earth as the un
witting subjects.
Synthetic chemicals have been a major force in these alter
ations. Through the creation and release of billions of pounds of
man-made chemicals over the past half century, we have been
making broadscale changes to the Earth’s atmosphere and even
in the chemistry of our own bodies. Now, for example, with the
stunning hole in the Earth’s protective ozone layer and, it appears,
the dramatic decline in human sperm counts, the results of this ex
periment are hitting home. From any perspective, these are two
huge signals of trouble. The systems undermined are among those
that make life possible. The magnitude of the damage that has
already occurred should leave any thoughtful person profoundly
shaken.
It is equally disturbing that the global scale of the experiment
makes it extremely difficult to assess the effects. Over the past fifty
years, synthetic chemicals have become so pervasive in the envi
ronment and in our bodies that it is no longer possible to define a
normal, unaltered human physiology. There is no clean, unconta
minated place, nor any human being who hasn’t acquired a con
siderable load of persistent hormone-disrupting chemicals. In this
experiment, we are all guinea pigs and, to make matters worse, we
have no controls to help us understand what these chemicals are do
ing. Faced with the question of whether synthetic chemicals are
contributing, for example, to learning disabilities, researchers have
typically set up studies comparing contaminated children with an
uncontaminated control group. Tragically, no children today are bom
chemical-free. In the search for relatively uncontaminated control
populations, researchers have ironically discovered the appalling uni
versality of this contamination. Even Inuits living a traditional life
style in remote regions of the Arctic have not escaped. The pollution
has come to them.
The early results from this unintended experiment raise thorny
and profound questions that reach far beyond the immediate chal
lenge of managing and eliminating the chemicals that have caused
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these problems. It is no longer sufficient to look for the next round
of substitutes for existing chemicals, for a new generation of suppos
edly less damaging synthetic compounds. The time has come to shift
the discussion to the global experiment itself.
What has this breathtaking plunge toward new technologies
wrought? It has yielded unparalleled health, luxury, and comfort for
some significant minority, at least, of the human population, but the
technologies themselves have often had a dark side that has only be
come evident decades later, after it is too late to recall them. When
questioned about the risks of releasing genetically engineered organ
isms into the environment, one of the world’s preeminent molecular
biologists saw no reason for hesitating. He told a group of journalists
that our society has to “be brave” and forge ahead with new tech
nologies despite the uncertainties. But what seems brave to some
seems foolish to others.
If the ozone hole and falling sperm counts are clear warnings
about the perils of proceeding with business as usual, where do we
go from here? Is there any way to anticipate the consequences of
our technology? If we remove hormone-disrupting chemicals from
the market, how can we be sure that their replacements won’t be cre
ating other nasty surprises thirty years hence? Is there any way to
stop the experiment with our children and the environment, an ex
periment that has been an accepted way of life in the twentieth cen
tury? Or is the prospect of such hair-raising surprises a part of the
Faustian bargain we have made in exchange for health, comfort, and
convenience?
When stopped short by one of these nasty surprises, such as the
ozone hole, we have typically set about in search of “safe” substi
tutes—a quest based on the unarticulated assumption that synthetic
chemicals can be put into the environment with impunity if chemi
cal companies and government regulators screen them properly for
safety. But proposed substitutes that may be “safe” for the ozone
layer pose other hazards, it turns out, through their capacity to trap
heat and accelerate greenhouse warming.
A similar pattern emerges in the history of pesticide oversight.
Like generals, pesticide regulators are always and perhaps inevita
bly fighting the last war. Again and again, they have vetted chemicals
OUR STOLEN FUTURE
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for the most recently recognized hazard only to be blindsided by
dangers they never thought to anticipate. They judged DDT by the
hazards of the previous generation of pesticides—the acutely toxic
arsenic compounds that could bring sudden death to farmers or
those unfortunate enough to eat food contaminated with residues.
Only after DDT had been spread as liberally as talcum powder across
the face of the Earth did we realize that DDT brought death as well,
but in a different way. When concerns emerged about the persis
tence of DDT and its impact on wildlife, regulators imposed con
trols, and less persistent compounds such as methoxychlor came
onto the market. Now we know that methoxychlor, which is still in
wide use, disrupts hormones.
There is a need to screen the thousands of chemicals in com
merce and to eliminate those that disrupt hormones. If we pro
ceed, however, as we have in the past, we will simply spread a new
generation of substitute chemicals across the face of the Earth. It
will be yet another chapter in this reckless experiment. Though
these new chemicals may be safer from the perspective of hor
mone disruption, it is likely they will have other unforeseen conse
quences—some relatively trivial and some perhaps as serious as the
ozone hole.
Judging from past experience, it may take a generation for the
next nasty surprise to emerge. When it comes it will show up where
we least expect it. Thirty years from now, our children may be strug
gling to stem another serious assault on the systems that sup
port life. Perhaps the next surprise will show up in the soil, one of
the least appreciated parts of our life-support system. The conse
quences would be dire indeed if human activities were to seriously
undermine the soil’s ability to recycle nutrients—a process of recy
cling and renewal that depends on a myriad of bacteria, fungi, and
insects. The safer bet, however, is that the surprise will be some
thing never even considered. If anything is certain, it is that we will
be blindsided again.
This caution does not arise from any propensity for pessimism
or dislike of technology. It arises from the very nature of our global
experiment and from our inescapable ignorance, which makes it im
possible to foresee consequences or guarantee safety. The dilemma
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FLYING BLIND
243
is simply stated: the Earth did not come with a blueprint or an in
struction book. When we conduct experiments on a global scale by
releasing billions of pounds of synthetic chemicals, we are tinkering
with immensely complex systems that we will never fully compre
hend. If there is a lesson in the ozone hole and our experience with
hormone-disrupting chemicals, it is this: as we speed toward the fu
ture, we are flying blind.
We can screen chemicals for hazards that have already con
fronted us such as hormone disruption and ozone depletion, but the
next nasty surprise will happen because we do not even know what
questions to ask. Nothing illustrates this point better than our expe
rience with two now infamous chemicals—CFCs and DDT.
Like DDT, ozone-depleting chlorofluorocarbons (or CFCs) were
touted as one of the safest substances ever invented, and like DDT,
they seemed one of the unalloyed blessings of progress when they
were first synthesized by Thomas Midgley Jr. in 1928. Midgley, one
of the pioneers in industrial invention, developed CFCs in response
to the demand for a safer alternative to the toxic and flammable
chemicals used as coolants in refrigerators. In 1941, he received
chemistry’s highest award for his work, the Priestley Prize. Making
his acceptance, Midgley, a man with an incorrigible theatrical streak
who loved to play Mr. Wizard, could not pass up the opportunity to
treat the audience to one of his favorite demonstrations. He poured
CFCs into a shallow dish, inhaled as the refrigerant vaporized, and
held his breath as he lighted a candle. Then he exhaled, extinguish
ing the candle triumphantly—again demonstrating that the chemical
was neither flammable nor toxic to humans and, therefore, unques
tionably safe.
CFCs were on the market for more than forty years before the
first shadow of suspicion fell on them. In 1970, James Lovelock, the
maverick scientist and inventor who would later become widely
known for the Gaia hypothesis, began to make measurements of the
atmosphere with his new invention—an electron capture detector
that increased the sensitivity of the gas chromatograph a thousand
fold. With this powerful new tool, it was now possible to detect
minute traces of synthetic chemicals in the atmosphere that are pres
ent in concentrations of parts per trillion Lovelock soon began to
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244
OUR STOLEN FUTURE
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find CFCs everywhere he looked, even in samples taken from a ship
that cruised to the southern tip of South America—a sign that CFCs
were now ubiquitous in Earth’s atmosphere.
By 1972, Lovelock had communicated his findings to Raymond
McCarthy, an official at Du Pont, the world’s leading manufacturer
of CFCs. Apparently concerned by the news that CFCs were accu
mulating in Earth’s atmosphere, McCarthy called a meeting of the
CFC manufacturers in the chemical industry to discuss “the ecology
of CFCs in the environment.” At the same time, he commissioned
several studies to consider the reactivity of CFCs.
Du Pont was no doubt reassured by the findings from these
studies, which concluded that CFCs did not appear to break down
into toxic or reactive compounds that might harm people or cause
environmental problems. Unfortunately, however, the eyes of the re
searchers were fixed only on the lower atmosphere. It appears no one
even considered possible threats to the ozone layer high up in the
stratosphere. That question would surface two years later in June
1974, when chemists Sherwood Rowland and Mario Molina pub
lished their now famous paper in the journal Nature, describing how
CFCs would eventually make their way to the stratosphere and at
tack ozone. Ultimately Du Pont would phase out its manufacturing
and distribution of CFCs. And in 1995 Rowland and Molina were
awarded the Nobel Prize for this research.
The history of DDT contains a similar paradox. The pesticide
was considered such a milestone on the road of human progress that
its developer, Paul Muller, was hailed as a savior and awarded the
Nobel Prize in 1948. In the short term, the chemical did seem won
drous. It killed insects while posing little direct threat to humans,
and by eliminating the mosquitoes that carry malaria, it saved count
less fives. But bke CFCs, DDT was at the same time invisibly attack
ing the foundation of life.
In the end, what we did not know proved to be more important
than what we did know. In the end, what we thought were the safest
chemicals proved to be among the most dangerous. And when the
ozone depletion predicted by Rowland and Molina appeared, it far ex
ceeded the worst-case scenario that atmospheric scientists had forecast.
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The situation confronting us is not one that lends itself to easy
prescriptions or simple answers. Our current economy and civiliza
tion are built on a foundation of fossil fuels and synthetic chemicals.
According to one chemical industry estimate, chlorinated synthetic
chemicals and the products made from them constitute forty-five
percent of the world’s GNP. If it has taken fifty years to work our way
into this dilemma, it will almost certainly take just as long or longer
to find our way out of it.
As we look toward the future and think about charting a new
course, it is critical to begin with a clear-eyed view of our situation.
As the experience over the past half century has demonstrated,
there is no way to put large quantities of man-made chemicals into
the environment without exposing our children and ourselves to
unknown risks. Many of these synthetic compounds may prove
harmless, but others may not. We must face the fact that there
is no way to guarantee the safety of synthetic chemicals, even those
that have been on the market for decades. CFCs had been in broad
use for fifty years before the ozone hole was discovered over Antarc
tica. The lag time before effects emerge in vast, complex sys
tems can give a false sense of safety and increase the opportunity for
catastrophe.
We must be ever mindful that for all the advances in science,
we still have only the most general understanding of the life systems
on which we have been experimenting—whether our own bodies or
Earth’s atmosphere. At the time that CFCs were invented, scientists
did not understand the ozone layer or its importance in shielding the
Earth from ultraviolet radiation. That came three years later through
the work of a British scientist, Sydney Chapman. DDT and other
hormone-disrupting chemicals were on the market for two decades
before researchers began to fathom the mysteries of the hormone
receptors and even longer before they discovered that synthetic
chemicals could mimic hormones and engage those receptors.
Ultimately, the risks that confront us stem from this gap be
tween our technological prowess and our understanding of the sys
tems that support life. We design new technologies at a dizzying
pace and deploy them on an unprecedented scale around the world
long before we can begin to fathom their possible impact on the
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OUR STOLEN FUTURE
global system or ourselves. We have plunged boldly ahead, never ac
knowledging the dangerous ignorance at the heart of the enterprise.
Such arrogant presumption may be an ineradicable part of
human nature. The ancient Greeks called it hubris. Throughout hu
man history, humans have risked the unknown, courting both suc
cess and catastrophe. What differs now is the stakes, the magnitude
of possible mistakes. Our activities no longer involve just one village
and its neighbor, one valley or the next. The scale of human activity
means that these experiments engage the planet.
As we race toward the future, we must never forget the funda
mental reality of our situation: we are flying blind. Our dilemma is
like that of a plane hurtling through the fog without a map or instru
ments. Instead of being able to provide a reliable radar system, scien
tists are peering through the cockpit window trying to warn of any
obstacles ahead. And usually, the most they can say is that the dark
mass looming into view might be a cloud bank. Or then again, it
might be a mountain.
So what do we do? Land the plane as quickly as possible, slow
down, or proceed full speed ahead because it would be incredibly ex
pensive and disruptive to cancel this trip?
These kinds of questions confront us today as we grapple with
the consequences of our half-century experiment with synthetic
chemicals. When confronted with a troubling environmental prob
lem, the first impulse has been to appoint a panel of experts in
the hopes that they can give us the right answer. Scientists can cer
tainly provide invaluable guidance, as the work described in this
book amply demonstrates. But science alone does not always have
the answer.
Deciding on a wise course involves a host of considerations and,
most of all, value judgments. It is not just a question of the quality
of science describing the problem but also of how we see the risks
and how much risk we are willing to entertain. Consider the con
venience that endocrine-disrupting plastics bring to human lives
against the risks they entail. If all that is at stake is the survival of a
single gull colony, it may be wise to wait for further scientific study
before embarking on an effort to reduce exposure. If, on the other
hand, it is a question of decreasing human sperm counts, prudence
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may dictate acting immediately rather than waiting to see whether
the downward trend continues.
Phasing out hormone-disrupting chemicals should be just
the first step, in our view. We must then move to slow down the
larger experiment with synthetic chemicals. This means first curtail
ing the introduction of thousands of new synthetic chemicals each
year. It also means reducing the use of pesticides as much as pos
sible, for these compounds are biologically active by design, and
billions of pounds are deliberately released into the environment
each year.
But these steps merely deal with the problems of which we have
some inkling, however crude. They help not at all with the next gen
eration of surprises, the next unexpected results from our massive al
terations of the planetary system. In this light, eroding ozone and
falling sperm counts cast dark shadows across the human future.
They confront us with the unavoidable question of whether to stop
manufacturing and releasing synthetic chemicals altogether. There
is no glib answer, no pat recommendation to offer. The time has
come, however, to pause and finally ask the ethical questions that
have been overlooked in the headlong rush of the twentieth century.
Is it right to change Earth’s atmosphere? Is it right to alter the chem
ical environment in the womb for every unborn child?
It is imperative that humans as a global community give serious
consideration to this question and begin a broad discussion that
reaches far beyond the usual participants—the chemical companies,
government regulators, farmers, economists, scientists, and environ
mental groups. This discussion must engage teachers and parents,
physicians and philosophers, artists and historians, spiritual leaders
such as the Pope and the Dalai Lama, and others who reflect the
richness and diversity of human experience and wisdom.
On a more practical front, we need to explore whether it is pos
sible to discontinue the global experiment without abandoning syn
thetic chemicals. Are there principles of chemical design and use
that would allow us the benefit of innovative materials without un
due exposure and risk? Considering the skyrocketing human popula
tion and a daunting agenda of global environmental problems, it
seems impossible to turn the clock back half a century and return to
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OUR STOLEN FUTURE
a material horizon bounded by wood, steel, and glass. At the same
time, any such exploration must always bear in mind that it is impos
sible to anticipate nasty surprises. The goal must therefore be to
keep human and environmental exposure to an absolute minimum.
How synthetic chemicals fit into a sustainable, healthy future re
mains unclear.
If it is too early to describe the precise road, it is possible to
signal the direction for this journey. For the past half century, the
commerce in cheap, abundant synthetic chemicals has shaped agri
culture, industrial processes, economies, and societies. It is impossi
ble to imagine the great migration of Americans to the steamy Sun
Belt without the CFCs that made it possible to air-condition homes,
cars, and public buildings. Similarly, the new generation of synthetic
pesticides that swept onto the market after World War II aided and
abetted the growth of specialized industrial farming that depended
exclusively on a chemical arsenal for pest control and abandoned
agricultural practices such as crop rotation, carefully timed planting,
or other methods to keep insects in check. The chemical age has cre
ated products, institutions, and cultural attitudes that require syn
thetic chemicals to sustain them.
The journey to a different future must begin by defining the
problem differently than we have until now. As a general rule, the
framing of a problem limits solutions more than a lack of ingenuity
or technology. The task is not to find substitutes for chemicals that
disrupt hormones, attack the ozone layer, or cause still undiscovered
problems, though it may be necessary to use replacements as a tem
porary measure. The task that confronts us over the next half cen
tury is one of redesign. When forced by the phaseout of CFCs to
reconsider the use of solvents when manufacturing electronic cir
cuitry, one research effort in the United States found a way to elimi
nate the need for CFCs or any other solvent by redesigning the
soldering process. Following such examples, we need to redesign not
only lawns, food packaging, and detergents, but also agriculture, in
dustry, and other institutional arrangements spawned by the chemi
cal age. We have to find better, safer, more clever ways to meet basic
human needs and, where possible, human desires. This is the only
wav to opt out of the experiment.
FLYING BLIND
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As we work to create a future where children can be born free of
chemical contamination, our scientific knowledge and technological
expertise will be crucial. Nothing, however, will be more important
to human well-being and survival than the wisdom to appreciate that
however great our knowledge, our ignorance is also vast. In this igno
rance we have taken huge risks and inadvertently gambled with sur
vival. Now that we know better, we must have the courage to be
cautious, for the stakes are very high. We owe that much, and more,
to our children.
4
APPENDIX:
THE WINGSPREAD
CONSENSUS STATEMENT
I
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Authors’ Note: In July 1991, a group of scientists, including Theo Colbom and Pete Myers, came together for the first time to discuss their
concerns about the prevalence and effect of endocrine disrupting
chemicals in the environment. That scientists from so many different
disciplines were brought together in the first place is remarkable, but
in the hope that their meeting might have some lasting effect they
reached consensus on the following statement. We have included it
here not only because it forms a succinct overview of the problem we
face but also as a starting point for scientists, policy makers, and con
cerned individuals about the direction that research and public policy
might take on this important issue. The scientists who signed this con
sensus are listed at the end of the statement, which follows. By includ
ing this list we do not imply that those listed (other than the present
authors) necessarily endorse the arguments or conclusions presented
elsewhere in this book.
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APPPENDIX
252
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Chemically-Induced Alterations in Sexual
Development: The Wildlife/Human Connection
THE PROBLEM
Many compounds introduced into the environment by human activity
are capable of disrupting the endocrine system of animals, including
fish, wildlife, and humans. The consequences of such disruption can
be profound because of the crucial role hormones play in controlling
development. Because of the increasing and pervasive contamination
of the environment by compounds capable of such activity, a multidis
ciplinary group of experts gathered in retreat at Wingspread, Racine,
Wisconsin, 26—28 July 1991 to assess what is known about the issue.
Participants included experts in the fields of anthropology, ecology,
comparative endocrinology, histopathology, immunology, mamma
logy, medicine, law, psychiatry, psychoneuroendocrinology, repro
ductive physiology, toxicology, wildlife management, tumor biology,
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and zoology.
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The purposes of the meeting were:
1. to integrate and evaluate findings from the diverse research dis
ciplines concerning the magnitude of the problem of endocrine
disruptors in the environment;
2. to identify the conclusions that can be drawn with confidence
from existing data; and
3. to establish a research agenda that would clarify uncertainties re
maining in the field.
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CONSENSUS STATEMENT
The following consensus was reached by participants at the workshop.
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1. We are certain of the following:
E A large number of man-made chemicals that have been re
leased into the environment, as well as a few natural ones, have
the potential to disrupt the endocrine system of animals, in-
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THE WINGSPREAD CONSENSUS STATEMENT
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eluding humans. Among these are the persistent, bioaccumula
tive, organohalogen compounds that include some pesticides
(fungicides, herbicides, and insecticides) and industrial chemi
cals, other synthetic products, and some metals.*
■ Many wildlife populations are already affected by these com
pounds. The impacts include thyroid dysfunction in birds and
fish; decreased fertility in birds, fish, shellfish, and mammals;
decreased hatching success in birds, fish, and turtles; gross
birth deformities in birds, fish, and turtles; metabolic abnor
malities in birds, fish, and mammals; behavioral abnormalities
in birds; demasculinization and feminization of male fish, birds,
and mammals; defeminization and masculinization of female
fish and birds; and compromised immune systems in birds and
mammals.
■ The patterns of effects vary among species and among com
pounds. Four general points can nonetheless be made: (1) the
chemicals of concern may have entirely different effects on the
embryo, fetus, or perinatal organism than on the adult; (2) the ef
fects are most often manifested in offspring, not in the exposed
parent; (3) the timing of exposure in the developing organism
is crucial in determining its character and future potential; and
(4) although critical exposure occurs during embryonic devel
opment, obvious manifestations may not occur until maturity.
■ Laboratory studies corroborate the abnormal sexual develop
ment observed in the field and provide biological mechanisms
to explain the observations in wildlife.
■ Humans have been affected by compounds of this nature, too.
The effect of DES (diethylstilbestrol), a synthetic therapeutic
agent, like many of the compounds mentioned above, are es’“Chemicals known to disrupt the endocrine system include: DDT and its degra
dation products, DEHP (di(2-ethylhexyl)phthalate), dicofol, HCB (hexachloro
benzene), kelthane, kepone, lindane and other hexachlorocyclohexane congeners,
methoxychlor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC
fungicides, certain PCB congeners, 2,3,7,8-TCDD and other dioxins, 2,3,7,8-TCDF
and other furans, cadmium, lead, mercury, tributyltin and other organo-tin com
pounds, alkyl phenols (non-biodegradable detergents and anti-oxidants present in
modified polystyrene and PVCs), styrene dimers and trimers, soy products, and lab
oratory animal and pet food products.
254
APPPENDIX
trogenic. Daughters born to mothers who took DES now suffer
increased rates of vaginal clear cell adenocarcinoma, various
genital tract abnormalities, abnormal pregnancies, and some
changes in immune responses. Both sons and daughters ex
posed in utero experience congenital anomalies of their repro
ductive system and reduced fertility. The effects seen in in
utero DES-exposed humans parallel those found in contami
nated wildlife and laboratory animals, suggesting that humans
may be at risk to the same environmental hazards as wildlife.
-W-<
2. We estimate with confidence that:
■ Some of the developmental impairments reported in humans
today are seen in adult offspring of parents exposed to syn
thetic hormone disruptors (agonists and antagonists) released
in the environment. The concentrations of a number of syn
thetic sex hormone agonists and antagonists measured in the
U.S. human population today are well within the range and
dosages at which effects are seen in wildlife populations. In
fact, experimental results are being seen at the low end of cur
rent environmental concentrations.
■ Unless the environmental load of synthetic hormone disrup
tors is abated and controlled, large scale dysfunction at the
population level is possible. The scope and potential hazard
to wildlife and humans are great because of the probability of
repeated and/or constant exposure to numerous synthetic chem
icals that are known to be endocrine disruptors.
■ As attention is focused on this problem, more parallels in wild
life, laboratory, and human research will be revealed.
3. Current models predict that:
■ The mechanisms by which these compounds have their impact
vary, but they share the general properties of (1) mimicking the
effects of natural hormones by recognizing their binding sites;
(2) antagonizing the effect of these hormones by blocking their
interaction with their physiological binding sites; (3) reacting
directly and indirectly with the hormone in question; (4) by al-
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THE WINGSPREAD CONSENSUS STATEMENT
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tering the natural pattern of synthesis of hormones; or (5) alter
ing hormone receptor levels.
■ Both exogenous (external source) and endogenous (internal
source) androgens (male hormones) and estrogens (female hor
mones) can alter the development of brain function.
■ Any perturbation of the endocrine system of a developing or
ganism may alter the development of that organism: typically
these effects are irreversible. For example, many sex-related
characteristics are determined hormonally during a window of
time in the early stages of development and can be influenced
by small changes in hormone balance. Evidence suggests that
sex-related characteristics, once imprinted, may be irreversible.
■ Reproductive effects reported in wildlife should be of concern
to humans dependent upon the same resources, e.g., contami
nated fish. Food fish is a major pathway of exposure for birds.
The avian (bird) model for organochlorine endocrine disrup
tion is the best described to date. It also provides support for
the wildlife/human connection because of similarities in the
development of the avian and mammalian endocrine systems.
4. There are many uncertainties in our predictions because:
■ The nature and extent of the effects of exposure on humans are
not well established. Information is limited concerning the dis
position of these contaminants within humans, especially data
on concentrations of contaminants in embryos. This is com
pounded by the lack of measurable endpoints (biologic mark
ers of exposure and effect) and the lack of multi-generational
exposure studies that simulate ambient concentrations.
a While there are adequate quantitative data concerning reduc
tion in reproductive success in wildlife, data are less robust con
cerning changes in behavior. The evidence, however, is sufficient
to call for immediate efforts to fill these knowledge gaps.
■ The potencies of many synthetic estrogenic compounds relative
to natural estrogens have not been established. This is important
because contemporary blood concentrations of some of the com
pounds of concern exceed those of internally produced estrogens.
■
256
APPPENOIX
hs
5. Our judgment is that:
■ Testing of products for regulatory purposes should be broadened
to include hormonal activity in vivo. There is no substitute for
*
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animal studies for this aspect of testing.
■ Screening assays for androgenicity and estrogemcity are available
for those compounds that have direct hormonal effects. Regula
tions should require screening all new products and by-products
for hormonal activity. If the material tests positive, further test
ing for functional teratogenicity (loss of function rather than ob
vious gross birth defects) using multigenerational studies should
be required. This should apply to all persistent, bioaccumulative
products released in the past as well.
■ It is urgent to move reproductive effects and functional terato
genicity to the forefront when evaluating health risks. The can
cer paradigm is insufficient because chemicals can cause severe
health effects other than cancer.
■ A more comprehensive inventory of these compounds is needed
as they move through commerce and are eventually released to
the environment. This information must be made more acces
sible. Information such as this affords the opportunity to re
duce exposure through containment and manipulation of food
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chains. Rather than separately regulating contaminants m wa
ter, air, and land, regulatory agencies should focus on the eco
system as a whole.
■ Banning the production and use of persistent chemicals has
not solved the exposure problem. New approaches are needed
i-------to reduce exposure to synthetic chemicals already in the environment and prevent the release of new products with similar
Il
characteristics.
s Impacts on wildlife and laboratory animals as a result of expo
sure to these contaminants are of such a profound and insidi
ous nature that a major research initiative on humans must be
undertaken.
■ The scientific and public health communities’ general lack ot
awareness concerning the presence of hormonally active envi
ronmental chemicals, functional teratogenicity, and the con-
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THE WINGSPREAD CONSENSUS STATEMENT
257
F
cept of transgenerational exposure must be addressed. Because
functional deficits are not visible at birth and may not be fully
manifested until adulthood, they are often missed by physi
cians, parents, and the regulatory community, and the causal
agent is never identified.
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6. To improve our predictive capability:
■ More basic research in the field of developmental biology
of hormonally responsive organs is needed. For example, the
amount of specific endogenous hormones required to evoke a
normal response must be established. Specific biologic markers
of normal development per species, organ, and stage of devel
opment are needed. With this information, levels that elicit
pathological changes can be established.
■ Integrated cooperative research is needed to develop both wild
life and laboratory models for extrapolating risks to humans.
■ The selection of a sentinel species at each trophic level in an
ecosystem is needed for observing functional deficits, while at
the same time describing the dynamics of a compound moving
through the system.
■ Measurable endpoints (biologic markers) as a result of exposure to exogenous endocrine disruptors are needed that inelude a range of effects at the molecular, cellular, organismal,
and population levels. Molecular and cellular markers are
important for the early monitoring of dysfunction. Normal
levels and patterns of isoenzymes and hormones should be
established.
■ In mammals, exposure assessments are needed based on body
burdens of a chemical that describe the concentration of a
chemical in an egg (ovum) which can be extrapolated to a dose
of the chemical to the embryo, fetus, newborn, and adult. Haz
ard evaluations are needed that repeat in the laboratory what is
being seen in the field. Subsequently, a gradient of doses for
particular responses must be determined in the laboratory and
then compared with exposure levels in wildlife populations.
53 More descriptive field research is needed to explain the annual
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258
APPPENDIX
influx to areas of known pollution of migratory species that
appear to maintain stable populations in spite of the relative
vulnerability of their offspring.
■ A reevaluation of the in utero DES-exposed population is re
quired for a number of reasons. First, because the unregulated,
large-volume releases of synthetic chemicals coincide with the
use of DES, the results of the original DES studies may have
been confounded by widespread exposure to other synthetic en
docrine disruptors. Second, exposure to a hormone during fetal
life may elevate responsiveness to the hormone during later life.
As a result, the first wave of individuals exposed to DES in utero
is just reaching the age where various cancers (vaginal, endome
trial, breast, and prostatic) may start appearing if the individuals
are at a greater risk because of perinatal exposure to estrogen-like
compounds. A threshold for DES adverse effects is needed. Even
the lowest recorded dose has given rise to vaginal adenocar
cinoma. DES exposure of fetal humans may provide the mostsevere-effect model in the investigation of the less potent effects
from environmental estrogens. Thus, the biological endpoints
determined in in utero DES-exposed offspring will lead the in
vestigation in humans following possible ambient exposures.
■ The effects of endocrine disruptors on longer-lived humans
may not be as easily discerned as in shorter-lived laboratory or
wildlife species. Therefore, early detection methods are needed
to determine if human reproductive capability is declining.
This is important from an individual level, as well as at the
population level, because infertility is a subject of great con
cern and has psychological and economic impacts. Methods
are now available to determine fertility rates in humans. New
methods should involve more use of liver-enzyme-system activ
ity screening, sperm counts, analyses of developmental abnor
malities, and examination of histopathological lesions. These
should be accompanied by more and better biomarkers of
social and behavioral development, the use of multigenerational histories of individuals and their progeny, and congener
specific chemical analyses of reproductive tissues and products,
including breast milk.
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THE WINGSPREAD CONSENSUS STATEMENT
259
Work Session participants included:
Dr. Howard A. Bern
Prof, of Integrative Biology
(Emeritus) and Research
Endocrinologist
Dept, of Integrative Biology and
Cancer Research Lab
University of California
Berkeley, CA
Dr. Phyllis Blair
Prof, of Immunology
Dept, of Molecular and Cell Biology
University of California
Berkeley, CA
Sophie Brasseur
Marine Biologist
Dept, of Estuarine Ecology,
Research
Institute for Nature Management
Texel, The Netherlands
Dr. Theo Colborn
Senior Fellow
World Wildlife Fund, Inc., and
W. Alton Jones Foundation, Inc.
Washington, DC
Dr. Gerald R. Cunha
Developmental Biologist
Dept, of Anatomy
University of California
San Francisco, CA
Dr. William Davis*
Research Ecologist
U.S. EPA
Environmental Research Lab
Sabine Island, FL
Dr. Klaus D. Dohler
Director Research
Development and Production
Pharma Bissendorf Peptide GmbH
Hannover, Germany
Mr. Glen Fox
Contaminants Evaluator
National Wildlife Research Center
Environment Canada
Quebec, Canada
Dr. Michael Fry
Research Faculty
Dept, of Avian Science
University of California
Davis, CA
Dr. Earl Gray*
Section Chief
Developmental and Reproductive
Toxicology Section
Reproductive Toxicology Branch
Developmental Biology Division
Health Effects Research Laboratory
U.S. EPA
Research Triangle Park, NC
Dr. Richard Green
Prof, of Psychiatry in Residence
Dept, of Psychiatry/NPI
School of Medicine
University of California
Los Angeles, CA
Dr. Melissa Hines
Asst. Prof, in Residence
Dept, of Psychiatry/NPI
School of Medicine
University of California
Los Angeles, CA
* Al though the research described in this article has been supported by the USEPA,
it does not necessarily reflect the views of the Agency and no official endorsement
should be inferred. Mention of trade names or commercial products does not con
stitute endorsement or recommendation for use.
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260
APPPENDIX
Mr. Timothy J. Kubiak
Environmental Contaminants
Specialist
Dept, of Interior
U.S. Fish and Wildlife Service
East Lansing, MI
Dr. John McLachlan
Director, Div. of Intramural
Research
Chief, Laboratory of Reproductive
and Developmental Toxicology
National Institute of
Environmental
Health Sciences
National Institutes of Health
Research Triangle Park, NC
Dr. J. P. Myers
Director
W. Alton Jones Foundation, Inc.
Charlottesville, VA
Dr. Richard E. Peterson
Prof, of Toxicology and
Pharmacology
School of Pharmacy
University of Wisconsin
Madison, WI
Dr. P. J. H. Reijnders
Head, Section of Marine
Mammalogy
Dept, of Estuarine Ecology
Research Institute for Nature
Management
Texel, The Netherlands
Dr. Ana Soto
Associate Prof.
Dept, of Anatomy and Cellular
Biology
Tufts University School of
Medicine
Boston, MA
Dr. Glen Van Der Kraak
Asst. Prof.
College of Biological Sciences
Dept, of Zoology
University of Guelph
Ontario, Canada
Dr. Frederick vom Saal
Prof.
College of Arts and Sciences
Division of Biological Sciences
University of Missouri
Columbia, MO
Dr. Pat Whitten
Asst. Prof.
Dept, of Anthropology
Emory University
Atlanta, GA
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Chapter 1: OMENS
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The paragraph beginning “In years of watching . . refers to C. Broley, “The
Plight of the American Bald Eagle,” Audubon Magazine 60:162-63, 171
(1958), and his wife, M. Broley, in Eagleman, Pellegrini and Cudahy, 1952.
“Although otters ...” is based on writings by Chris Mason, including
C. Mason, T. Ford, and N. Last, “Organochlorine Residues in British Ot
ters,” Bulletin of Environmental Contamination and Toxicology 36:656-61
(1986); and C. Mason and S. Macdonald, Otters: Ecology and Conservation,
Cambridge University Press, 1986.
“In the post-World War II. . .” refers to a series of papers by Richard
Aulerich and Robert Ringer, that includes R. Aulerich, R. Ringer, and S. Iwamoto, “Reproductive Failure and Mortality in Mink Fed on Great Lakes
Fish,” Journal of Reproduction and Fertility Supplement 19:365-76 (1973).
“Curiously, other mink ranchers . . .” comes from D. Dutton, Worse
Than the Disease: Pitfalls of Medical Progress, Cambridge University Press,
1988.
“The sight of . ..” is taken from personal conversations with Michael
Gilbertson and a paper by M. Gilbertson, T. Kubiak, J. Ludwig, and G. Fox,
“Great Lakes Embryo Mortality, Edema, and Deformities Syndrome
(GLEMEDS) in Colonial Fish-Eating Birds: Similarity to Chick-Edema Dis
ease,” Journal of Toxicology and Environmental Health 33 (4) :455—520 (1991).
“Even the trained eye .. leans on work from a number of researchers:
G. Hunt and M. Hunt, “Female-Female Pairing in Western Gulls (Larus occidentalis) in Southern California,” Science 196:1466-67 (1977); M. Conover
262
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and G. Hunt, “Female-Female Pairing and Sex Ratios in Gulls: An Historical
Perspective,” Wilson Bulletin, 96(4):619-25 (1984); D. Fry and M. Toone,
“DDT-Induced Feminization of Gull Embryos,” Science 213:922—24 (1981);
G. Fox, S. Teeple, A. Gilman, F. Anderka, and G. Hogan, “Are Lake Ontario
Herring Gulls Good Parents?” in Proceedings of the Fish-Eating Birds of the
Great Lakes and Environmental Contaminants Symposium, December 2-3,
1976, Co-sponsored by the Toxic Chemical Division and Ontario Region,
Canadian Wildlife Service, pp. 76-90 (1976); and personal communication
(1994) with Ian Nisbet, North Falmouth, and Jeremy Hatch, University of
Massachusetts, Boston.
The section about Florida alligators stems from: A. Woodward, H. Per
cival, M. Jennings, and C. Moore, “Low Clutch Viability of American Alli
gators on Lake Apopka,” Florida Science 56:52-63 (1993); and L. Guillette,
T. Gross, D. Gross, A. Rooney, and H. Percival, “Gonadal Steroidogenesis
In Vitro from Juvenile Alligators Obtained from Contaminated or Control
Lakes,” Environmental Health Perspectives 103(4):31—36 (1995). This sec
tion was also supported by personal communications with Louis Guillette,
University of Florida, Gainesville, 1994-95.
“The first signs of the epidemic . ..” relates to a series of events
described in R. Dietz, M.-P. Heide-Jprgensen, and T. Harkonen, “Mass
Deaths of Harbor Seals (Phoca vitulina) in Europe,” Ambio 18(5):258—264
(1989).
The section about dolphins beginning “Although fishermen and
yachtsmen . ..” discusses the research of Alex Aguilar and a number of col
laborators from around the world. See A. Aguilar and J. Raga, “The Striped
Dolphin Epizootic in the Mediterranean Sea,” Ambio 22(8):524—28 (1993);
K. Kannan, S. Tanabe, A. Borrell, A. Aguilar, S. Focardi, and R. Tatsukawa,
“Isomer-Specific Analysis and Toxic Evaluation of Polychlorinated Biphe
nyls in Striped Dolphins Affected by an Epizootic in the Western Medi
terranean Sea,” Archives of Environmental Contamination and Toxicology
25:227-33 (1993); J. Forcada, A. Aguilar, P. Hammond, X. Pastor, and
R. Aguilar, “Distribution and Numbers of Striped Dolphins in the Western
Mediterranean Sea After the 1990 Epizootic Outbreak,” Marine Mammal
Science 10(2):l37—50 (1994); and A. Aguilar and A. Borrell, “Abnormally
High Polychlorinated Biphenyl Levels in Striped Dolphins (Stenella
coeruleoalba) Affected by the 1990-1992 Mediterranean Epizootic,” The
Science of the Total Environment 154:237-47 (1994).
“Even a high school...” refers to E. Carlsen, A. Giwercman, N. Keiding,
and N. Skakkebaek, “Evidence for Decreasing Quality of Semen During Past
50 Years,” British Medical Journal 305:609-13 (1992).
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Chapter 2: HAND-ME-DOWN POISONS
The paper about herring gulls is R. Moccia, G. Fox, A. Britton, The Journal
of Wildlife Diseases 22(l):60-70 (1986).
For further information concerning the paragraph beginning “Flick.
Another document...see T. Colborn, A. Davidson, S. Green, R. Hodge,
C. Jackson, and R. Liroff, Great Lakes, Great Legacy?, The Conservation
Foundation and the Institute for Research on Public Policy, 1990; and G. Fox,
“What Have Biomarkers Told Us About the Effects of Contaminants on
the Health of Fish-Eating Birds in the Great Lakes? The Theory and a Litera
ture Review/’ Journal of Great Lakes Research 19(4):722-36 (1993).
For more information about opportunistic species, loss of diversity, and
overloading of a system by rapidly reproducing organisms alluded to starting
with “The improvements since then . .. /’ see D. Rapport, H. Regier, and
T. Hutchinson, “Ecosystem Behavior Under Stress,” The American Naturalist
125(5):617-38 (1985); H. Regierand G. Baskerville, “Sustainable Redevelop
ment of Degraded Ecosystems,” in Sustainable Development of the Biosphere,
W. Clark and R. Munn, eds., Cambridge University Press, 1986. The explo
sion of double-crested cormorants, not only in the Great Lakes, but across
the United States after DDT use was curtailed, is an example of a species that
took off like a weed, filling niches that were left vacant by more sensitive
species. “She had already . .stems from general opinion polls in Canada
and from the joint report by the National Research Council of the United
States and The Royal Society of Canada, “The Great Lakes Water Quality
Agreement: An Evolving Instrument for Ecosystem Management,” 1985.
“John Harshbarger. . .” refers to a series of papers that include: P. Bau
mann and J. Harshbarger, “Frequencies of Liver Neoplasia in a Feral Fish
Population and Associated Carcinogens,” Marine Environmental Research
17:324-27 (1985); J. Black, “Epidermal Hyperplasia and Neoplasia in Brown
Bullheads (Ictalurus nebulosus) in Response to Repeated Applications of
a PAH Containing Extract of Polluted River Sediment,” in Polynuclear
Aromatic Hydrocarbons: Seventh International Symposium, on Formation,
Metabolism and Measurement, M. Cooke and A. Dennis, eds., Battelle, 1982,
pp. 99-111; A. Maccubbin, P. Black, L. Trzeciak, and J. Black, “Evidence for
Polynuclear Aromatic Hydrocarbons in the Diet of Bottom-Feeding Fish,”
Bulletin of Environmental Contamination and Toxicology 34:876-82 (1985).
“Those trying to discover ...” mentions a keynote address at the
Toronto meeting by B.-E. Bengtsson. For further reading see B.-E. Bengtsson,
A. Bergman, I. Brandt, C. Hill, N. Johansson, A. Sodergren, and J. Timlin,
8
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NOTES
“Reproductive Disturbances in Baltic Fish: Research Programme for the Pe
riod 1994/95 to 1997/98” in a report for the Swedish Environmental Protec
tion Agency, 1994; and L. Norrgren, “Report from the Uppsala Workshop on
Reproduction Disturbances in Fish,” Report #4346, Swedish Environmental
Protection Agency, Research and Development Department, 1994.
The paragraphs that follow “In herring gull. ..” explain in more detail
the episodes cited in Chapter 1 under the Channel Islands, Southern Cali
fornia, episode; see those citations.
“Earlier experiments by other ...” discusses data fully covered in D. Fry,
C. Toone, S. Speich, and R. Peard, “Sex Ratio Skew and Breeding Patterns
of Gulls: Demographic and Toxicological Considerations,” Studies in Avian
Biology 10:26-43 (1987); and T. Kubiak, H. Harris, L. Smith, T. Schwartz,
D. Stalling, J. Trick, L. Sileo, D. Docherty, and T. Erdman, “Microcontami
nants and Reproductive Impairment of the Forster's Tern on Green Bay,
Lake Michigan—1983,” Archives of Environmental Contamination and Tox
icology 18:70^27 (1989).
“Fox and others ...” refers to G. Fox, A. Gilman, D. Peakali, F. Anderka, “Behavioral Abnormalities of Nesting Lake Ontario Herring Gulls,”
Journal of Wildlife Management 42(3):477-83 (1978).
The comment about “gay gulls” (in the paragraph that starts with “As
Colborn tackled . . .”) refers to J. Diamond, “Goslings of Gay Geese,” Na
ture 340:101 (1989). In this article Diamond points out that female-female
pairing had never been reported in the literature before the 1950s.
The endocrinology textbook referred to is G. Hedge, H. Colby, and
R. Goodman, Clinical Endocrine Physiology, W. B. Saunders, 1987.
“It dawned on Colborn ...” refers to a series of reports, some of which
are: G. Fein, J. Jacobson, S. Jacobson, P. Schwartz, and J. Dowler, “Prenatal
Exposure to Polychlorinated Biphenyls: Effects on Birth Size and Gesta
tional Age,” Journal of Pediatrics 105 (2):315-20 (1984); S. Jacobson, G. Fein,
J. Jacobson, P. Schwartz, and J. Dowler, “The Effect of Intrauterine PCB
Exposure on Visual Recognition Memory,” Child Development 56:853-60
(1985); J. Jacobson, S. Jacobson, and H. Humphrey, “Effects of In Utero
Exposure to Polychlorinated Biphenyls and Related Contamination on
Cognitive Functioning in Young Children,” Journal of Pediatrics 116:38—45
(1990); and J. Jacobson, S. Jacobson, and H. Humphrey, “Effects of Expo
sure to PCBs and Related Compounds on Growth and Activity in Chil
dren,” Neurotoxicology and Teratology 12:319-26 (1990).
For a comprehensive overview of chemicals found in breast milk, see
A. Jensen and S. Slorach, Chemical Contaminants in Human Milk, CRC
Press, 1991. Also see K. Thomas and T. Colborn, “Organochlorine Endocrine
W.'
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265
Disruptors in' Human Tissue,n in Chemically Induced Alterations in Sexual
and Functional Development: The Wildlife-Human Connection, T. Colbom
and C. Clement, eds., Princeton Scientific Publishing, 1992, pp. 365-94.
“Of course! . . discusses the problem of biomagnification; see R. Norstrom, D. Hallett, and R. Sonstegard, “Coho Salmon (Oncorhynchus kisutch)
and Herring Gulls (Larus arentatus) as Indicators of Organochlorine Conta
mination in Lake Ontario,” Journal of the Fisheries Research Board of Canada
35(11):1401—1409 (1978). These authors reported that PCBs biomagnified
25 million times from Lake Ontario water to the herring gull.
The foundation for this chapter was Colbom’s report under contract
to Darrell Piekarz, Environment Canada, Conservation and Protection, En
vironmental Interpretation Division, Ottawa, Canada, “The Great Lakes
Toxics Working Paper,” Contract Number: KE144-7-6336, April 19, 1988.
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Chapter 3: CHEMICAL MESSENGERS
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For the reader who wants to delve deeper into the major theme of this
chapter, we recommend: F. vom Saal, “The Intrauterine Position Phenome
non: Effects on Physiology, Aggressive Behavior, and Population Dynamics
in House Mice,” in Biological Perspectives on Aggression, K. Flannelly,
R. Blanchard, and D. Blanchard, eds. (no. 169 in a series entitled Progress in
Clinical Biology Research); Liss, 1984, pp. 135-79; F. vom Saal, “Sexual Dif
ferentiation in Litter Bearing Mammals: Influence of Sex of Adjacent Fe
tuses in Utero,” Journal of Animal Science 67:1824-40 (1989); and F. vom
Saal, M. Montano, and M. Wang, “Sexual Differentiation in Mammals,” in
Chemically Induced Alterations in Sexual and Functional Development: The
Wildlife-Human Connection, T. Colbom and C. Clement, eds., Princeton
Scientific Publishing, 1992, pp. 17-83.
“The sisters also ...” refers to F. vom Saal and F. Bronson, “Sexual
Characteristics of Adult Female Mice Are Correlated with Their Blood Testos
terone Levels During Prenatal Development,” Science 208:597-99 (1980).
“Not so fast . . .” is supported by the vom Saal paper on intrauterine
position and J. Vandenbergh, “Regulation of Puberty and Its Consequences
on Population Dynamics of Mice,” American Zoologist 27:891-98 (1987).
“Even more amazing ...” refers to a report in the Science Section of
the New York Times, Tuesday, March 31, 1992, “Prenatal Womb Position
and Supermasculinity,” in which Bennett Galef and coworkers, working
with Mongolian gerbils, are quoted as stating that “almost everything we’ve
looked at behaviorally is affected by intrauterine position.” See also
11
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M. Clark, P. Karpiuk, and B. Galef, “Hormonally Mediated Inheritance ok
Acquired Characteristics in Mongolian Gerbils,” Nature 364:712 (1993).
“Interestingly, some studies. . refers to F. vom Saal, D. Quadagno,
M. Even, L. Keisler, D. Keisler, and S. Khan, “Paradoxical Effects of Mater
nal Stress on Fetal Steroids and Postnatal Reproductive Traits in Female
Mice from Different Intrauterine Positions,” Biology of Reproduction 43:
751-61 (1990).
. .
“Whatever the source .. .” cites D. McFadden, “A Masculinizing Effect
on the Auditory Systems of Human Females Having Male Go-Twins,” Pro
ceedings of the National Academy of Science 90:11900-11904 (1993).
The calculations in the paragraph starting “The striking . . . are
based on a standard medicine dropper delivering 20 drops per milliliter or
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cubic centimeter.
.
For further reading related to the paragraph starting with In girls, the
change . . . ,” see F. vom Saal, C. Finch, and J. Nelson, “Natural History and
Mechanisms of Reproductive Aging in Humans, Laboratory Rodents and
Other Selected Vertebrates” in The Physiology of Reproduction, 2nd ed„
E Knobil and J. Neill, eds., Plenum, 1994, pp. 1213-1314.
“An individual who gets . . .” mentions Charles Phoenix, who also
worked with Robert Goy. See C. Phoenix, R. Goy, A. Gerall, and W. Young,
“Organizing Action of Prenatally Administered Testosterone Propionate on
the Tissues Mediating Mating Behavior in the Female Guinea Pig,” Endo
crinology 65:369-82 (1959).
To read more about sexual differentiation, see Behavioral Endocrinol
ogy, J.,Becker, S. Marc, and D. Crews, eds., MIT Press, 1993; and S. LeVay,
The Sexual Brain, MIT Press, 1993.
Chapter 4: HORMONE HAVOC
“From the very beginning . . describes the work of R. Greene, M. Burnll,
and A Ivv “Experimental Intersexuality: The Paradoxical Effects of Estro
gens on the Sexual Development of the Female Rat,” Anatomical Record
74(4):429-38 (1939); and R. Greene, M. Burrill, and A. Ivy, ‘•Experimental
Intersexuality: Modification of Sexual Development of the White Rat with
a Synthetic Estrogen,” in Proceedings of the Society for Experimental Bio -
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ogy and Medicine 41:169—70 (1939).
For further reading about the passage starting “This cautionary evi
dence . . . see D. Dutton, Worse Than the Disease: Pitfalls of Medical
Progress, Cambridge University Press, 1988.
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“The Northwestern University rat studies . .reflects a conversation
with John McLachlan on May 5, 1994, who at that time was chief at the
Laboratory of Reproductive and Developmental Toxicology, National Insti
tute of Environmental Health Sciences.
“Before doctors . . refers to Insight Team of the Sunday Times of
London, Suffer the Children: The Story of Thalidomide, Viking, 1979.
“As would later . .also refers to the Insight Team’s book.
"Tor ordinary people . .refers to “The Full Story of the Drug Thal
idomide,” Life magazine, August 10, 1962.
“Would doctors have . . .” was reenforced by the discussion with John
McLachlan on May 5, 1994, mentioned earlier.
“The most painful aspect. . .” refers to W. Dieckmann, M. Davis,
L. Rynkiewicz, and R. Pottinger, “Does the Administration of Diethylstilbe
strol During Pregnancy Have Therapeutic Value?” American Journal of Ob
stetrics and Gynecology 66(5): 1062 (1953); and Y. Brackbill and H. Berendes,
“Dangers of Diethylstilboestrol: Review of a 1953 Paper,” a letter in Lancet
2:520 (1978).
The closing of the paragraph that begins “When the cluster ...”
refers to the book by D. Dutton.
“Ulfelder just couldn’t ...” describes a scene from R. Meyers, D. E. S.:
The Bitter Pill, Seaview/Putnam, 1983, pp. 93-94.
The paragraph that follows refers to A. Herbst, H. Ulfelder, and D. Poskanzer, “Adenocarcinoma of the Vagina: Association of Maternal Stilbestrol
Therapy with Tumor Appearance in Young Women,” New England Journal
of Medicine 284:878-81 (1971). Herbst, who played an invaluable role in
bringing the DES tragedy to light, continues to follow the medical histories
of the DES offspring.
“Regardless of the compelling ...” quotes T. Dunn and A. Green,
“Cysts of the Epididymis, Cancer of the Cervix, Granular Cell Myoblas
toma, and Other Lesions After Estrogen Injection in Newborn Mice,” Journal
of the National Cancer Institute 31:425-38 (1963); A. Herbst and H. Bern,
eds., Developmental Effects of Diethylstilhestrol (DES) in Pregnancy,
Thieme-Stratton, 1981, p. 1; and N. Takasugi and H. Bern, “Tissue
Changes in Mice with Persistent Vaginal Cornification Induced by Early
Postnatal Treatment with Estrogen,” Journal of the National Cancer Institute
33:855-65 (1964).
“Before long, the group ..refers to R. Newbold and J. McLachlan,
“Vaginal Adenosis and Adenocarcinoma in Mice Exposed Prenatally or
Neonatally to Diethylstilbestrol,” Cancer Research 42:2003-11 (1982).
“McLachlan and his colleagues . . .” cites J. McLachlan, R. Newbold,
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and B. Bullock, “Reproductive Tract Lesions in Male Mice Exposed Prenatally to Diethylstilbestrol,” Science 190:991-92 (1975).
“No doubt because . . refers to W. Gill, “Effects on Human Males
of In-Utero Exposure to Exogenous Sex Hormones,” in Toxicity of Hor
mones in Perinatal Life, T. Mon and H. Nagasawa, eds., ORC Press, 1988,
5g#*
pp. 162-74.
“Friedman pursued his hunch . . cites B. Tilley, A. Barnes, E. Bergstralh, D. Labarthe, K. Noller, T. Colton, and E. Adam, “A Comparison of
Maternal History Recall and Medical Records: Implications for Retrospec
tive Studies,” American Journal of Epidemiology, 121 (2) :269—81 (1985).
“Friedman decided to . . .” describes the frustrations mentioned in
D. Schottenfeld, M. Warshauer, S. Sherlock, A. Zauber, M. Leder, and
R. Payne, “The Epidemiology of Testicular Cancer in Young Adults,” Amer
ican Journal of Epidemiology, 112(2):232—46 (1980).
For more information about the paragraph opening “As was the
case
see C. Orenberg, D. E. S.: The Complete Story, St. Martin’s, 1981,
pp.46-47.
“In immune system . . .” discusses T cells, which comprise a small
part of the total population of white blood cells (lymphocytes) in the im
mune system. T cells get their name because they differentiate in the thy
mus gland whereas the other cells in the immune system differentiate in
the fetal liver, spleen, and adult bone marrow. T cells function as the first
line of defense against viruses and other foreign material in the body.
Among their number are the natural killer cells (NK) that target and kill
cells that have been attacked by viruses or have been transformed into can
cerous cells.
After reading “Although DES exposed mice ...” the reader might
want to consult I. Palmlund, R. Apfel, S. Buitendijk, A. Cabau, and J. Fors
berg, “Effects of Diethylstilbestrol (DES) Medication During Pregnancy:
Report From a Symposium at the 10th International Congress of ISPOG,
Journal of Psychosomatic Obstetrical Gynaecology 14:71-89 (1993). This
paragraph also mentions a possible link between DES prenatal exposure and
rheumatic fever. For more information see P. Blair, Immunologic Studies of
Women Exposed In Utero to Diethylstilbestrol,” in Chemically Induced Al
terations in Sexual and Functional Development: The Wildlife-Human Con
nection, T. Colborn and C. Clement, eds., Princeton Scientific Publishing,
1992, pp. 289-93; and P. Blair, K. Noller, J. Turiel, B. Forghani, and S. Ha
gens, “Disease Patterns and Antibody Responses to Viral Antigens in
Women Exposed In Utero to Diethylstilbestrol,” in Chemically Induced Al
terations, pp. 283—88. Also see D. Vvingard and J. Turiel, Long-1 erm
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3
Effects of Exposure to Diethylstilbestrol,” Journal of Western Medicine
149:551-54 (1988).
Much of what follows “The animal studies ...” leans heavily on
M. Hines, “Surrounded by Estrogens? Considerations for Neurobehavioral De
velopment in Human Beings,” in Chemically Induced Alterations, pp. 261-81.
It is important to point out that other hormones have been used for
the same purpose as DES, such as progesterone and testosterone, although
their effects in offspring have not been as carefully documented.
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Chapter 5: FIFTY WAYS TO LOSE
YOUR FERTILITY
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“Twelve years after.. .” refers to H. Burlington and V. Lindeman, “Effect of
DDT on Testes and Secondary Sex Characters of White Leghorn Cock
erels,” Proceedings of the Society for Experimental Biology and Medicine
74:48-51 (1950).
“The body has hundreds ...” discusses orphan receptors studied by
a team at the National Institutes of Environmental Health Sciences. See
J. McLachlan, R. Newbold, C. Teng, and K. Korach, “Environmental Estro
gens: Orphan Receptors and Genetic Imprinting,” in Chemically Induced
Alterations in Sexual and Functional Development: The Wildlife-Human
Connection, T. Colborn and C. Clement, eds., Princeton Scientific Publish
t
ing, 1992, pp. 107-12.
“They fit together ...” describes mechanisms of hormone binding.
See K. Korach, P. Sarver, K. Chae, J. McLachlan, and J. McKinney, “Es
trogen Receptor-Binding Activity of Polychlorinated Hydroxybiphenyls:
Conformationally Restricted Structural Probes,” Molecular Pharmacology
33:120-26 (1987); and J. McLachlan, “Functional Toxicology: A New Ap
proach to Detect Biologically Active Xenobiotics,” Environmental Health
Perspectives 101 (5):386-87 (1993).
For those who want to read more about the sensitivity of the fetus, we
suggest H. Bern, “The Fragile Fetus” in Chemically Induced Alterations,
pp. 9-15.
“As scientists have explored ...” refers to A. Salhanick, C. Vito, and
T. Fox, “Estrogen-Binding Proteins in the Oviduct of the Turtle, Chrysemys
picta: Evidence for a Receptor Species,” Endocrinology, 105 (6): 1388-95 (1979).
The Australian sheep incident described in the paragraph starting “The
early 1940s. . .” comes from H. Bennetts, E. Underwood, and F. Shier, “A Spe
cific Breeding Problem of Sheep on Subterranean Clover Pastures in Western
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Australia,” Austral.® Vatertao. laumal 22:2-12 ( 946); personal comnurmcation with Norman Adams, CSIRO Drvision of Animal Production, PO
Wembley, Australia; and N. Adams, “Organizational and Activational Effects
of Phytoestrogens on the Reproductive Tract of the Ewe (in Pre“>.
“Surprisingly, plant evolution
leans on K. Setche l, Naturally
Occurring Non-Steroidal Estrogens of Dietary Origin, in Estjm m
Environment II: Influences on Development, ). McUchlan ed Elsever,
198S; and R. Bradbury and D. White, “Estrogens and Related Substances in
Plants "Vitamins and Hormones 12:207-33 (1954).
“For such a defensive strategy..refers to C. Hughes,
Mimicry of Reproductive Hormones and Modulation of febr-ore Ferhhty
by Phytoestrogens,” Environmental Health Perspectives 78:171-75 (1988).
“Humans long ago . . discusses J. M. Riddle, Contraception
ContTaception and
Abortion from the Ancient World to the Renaissance, Harvard University
Wi
5S ;
PreSS’“There is no ..
begins several pages about the work of Pat Whittem
See P. Whitten, “Chemical Revolution to Sexual Revolution: Historical
Chanses in Human Reproductive Development,” in Chemically Induced
terutions, pp. 311-34; P Whitten and F. Naftolin, “Effects of a Phytoestro
gen Diet on Estrogen-Dependent Reproductive Processes in Immature
Female Rats,” Steroids 57:5M1 (1992); P. Whitten, E Russell, and E
Naftolin, “Effects of a Normal, Human-Concentrahon, Phytoestrogen D.et
on Rat Uterine Growth,” Steroids 57:98-106 (1992); and P. Whitt®, C. Uiwis,
and F. Naftolin, “A Phytoestrogen Diet Induces the Premature ovu a ory
Syndrome in Lactationally Exposed Female Rats,” Biology of Reproduction
49-1117-21 (1993).
r
,.
“When male workers in a chemical plant . . .” refers to a discovery
cited in P. Guzelian, “Fourteen Workers Exposed to Pesticide KeP™e re
Probably Sterile, Researchers Report,” Occupational Health and Safety Let6 “To dS researchers...” refers to T. Colbom, F. vom Saal, and A Soto,
“Developmental Effects of Endocrine-Disrupting
in^Wildlife
and Humans,” Environmental Health Perspectives iOf(>):3f8-184 (^ ■ - .
This paragraph also introduces three synthetic chemicals that will be ad
dressed again and again throughout this book: PCBs dioxins, and furans^
Chemicals are grouped in these families because they share a common
chemical structure, but each family member differs in the arrangement
the chlorine atoms on its common structure. These family members are
called congeners. The most famous of the dioxins, because of its toxicity,
2,3,7,8-TCDD (tetrachlorodibenzo-para-dioxm), is what is common y re
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271
ferred to as “dioxin.” The other members of the dioxin family and PCBs and
furans are referred to by their respective chemical structure. Furans are sim
ilar in structure to dioxins but are of lower toxicity.
“Most discussions . . .” refers to the problem caused by substituting in
adequately tested new chemicals for old-time chemicals that are now known
to be toxic problems. For example, see A. Murk, J. van den Berg, J. Koeman,
and A. Brouwer, “The Toxicity of Tetrachlorobenzyltoluenes (Ugilec 141)
and Polychlorobiphenyls (Aroclor 1254 and PCB-77) Compared in Ah-Responsive and Ah-Nonresponsive Mice,” Environmental Pollution 72:57-67
(1991). In this study, the researchers found that a German substitute for
PCBs, Ugilec 141, was bioaccumulating in fish in the Rhine River and is as
toxic as the products it was designed to replace. This would not have been
discovered without applying forensic science in the field: traditional monitor
ing would have missed this product in the fish.
In reading the paragraph starting “As the number . . . ,” bear in mind
that the published 1993 number of chemicals (51) with endocrine or repro
ductive effects has already increased, although not all of the new discoveries
have been reported in the scientific literature to date (1995).
The section that opens “If some scientists . . .” leans on the research
of a team of reproductive toxicologists at the U.S. Environmental Protec
tion Agency’s Health Effects Research Laboratory, North Carolina. See
L. Gray, J. Ostby, and W. Kelce, “Developmental Effects of an Environ
mental Antiandrogen: The Fungicide Vinclozolin Alters Sex Differentiation
of the Male Rat,” Toxicology and Applied Pharmacology 129:46-52 (1994);
and W. Kelce, C. Stone, S. Laws, L. Gray, J. Kemppainen, and E. Wilson,
“Persistent DDT Metabolite p,p'-DDE is a Potent Androgen Receptor An
tagonist,” Nature 375:581-85 (1995).
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Chapter 6: TO THE ENDS OF THE EARTH
Guidance for polar bear natural history and behavior came from I. Stirling,
Polar Bears, University of Michigan Press, 1988; and Thor Larsen, ‘Tolar Bear
Denning and Cub Production in Svalbard, Norway,” Journal of Wildlife
Management 49(2):320-26 (1985).
Based on what ...” is based on an Associated Press report by Doug
Mellgren, “Norwegian Researchers Fear PCBs Threaten Polar Bears’ Fertil
ity,” January 4, 1993.
“Some Svalbard bears . . .” refers to G. Norheim, J Slcaare, and 0. Wiig,
Some Heavy Metals, Essential Elements, and Chlorinated Hydrocarbons
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NOTES
in Polar Bear (Ursus maritimus) at Svalbard/’ Environmental Pollution
77(1):51-57 (1992).
“The story of. . uses the term persistent, which is based on a defin
ition by the U.S. and Canadian International Joint Commission in their
Sixth Biennial Report on Great Lakes Water Quality, 1992: “Any toxic
substance with a half-life in water of greater than eight weeks.” (p. 26)
They recommend that the definition apply to all media: water, air, sedi
ment, soil, and biota.
“The person to first..refers to “Report of a New Chemical Hazard,”
a news item in New Scientist 32:612 (1966).
“Our imaginary PCB molecule ...” introduces PCB congener 153.
The following are selected papers that describe in more detail the nature of
PCB congener 153: L. Hansen, “Environmental Toxicology of Polychlori
nated Biphenyls,” Polychlorinated Biphenyls (PCBs): Mammalian and Envi
ronmental Toxicology, S. Safe, ed., Springer-Verlag, 1987, pp. 15-48; D. Ness,
S. Schantz, J. Moshtaghian, and L. Hansen, “Effects of Perinatal Exposure
to Specific PCB Congeners on Thyroid Hormone Concentrations and Thy
roid Histology in the Rat,” Toxicology Letters 68:311-23 (1993) [Thyroid
hormone production in rat pups whose mothers were exposed to PCB-153
was depressed. The pups’ brain and body weights were lower and their livers
were larger than unexposed pups.]; and B. Bush, A. Bennett, and J. Snow,
“Polychlorobiphenyl Congeners, p,p’-DDE, and Sperm Function in Hu
mans,” Archives of Environmental Contamination and Toxicology 15:333-41
(1986) [In this study, three PCB congeners (153, 138, and 114) were in
versely associated with sperm motility in samples from men with less than
20 million sperm per milliliter.].
Much of what appears in the paragraph starting “Our imaginary PCB
molecule .. .” was taken from the record of Federal Civil Action L92-CV2137: Robert K. Joiner and Karen P. Joiner v. General Electric Company,
Westinghouse Electric Company, and Monsanto Company: Deposition of re
tired Monsanto employee William B. Papageorge, July 22, 1993.
“These ubiquitous metal . . .” relies on conversations with Diane
Herndon of the public information center at Monsanto, other Monsanto of
ficials, and Edward Bates, Jr., an engineer and manager of transformer tests
at General Electric’s power transformer plant, Pittsfield, Massachusetts,
from 1940 until his retirement in the mid-1980s. All were invaluable in
helping us reconstruct as much as possible the details of how Aroclors were
used in GE’s manufacturing process in Pittsfield. After all these years, some
of the precise details v/ere impossible to establish.
“Within hours . .describes bioaccumulation as in S. Hooper, C. Pct-
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273
tigrew, and G. Sayler, “Ecological Fate, Effects and Prospects for the Elimi
nation of Environmental Polychlorinated Biphenyls (PCBs),” Environmen
tal Toxicology and Chemistry 9:655-67 (1990).
As with so many species, there is concern over the decline of the
American eel mentioned in the paragraph starting “Before long. . . .” For
a comprehensive account of the status of the American eel in the St. Law
rence River see M. Castonguay, P. Hodson, C. Couillard, M. Eckersley,
J.-D. Dutil, and G. Verreault, “Why Is Recruitment of the American Eel,
Anguilla rostrata, Declining in the St. Lawrence River and Gulf?” Canadian
Journal of Fisheries and Aquatic Sciences 51:479-88 (1994).
The section starting “The eel’s flesh ...” is based on the following:
H. Iwata, S. Tanabe, N. Sakai, and R. Tatsukawa, “Distribution of Persistent
Organochlorines in Oceanic Air and Surface Seawater and the Role of Ocean
in Their Global Transport and Fate,” Environmental Science and Technology
27(6): 1080—98 (1993); F. Wania and D. Mackay, “Global Fractionation and
Cold Condensation of Low Volatility Organochlorine Compounds in Polar
Regions,” Ambio 22(1): 10—18 (1993); and M. Oehme, “Further Evidence for
Long-range Air Transport of Polychlorinated Aromates and Pesticides: North
American and Eurasia to the Arctic,” Ambio 20(7)293-97 (1991).
“The gray green . ..” depends upon information in D. Muir, R. Norstrom, M. Simon, “Organochlorine Contaminants in Arctic Marine Food
Chains: Accumulation of Specific Polychlorinated Biphenyls and ChlordaneRelated Compounds,” Environmental Science and Technology 22 (9): 1071-79,
(1988) and personal communication with Derek Muir, 1995.
“While prenatal exposure . ..” raises questions concerning breast
milk. See A. Smith, “Infant Exposure Assessment for Breast Milk Dioxins
and Furans Derived from Waste Incineration Emissions,” Risk Analysis
7(3):347-53 (1987).
“The contamination of. ..” reflects E. Dewailly, A. Nantel, J. Weber,
and F. Meyer, “High Levels of PCBs in Breast Milk of Inuit Women from
Arctic Quebec,” Bulletin of Environmental Contamination and Toxicology
43:641-46 (1989); E. Dewailly, P. Ayotte, S. Bruneau, C. LaLiberte, D. Muir,
and R. Norstrom, “Human Exposure to Polychlorinated Biphenyls Through
the Aquatic Food Chain in the Arctic,” Dioxin ’93: 13th International Sym
posium on Chlorinated Dioxins and Related Compound, Vienna, September
1993, 14:173-75 (1993); and D. Kinloch, H. Kuhnlein, and D. Muir, “Inuit
Foods and Diet: A Preliminary Assessment of Benefits and Risks,” The Sci
ence of the Total Environment 122:247-78 (1992).
Probably the most disturbing information concerning exposure to per
sistent chemicals in the Arctic is revealed in D. Gregor, A. Peters, C. Teixeira,
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N. Jones, and C. Spencer, “The Historical Residue Trend of PCBs in the
Agassiz Ice Cap, Ellesmere Island, Canada,” The Science of the Total Envi
ronment 160/161:117-26 (1995). The authors found there was no change in
average PCB deposition between 1963 and 1993 on Ellesmere Island situ
ated west of Greenland and 500 miles from the North Pole. PCB-153 was
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among the PCB congeners measured in this study.
Chapter 7: A SINGLE HIT
i
For more information about the work mentioned in the paragraph starting
“A few months later...,” see R. Peterson, R. Moore, T. Mably, D. Bjerke,
and R. Goy, “Male Reproductive System Ontogeny: Effects of Perinatal
Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin” in Chemically Induced
Alterations in Sexual and Functional Development: The Wildlife-Human
Connection, T. Colborn and C. Clement, eds., Princeton Scientific Publish
ing, 1992, pp. 175-93.
The lay reader who wishes to know more about dioxin (known as
2,3,7,8-TCDD for short) should consult “Putting the Lid on Dioxins: Pro
tecting Human Health and the Environment,” a joint report by Physicians for
Social Responsibility and the Environmental Defense Fund, 1994. For those
with a technical background, we recommend examining the six-volume Ex
ternal Review Draft Dioxin Reassessment, released by the U.S. Environmen’ tai Protection Agency’s Office of Research and Development in June 1994,
EPA/600/BP-92/001; S. Safe, “Comparative Toxicology and Mechanism of
Action of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans,” Annual
Review of Pharmacology and Toxicology 26:371-99 (1986); and S. Safe, Poly
chlorinated Biphenyls (PCBs), Dibenzo-p-dioxins (PCDDs), Dibenzofurans
(PCDFs), and Related Compounds: Environmental and Mechanistic Con
siderations Which Support the Development of Toxic Equivalency Factors
(TEFs),” Critical Reviews in Toxicology 21 (1):51—88 (1990).
Figures in this chapter for production and releases of dioxincontaminated material were taken from “Veterans and Agent Orange: Health
Effects of Herbicides Used in Vietnam;” Institute of Medicine, National
Academy of Sciences, 1993; M. Gough, Dioxin, Agent Orange: The Facts,
Plenum, 1986; and “The Health Risks of Dioxin” hearing before the Human
Resources and Intergovernmental Relations Subcommittee of the Commit
tee on Government Operations, House of Representatives, June 10, 1992.
For the reader interested in following the cancer studies from Severe, we
recommend P. Bertazzi, A. Pesatori, D. Consonni, A. Tironi, M. Landi, and
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C. Zocchetti, “Cancer Incidence in a Population Accidentally Exposed to
2.3.7.8-Tetrachlorodibenzo-para-dioxin, ” Epidemiology 4(5):398—406 (1993).
We further recommend A. Pesatori, D. Consonni, A. Tironi, C. Zocchetti,
and P. Bertazzi, “Cancer in a Young Population in a Dioxin-Contaminated
Area,” International Journal of Epidemiology 22(6): 1010—13 (1993); and
P. Bertazzi, C. Zocchetti, A. Pesatori, S. Guercilena, M. Sanarico, and
L. Radice, “Ten-Year Mortality Study of the Population Involved in the
Seveso Incident in 1976,” American Journal of Epidemiology 129 (6):1187-1200
(1989). The Pesatori et al., 1993, study revealed an increase in thyroid can
cer, which, as the authors state, is consistent with “experimental findings
and previous observations in humans.” (p. 1010)
“In this case ..refers to G. Smoger, P. Kahn, G. Rodgers, S. Suffin,
and P. McConnachie, “In Utero and Postnatal Exposure to 2,3,7,8-TCDD in
Times Beach, Missouri: 1. Immunological Effects: Lymphocyte Phenotype
Frequencies,” Dioxin '93: 13th International Symposium on Chlorinated
Dioxins and Related Compounds, Vienna, September 1993; and D. Cantor,
G. Holder, W. Cantor, P. Kahn, G. Rodgers, G. Smoger, W. Swain, H. Berger,
and S. Suffin, “In Utero and Postnatal Exposure to 2,3,7,8-TCDD in Times
Beach, Missouri: 2. Impact on Neurophysiological Functioning,” Dioxin ’93.
“The EPA’s reassessment...” refers to L. Gray and J. Ostby, “In Utero
2.3.7.8-Tetrachlorodibenzo-p-dioxin (TCDD) Alters Reproductive Morphol
ogy and Function in Female Rat Offspring,” Toxicology and Applied Pharma
cology (in press, 1995). Also see L. Gray, W. Kelce, E. Monosson, J. Ostby,
and L. Birnbaum, “Exposure to TCDD During Development Permanently
Alters Reproductive Function in Male Long Evans Rats and Hamsters: Re
duced Ejaculated Epididymal Sperm Numbers and Sex Accessory Gland
Weights in Offspring with Normal Androgenic Status,” Toxicology and
Applied Pharmacology 131:108-18 (1995).
“Well before their ...” mentions the work of Dorothea Sager; see
D. Sager, D. Girard, and D. Nelson, “Early Postnatal Exposure to PCBs: Sperm
Function in Rats,” Environmental Toxicology and Chemistry 10:737-46
(1991) for an overview.
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Chapter 8: HERE, THERE,
AND EVERYWHERE
Drs. Soto and Sonnenschein published a paper that describes how they arrived
at their hypothesis concerning estrogenic action on cellular proliferation,
“Mechanism of Estrogen Action on Cellular Proliferation: Evidence for Indi-
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NOTES
rect and Negative Control on Cloned Breast Tumor Cells,” Biochemical and
Biophysical Research Communication 122:1097—1103 (1984). This was fol
lowed by A. Soto and C. Sonnenschein, “Cell Proliferation of Estrogen-Sensi
tive Cells: The Case for Negative Control,” Endocrine Reviews 8:44-52 (1987).
“By 1985 ...” describes work that is discussed more in depth in A. Soto
and C Sonnenschein, “The Role of Estrogens on the Proliferation of Human
Breast Tumor Cells (MCF-7),” Journal of Steroid Biochemistry 23:87-94,
(1985); and C. Sonnenschein, J. Papendorp, and A. Soto, “Estrogenic Effect
of Tamoxifen and Its Derivatives on the Proliferation of MCF-7 Human
Breast Tumor Cells,” Life Sciences 37:387-94 (1985).
As a follow-up to the paragraph starting “In the end ...,” see A. Soto,
H Justicia, J. Wray, and C. Sonnenschein, “p-Nonylphenol: A Estrogenic
Xenobiotic Released from ‘Modified’ Polystyrene,” Environmental Health
Perspectives 92A67-73 (1991); and A. Soto, T. Lin, H. Justicia, R. Silvia,
and C. Sonnenschein, “An ‘In Culture’ Bioassay to Assess the Estrogemcity
of Xenobiotics (E-SCREEN),” in Chemically Induced Alterations in Sexual and
Functional Development: The Wildlife-Human Connection, T. Colbom and
C. Clement, eds., Princeton Scientific Publishing, 1992, pp. 295-309.
The passage starting “They also learned ...” comes from a report by
the Chemical Manufacturer Association’s Alkylphenol and Ethoxylates
Panel, “Alkylphenol Ethoxylates: Human Health and Environmental Ef
fects,” October 1993. For a recent discussion about the stability of the
alkylphenols see W.-Y. Shiu, K.-C. Ma, D. Varhamdkova, and D. Mackay,
“Chlorophenols and Alkylphenols: A Review and Correlation of Environmen
tally Relevant Properties and Fate in an Evaluative Environment,” Chemos
phere 29(6):1155-1224 (1994). These chemicals have little tendency to
evaporate and therefore remain in water and soil. The authors admit that
their work is “merely a first attempt to elucidate the environmental fate of
this important and interesting class of chemicals.”
“By strange coincidence ...” refers to A. Krishnan, P. Stathis, S. Permuth, L. Tokes, and D Feldman, “Bisphenol-A: An Estrogenic Substance Is
Released from Polycarbonate Flasks During Autoclaving,” Endocrinology
132(8):2279-86 (1993). Officials of GE Plastics Company contend that poly
carbonate containers are unlikely to leach bisphenol-A in normal use because
they would not be subjected to the high temperatures used in the Stanford lab
for sterilization. (This is based on conversations with Diana Nichols, commu
nications, and Tim Ullman, manager of global product stewardship, Pittsfield,
Massachusetts.) The authors have not seen independent tests that assess the
leaching properties of polycarbonates at various water temperatures in the
presence of various kinds of cleaning agents or after extended use.
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277
For more information concerning the section that begins “In this
same period ...see J. Sumpter and S. Jobling, “Vitellogenesis as a Bio
marker for Oestrogen Contamination of the Aquatic Environment/’ in The
Proceedings of the Estrogens in the Environment Conference, Environmental
Health Perspectives Supplements (in press, 1995); S. Jobling, T. Reynolds,
R. White, M. Parker, and J. Sumpter, “A Variety of Environmentally Persis
tent Chemicals, Including some Phthalate Plasticizers, Are Weakly Estro
genic/’ Environmental Health Perspectives 103(6):582—87 (1995); C. Purdom,
P. Hardiman, V. Bye, N. Eno, C. Tyler, and J. Sumpter, “Estrogenic Effects
of Effluents from Sewage Treatment Works/’ Chemistry and Ecology
8:275-85 (1994); and S. Jobling and J. Sumpter, “Detergent Components
in Sewage Effluent Are Weakly Oestrogenic to Fish: An In Vitro Study Using
Rainbow Trout (Oncorhynchus mykiss) Hepatocytes/’ Aquatic Toxicology
27:361-72 (1993).
“Spurred by the Tufts ..refers to J. Brotons, M. Olea-Serrano, M. Vil
lalobos, V. Pedraza, N. Olea, “Xenoestrogens Released from Lacquer Coat
ings in Food Cans,” Environmental Health Perspectives 103(6):608—12 (1995).
“All of the incidents ..refers to W. Kelce, C. Stone, S. Laws,
L. Gray, J. Kemppainen, and E. Wilson, “Persistent DDT Metabolite p,pDDE Is a Potent Androgen Receptor Antagonist,” Nature 375:581-85
(1995). In their continuing work every estrogenic compound they have
tested thus far also binds to the androgen (male) receptor and the proges
terone receptor. It appears that not only are the receptors promiscuous, but
our hormones and their synthetic copycats are promiscuous as well (per
sonal communication with Earl Gray, July 1995).
“Such assertions seem .. .” is based on a discussion with an attorney,
David Viadeck, director of the Public Citizen Litigation Group, Washington,
D.C., who has litigated cases on trade secrets.
For more reading on global and regional contaminant trends (mentioned
in the paragraph starting “Oftentimes, the studies ...”), see B. Loganathan and
K. Kannan, “Global Organochlorine Contamination Trends: An Overview,”
Ambio 23(3):187-91 (1994); and B. Loganathan, S. Tanabe, Y. Hidaka,
M. Kawano, H. Hidaka, and R. Tatsukawa, “Temporal Trends of Persistent
Organochlorine Residues in Human Adipose Tissue from Japan, 1928-1985,”
Environmental Pollution 81:31-39 (1993).
For historical information concerning the information on chemical
production see A. Ihde, The Development of Modern Chemistry, Harper and
Row, 1970; and M. Holdgate, A Perspective of Environmental Pollution,
Cambridge University Press, 1979.
“Around the world ...” uses figures from The World Environment
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NOTES
1972-1992; Two Decades of Challenge, M. Tolba and O. El-Kholy, eds.,
Chapman and Hall, 1992.
For more information on the production of pesticides, see C. Edwards
The Impact of Pesticides on the Environment,” in The Pesticide Question:
Environment, Economics, and Ethics, D. Pimentel and H. Lehman, eds.,
Chapman and Hall, 1993; D. Pimentel, “The Dimensions of the Pesticide
Question,” in Ecology, Economics, Ethics: The Broken Circle, F. Bormann and
S. Kellert, eds, Yale University Press, 1991; A. Aspelin, “Pesticide Industry
Sales and Usage, 1992 and 1993 Market Estimates Report,” U.S. Environmen
tal Protection Agency Report EPA/733/K-94/001, 1994; U.S. Food and Drug
Administration, “Food and Drug Administration Pesticide Program Residues
in Foods—1989,” Journal of the Association of Official Analytical Chemistry
73:127A-146A (1990); U.S. Congressional Office of Technology Assessment,
Pesticide Residues in Food: Technologies for Detection, Washington, D.C,
1988; S. Dogheim, E. Nasr, M. Almaz, and M. El Tohamy, “Pesticide Residues
in Milk and Fish Samples Collected in Two Egyptian Govemorato,” Journal of
the Association of Official Analytical Chemistry 73:19-21 (1990) [cited in
Pimentel]; D. Acquay, M. Biltonen, P. Rice, M. Silva, J. Nelson, V. Lipner,
S. Giordano, A. Horowitz, and M. D’Amore, “Assessment of Environmental
and Economic Impacts of Pesticide Use,” in The Pesticide Question; and
B. Hileman, “Concerns Broaden over Chlorine and Chlorinated Hydrocar
bons,” Chemical and Engineering News, April 19, 1993, pp. 11-20.
’ The paragraph starting “The world trade ....” closes with a statement
supported by Loganathan et al, 1994.
“In 1991, the U.S....” refers to the findings of Carl Smith at the Foun
dation for Advancements in Science and Education (FASE), Los Angeles, Cab
iforma, reported in “Exporting Banned and Hazardous Pesticides, 1991
Statistics: The Second Export Survey by the FASE Pesticide Project, 1993.
Using customs records, Smith has since discovered that approximately a ton of .
DDT per day was shipped from the United States in 1992 (personal commu
nication, July 1995). Smith also notes that customs records as a rule omit the
technical names of pesticides; thus his figures are conservative estimates.
“Contrary to assertions . . .” refers to Kelce et al, 1995.
Chapter 9: CHRONICLE OF LOSS
For further reading on the status of the St. Lawrence beluga population, see
L. Pippard, “Status of the St. Lawrence River Population of Beluga, Delphinapterus leucas,” The Canadian Field-Naturalist 99:438-50 (1985).
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The population figures cited in the paragraph starting “For years, sci
entists ...” are based on aerial surveys in 1990, cited by P. Beland in a report
for the Canadian World Wildlife Fund’s Wildlife Toxicology Fund, “Toxi
cology and Pathology of Marine Mammals,” May 1992. See also P. Beland,
untitled article in Whalewatcher: Journal of the American Cetacean Society
28(1)3-5 (1994); and P. Beland, A. Vezina, and D. Martineau, “Potential
for Growth of the St. Lawrence (Quebec, Canada) Beluga Whale (Delphinapterus leucas) Population Based on Modelling,” Journal du Conseil inter
national pour Exploration de la Mer 45:22-32 (1988).
For further information after reading the paragraph starting “Even
the first . ..,” see D. Martineau, P. Beland, C. Desjardins, and A. Lagacee,
“Levels of Organochlorine Chemicals in Tissues of Beluga Whales (Delphinapterus leucas) from the St. Lawrence Estuary, Quebec, Canada,” Archives
of Environmental Contamination and Toxicology 16:137-47 (1987); P. Beland,
S. De Guise, C. Girard, A. Lagacee, D. Martineau, R. Michaud, D. Muir,
R. Norstrom, E. Pelletier, S. Ray, and L. Shugart, “Toxic Compounds and
Health and Reproductive Effects in St. Lawrence Beluga Whales,” Journal
of Great Lakes Research 19(4):766-75 (1993); and S. De Guise, A. Lagacee,
and P. Beland, “Tumors in St. Lawrence Beluga Whales (Delphinapterus
leucas),” Veterinary Pathology 31:444-49 (1994).
“The autopsy continued . . .,” which discusses Booly’s condition, can
be further explored in S. De Guise, A. Lagacee, and P. Beland, “True Her
maphroditism in a St. Lawrence Beluga Whale (Delphinapterus leucas),”
Journal of Wildlife Disease 30(2):287-90 (1994).
“Was Booly an accident ...” suggests that pollution may have
reached a peak about the time Booly was bom; see G. Sanders, S. Eisenreich,
and K. Jones, “The Rise and Fall of PCBs: Time-Trend Data from Temper
ate Industrialized Countries,” Chemosphere 29 (9—11):2201—2208 (1994).
Sanders et al. provide figures for PCB loading in water and peat compared
with production in the United Kingdom (Loch Ness) and the United States
that support that conclusion.
“Such reproductive problems . . .” refers to P. Reijnders, “Reproductive
Failure in Common Seals Feeding on Fish From Polluted Coastal Waters,”
Nature 324:456-57 (1986). For more reading about the immune status of
marine mammals, see A. Osterhaus, “Seal Death,” Nature 334:301-302
(1988); A. Osterhaus, J. Groen, P. De Vries, F. UytdeHaag, B. Klingeborn,
and R. Zarnke, “Canine Distemper Virus in Seals,” Nature 335:403-404
(1988); A. Osterhaus and E. Vedder, “Identification of Virus Causing Re
cent Seal Deaths,” Nature 335:20 (1988); A. Osterhaus, J. Groen, F. Uytdehaag, I. Visser, M. Bildt, A. Bergman, and B. Klingeborn, “Distemper Virus
I
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in Baikal Seals,” Nature 338:209-10, 1989; P. Ross, R. de Swart, I. Visser,
L. Vedder, W. Murk, W. Bowen, and A. Osterhaus, "Relative Immunocom
petence of the Newborn Harbour Seal, Phoca vitulina^ Veterinary Im
munology and Immunopathology 42:331-48 (1994); P. Ross, R. de Swart,
P. Reijnders, H. Van Loveren, J. Vos, and A. Osterhaus, "ContaminantRelated Suppression of Delayed-Type Hypersensitivity and Antibody Re
sponses in Harbor Seals Fed Herring from the Baltic Sea,” Environmental
Health Perspectives 103(2): 162—67 (1995); and R. de Swart, "Impaired
Immunity in Seals Exposed to Bioaccumulated Environmental Contami
nants,” Ph.D. thesis, Erasmus University, Rotterdam, Netherlands, 1995.
For a recent discussion about the St. Lawrence beluga whale popula
tion, see S. De Guise, D. Martineau, P. Beland, and M. Fournier, "Possible
Mechanisms of Action of Environmental Contaminants on St. Lawrence
Beluga Whales (Delphinapterus leucas),” Environmental Health Perspectives
Supplements 103(4):73-77 (1995).
The close of the paragraph that opens “The first clue ...” refers to
M. Roelke, J. Martenson, and S. O'Brien, "The Consequences of Demo
graphic Reduction and Genetic Depletion in the Endangered Florida Pan
ther,” Current Biology 3:340-50 (1993). See also C. Facemire, T. Gross, and
L. Guillette, "Reproductive Impairment in the Florida Panther: Nature or
Nurture?” Environmental Health Perspectives Supplements 103(4):79—86
(1995).
"With this insight . . .” refers to A. Woodward et al., 1993, cited in
Chapter 1, and L. Guillette, T. Gross, G. Masson, J. Matter, H. Percival,
and A. Woodward, "Developmental Abnormalities of the Gonad and Ab
normal Sex Hormone Concentrations in Juvenile Alligators from Contami
nated and Control Lakes in Florida,” Environmental Health Perspectives
102:680-88, 1994; L. Guillette, D. Crain, A. Rooney, and D. Pickford, "Orga
nization Versus Activation: The Role of Endocrine-Disrupting Contaminants
(EDCs) During Embryonic Development in Wildlife,” Environmental Health
Perspectives Supplement (in press); and L. Guillette and D. Crain, "EndocrineDisrupting Contaminants and Reproductive Abnormalities in Reptiles,”
Comments on Toxicology (in press).
For more information about temperature influence (mentioned in the
paragraph starting "In turtles, sex is determined ...”), see D. Crews,
J. Bergeron, J. Bull, D. Flores, A. Tousignant, J. Skipper, and T. Wibbels,
"Temperature-Dependent Sex Determination in Reptiles: Proximate Mecha
nisms, Ultimate Outcomes and Functional Outcomes,” Developmental Genet
ics 15:297-312 (1994). This paper describes the authors' findings following the
painting of turtle eggs with single PCB congeners during incubation.
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281
“In the Great Lakes ...” refers to the doctoral dissertation of W. Bower
man, “Regulation of Bald Eagle (Haliaeetus leucocephalus) Productivity in
the Great Lakes Basin: An Ecological and Toxicological Approach,” Michigan
State University, Department of Fisheries and Wildlife, 1993, and personal
communication with Bowerman, and with Dave Best and Letha Williams,
U.S. Fish and Wildlife Service. For an excellent review and analysis of
the literature on contaminants in Great Lakes birds, see J. Giesy, J. Ludwig,
and D. Tillitt, “Deformities in Birds of the Great Lakes Region: Assigning
Causality,” Environmental Science and Technology 28(3): 128-35 (1994).
“An eagle's diet ..describes the research of Karen Kozie, as re
ported in T. Colborn, “Epidemiology of Great Lakes Bald Eagles,” Journal
of Toxicology and Environmental Health 33 (4) :395—453 (1991).
“Based on environmental ...” refers to the syndrome called GLEMEDS cited in Chapter 1.
“In 1993, the bald eagles . . .” refers to findings in W. Bowerman,
T. Kubiak, J. Holt, D. Evans, R. Eckstein, C. Sindelar, D. Best, and K. Kozie,
“Observed Abnormalities in Mandibles of Nestling Bald Eagles Haliaeetus
leucocephalus,” Bulletin of Environmental Contamination and Toxicology
53:450-57 (1994), and personal communication with Carol Schuler, Port
land Field Office, U.S. Fish and Wildlife Service.
The section of this chapter devoted to the mink is taken from the
writings of Richard Aulerich and Robert Ringer as cited in R. Aulerich et al.,
1973, mentioned in the notes to Chapter 1, and R. Aulerich and R. Ringer,
“Current Status of PCB Toxicity to Mink, and Effect on Their Reproduc
tion,” Archives of Environmental Contamination and Toxicology 6:279-92
(1977).
The section of this chapter devoted to otters (starting with “In Britain
and Europe ...”) leans on the following literature: C. Mason, “Role of Con
taminants in the Decline of the European Otter,” Proceeding of the Expert
Consultation Meeting on Mink and Otter, International Joint Commission,
Windsor, Ontario, 1991; R. Foley, S. Jackling, R. Sloan, and M. Brown,
“Organochlorine and Mercury Residues in Wild Mink and Otter: Comparison
with Fish,” Environmental Toxicology and Chemistry 7:363-74 (1988); and
C. Henny, L. Blus, S. Gregory, and C. Stafford, “PCBs and Organochlorine
Pesticides in Wild Mink and River Otters from Oregon,” in Proceedings of
Worldwide Furbearer Conference, J. Chapman and D. Pursley, eds., Frost
burg, Maryland, 1981, pp. 1763-80.
The history discussed in the paragraph starting “The demise of . . .” is
described in much greater detail in T. Colborn, A. Davidson, S. Green,
R. Hodge, C. Jackson, and R. Liroff, Great Lakes, Great Legacy?, The Con-
i
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NOTES
servation Foundation and the Institute for Research on Public Policy, 1990.
The reference to dioxin in this paragraph is based on M. Walker and R. Pe
terson, “Toxicity of Polychlorinated Dibenzo-p-Dioxins, Dibenzofurans,
and Biphenyls During Early Development in Fish, in Chemically Induced
Alterations in Sexual and Functional Development: The Wildlife-Human
Connection, T. Colborn and C. Clement, eds., Princeton Scientific Publish
ing, 1992, pp. 195-202; and P. Cook, D. Kuehl, M. Walker, and R. Peterson,
“Bioaccumulation and Toxicity of TCDD and Related Compounds in
Aquatic Ecosystems,” Banbury Report 35: Biological Basis for Risk Assess
ment of Dioxins and Related Compounds, Cold Spring Harbor Laboratory
Press, 1991, pp. 143-67; and personal communication with Phil Cooke,
U.S. Environmental Protection Agency, Duluth, Minnesota, 1995.
For more information about the conditions described in the passage
starting “Egg mortality . . . ,” see J. Leatherland, Endocrine and Reproduc
tive Function in Great Lakes Salmon,” in Chemically Induced Alterations,
..
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pp. 129-45.
The paragraph commencing “In Europe and Scandinavia . . . leads
into a section on marine mammals that is based on work already cited
throughout. See especially the section in Chapter 1 on marine mammal
die-offs. For further reviews, see P. Reijnders and S. Brasseur, Xenobiotic
Induced Hormonal and Associated Developmental Disorders in Marine
Organisms and Related Effects in Humans: An Overview,” in Chemically
Induced Alterations, pp. 159—74; J. Raloff, “Something s Fishy: Marine Epi
demics May Signal Environmental Threats to the Immune System, Science
News, 146:8-9 (1994); and T. Colborn and M. Smolen, “An Epidemiological
Analysis of Persistent Organochlorine Contaminants in Cetaceans, Re
views of Environmental Contaminants and Toxicology (in press).
“A second study ...” refers to the work of G. Lahvis and coworkers
R. Wells, D. Casper, and C. Via, reported in “In Vitro Lymphocyte Response
of Bottlenose Dolphins (Tursiops truncatus): Mitogen-Induced Proliferation,
Marine Environmental Research 35:115-19 (1993); and G. Lahvis, R. Wells,
D. Kuehl, J. Stewart, H. Rhinehart, and C. Via, “Decreased Lymphocyte Re
sponses in Free-Ranging Bottlenose Dolphins (Tursiops truncatus) Are Associ
ated with Increased Concentrations of PCBs and DDT in Peripheral Blood,
Environmental Health Perspectives Supplements 103(4):67—72 (1995).
As a follow-up to the paragraph starting “Even less is known . . . , see
R. Stebbins and N. Cohen, A Natural History of Amphibians, Princeton Uni
versity Press, 1995; and A. Blaustein, D. Wake, and W. Sousa, “Amphibian
Declines: Judging Stability, Persistence, and Susceptibility of Populations to
Local and Global Extinctions,” Conservation Biology 8(l):60-71 (1994).
I
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283
Chapter 10: ALTERED DESTINIES
I
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The paragraph opening “The relevance of..leads into a discussion of the
work of F. vom Saal, S. Nagel, P. Palanza, M. Boechler, S. Parmigiani, and
W. Welshons, reported in “Estrogenic Pesticides: Binding Relative to Estra
diol in MCF-7 Cells and Effects of Exposure During Fetal Life on Subsequent
Territorial Behavior in Male Mice,” Toxicology Letter (in press, 1995).
“At the end .. refers to the Wingspread Consensus Statement,
which is Chapter One in Chemically Induced Alterations in Sexual and
Functional Development: The Wildlife-Human Connection, T. Colbom and
C. Clement, eds., Princeton Scientific Publishing, 1992. It is printed in the
Appendix of this book.
“Based on warnings . .is supported by R. Newbold, B. Bullock, and
J. Mclachlan, “Uterine Adenocarcinoma in Mice Following Developmental
Treatment with Estrogens: A Model for Hormonal Carcinogenesis,” Cancer
Research 50:7677-81 (1990); H. Bern and F. Talamantes, “Neonatal Mouse
Models and their Relation to Disease in the Human Female,” in Developmen
tal Effects of Diethylstilbestrol (DES) in Pregnancy, A. Herbst and H. Bem,
eds., Thieme-Stratton, 1981, pp. 129-47; and B. Bullock, R. Newbold, and
J. McLachlan, “Lesions of Testis and Epididymis Associated with Prenatal
Diethylstilbestrol,” Environmental Health Perspectives 77:29-31 (1988).
“Laboratory experiments ...” refers to L. Birnbaum, “Endocrine Effects
of Prenatal Exposures to PCBs, Dioxins, and Other Xenobiotics: Implica
tions for Policy and Future Research,” Environmental Health Perspectives
102(8):676-79 (1994).
“The most dramatic . . .” refers to E. Carlsen et al., 1992, cited in
Chapter 1.
The passage starting “The study is ...” points out the difficulty of
recognizing a reduction in sperm count. Traditionally, andrologists consid
ered a sperm count under 50 million sperm per milliliter a signal of a reduc
tion in fertility. More recently, this benchmark has been lowered to 20
million sperm per milliliter. However, even at 20 million sperm per milli
liter most men can produce viable offspring, given sufficient opportunity.
The skeptics include P. Bromwich, J. Cohen, I. Stewart, and A. Walker,
“Decline in Sperm Counts: An Artifact of Changed Reference Range of
‘Normar?” British Medical Journal 309:19-22 (1994); and G. Olsen, K. Bodner,
J. Ramlow, C. Ross, and L. Lipshultz, “Have Sperm Counts Been Reduced
50 Percent in 50 Years? A Statistical Model Revisited,” Fertility and Sterility
63(4):887-93 (1995).
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284
f'
NOTES
“This debate stimulated . . .n refers to J. Auger, J. Kunstmann,
F. Czyglik, and P. Jouannet, “Decline in Semen Quality Among Fertile
Men in Paris During the Past 20 Years/’ New England Journal of Medicine
B2(5):281-85 (1995); K. Van Waeleghem, N. De Clercq, L. Vermeulen,
F. Schoonjans, and F. Comhaire, “Deterioration of Sperm Quality in Young
Belgian Men During Recent Decades,” in Abstracts of the Annual Meeting
of the ESHRE, Brussels, 1994, p. 73; and D. Irvine, “Falling Sperm Quality,”
letter to the editor, British Medical Journal, 309:131 (1994).
“When Sharpe and Skakkebaek . . .” refers to their article, R. Sharpe
and N. Skakkebaek, “Are Oestrogens Involved in Falling Sperm Counts and
Disorders of the Male Reproductive Tract?” Lancet 341:1392-95 (1993).
For more information on undescended testicles, see C. Chilvers, M. Pike,
D. Forman, K. Fogelman, and M. Wadsworth, “Apparent Doubling of Fre
quency of Undescended Testis in England and Wales in 1962-81,” Lancet
330-32 (1984); and J. Hutson, M. Baker, M. Terada, B. Zhou, and G. Pax
ton, “Hormonal Control of Testicular Descent and the Cause of Cryp
torchidism,” Reproduction, Fertility, and Development 6:151-56 (1994). The
latter describes what is known about testicular descent, the multifactorial
etiology of cryptorchidism, and mentions the role estrogens, anti-androgens,
and Mullerian inhibiting substances (MIS) play in prenatal differentiation
of tissue that could become ovary or testis.
“Synthetic chemicals have . . .” mentions Dorothea Sager; her work
was cited in Chapter 7. The paragraph closes with a description of the work
of Brian Bush and associates cited in Chapter 6.
“Before biological research ...” refers to reports from the National
Center for Health Statistics, Hyattsville, Maryland; and Congressional Of
fice of Technology Assessment, “Infertility: Medical and Social Choices,”
U.S. Government Printing Office, May 1988. The $2 billion is a figure
gleaned from an interview with Joyce Zeitz of the American Fertility Society,
Birmingham, Alabama.
“Prenatal exposure .. .” refers to a discussion in Chapter 3. See cita
tions there.
“In ongoing studies ...” touches on F. vom Saal, M. Dhar, V. Ganjam,
and W. Welshons, “Prostate Hyperplasia and Increased Androgen Recep
tors in Adulthood Induced by Fetal Exposure to Estradiol in Mice,” Ab
stract for the Fall Meeting of the Society for Basic Urologic Research,
Stanford University, 1994.
“Even in males . . .” refers to S. Ho and M. Yu, “Selective Increase in
Type II Estrogen-Binding Sites in the Dysplastic Dorsolateral Prostates of
Noble Rats,” Cancer Research 53:528-32 (1993), personal communication
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285
with Ho, 1995, and from a discussion with Dr. Ronald McDaniels, Abbott
Pharmaceuticals, and a paper, J. Oesterling, “Benign Prostatic Hyperplasia:
Diagnosis and Treatment Options/’ New England Journal of Medicine
332(2):99 (1995). Oesterling states that 400,000 transurethral resections of
the prostate are performed each year at a cost of 5 billion dollars. Mc
Daniels estimates an additional 1 billion dollars for drug therapy.
The figures concerning breast cancer in the passage starting “Over the
past . . .” come from a review of the National Cancer Institute, SEER Sta
tistics, and reviews of existing data by the authors.
“Despite more sophisticated ...” uses data from Centers for Disease
Control, “Radical Prostatectomies—Wisconsin, 1982-1992,” Morbidity and
Mortality Weekly Report 42(32):620—21, 627 (1993); and “Trends in Prostate
Cancer—United States, 1980-1988,” Morbidity and Mortality Weekly Re
port 41:401-404 (1992).
“In tubal or ectopic ...” states that repeated tubal pregnancies can
result in infertility. There are no official estimates on the proportion of
female infertility caused by endometriosis, but Zeitz of the American Fer
tility Society estimates that it might be responsible for twenty percent of
the cases. The other two leading causes are ovulatory and tubal problems—
problems reported in DES daughters.
For historical information about “Endometriosis, a poorly . . . ,” see
J. Older, “Leaches and Laudanum: Grandmother and You: Historical High
lights,” Endometriosis7 Scribners, 1964. The National Institute of Child Health
publication mentioned is “Facts About Endometriosis,” No. 91-2413 (no date).
“After years of debate ...” was drawn from a conversation with Mary
Lou Balweg, The Endometriosis Association, Milwaukee, Wis. 1994; and from
S. Rier, D. Martin, R. Bowman, W. Dmowski, and J. Becker, “Endometriosis in
Rhesus Monkeys (Macaca mulatta) Following Chronic Exposure to 2,3,7,8Tetrachlorodibenzo-p-dioxin,” Fundamental and Applied Toxicology 21:433-41
(1993).
“Animal studies also . . .” also leans on Rier et al., 1993, and mentions
V. Leoni, L. Fabiani, G. Marinelli, G. Puccetti, G. Tarsitani, A. De Carolis,
N. Vescia, A. Morini, V. Aleandri, V. Pozzi, F. Cappa, and D. Barbati, “PCB
and Other Organochlorine Compounds in Blood of Women with or With
out Miscarriage: A Hypothesis of Correlation,” Ecotoxicology and Environ
mental Safety 17:1-11 (1989).
In connection with the paragraph opening “But by far ... ,” see
D. Davis and H. Freeman, “An Ounce of Prevention,” Scientific American,
September 1994, p. 112.
'Because total estrogen . . .” refers to D. Hunter and K. Kelsey, “Pesti-
!
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NOTES
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cide Residues and Breast Cancer: The Harvest of a Silent Spring?” Journal
of the National Cancer Institute 85(8):598-99 (1993).
For more information concerning the paragraph starting “The most
notable . . .see P. Pujol, S. Hilsenbeck, G. Chamness, and R. Elledge,
“Rising Levels of Estrogen Receptor in Breast Cancer over 2 Decades,”
Cancer 74(5):1601-1606 (1994).
For the passage that begins “In 1993, a group ...see D. Davis,
H. Bradlow, M. Wolff, T. Woodruff, D. Hoel, and H. Anton-Culver, “Med
ical Hypothesis: Xenoestrogens as Preventable Causes of Breast Cancer,”
Environmental Health Perspectives 101 (5):372—77 (1993).
“Researchers have been . ..” refers to E. Dewailly, S. Dodin, R. Verreault, P. Ayotte, L Sauve, J. Morin, and J. Brisson, “High Organochlorine
Body Burden in Women with Estrogen Receptor-Positive Breast Cancer,”
Journal of the National Cancer Institute 86(3) :232—34 (1994).
“Two other studies ...” refers to M. Wolff, P. Toniolo, E. Lee, M. Rivera,
and N. Dubin, “Blood Levels of Organochlorine Residues and Risk of Breast
Cancer,” Journal of the National Cancer Institute 85 (8):648—52 (1993). How
ever, N. Krieger, M. Wolff, R. Hiatt, M. Rivera, J. Vogelman, and N. Orentreich, “Breast Cancer and Serum Organochlorines: A Prospective Study
Among White, Black, and Asian Women,” Journal of the National Cancer
Institute 86(8):589-99 (1994), found that breast cancer patterns varied
among racial groups. They found a positive but not statistically significant
association between DDT and breast cancer in Caucasians and AfricanAmericans, but no association for Asians. See a letter from M. Wolff and P.
Landrigan, “Response to Environmental Estrogens Stir Debate,” Science
266:526-27 (1994).
“Among cancer victims . . .” refers to D. Hoel, D. Davis, A. Miller,
E. Sondik, and A. Swerdlow, “Trends in Cancer Mortality in 15 Indus
trialized Countries, 1969-1986,” Journal of the National Cancer Institute
84(5):313-20 (1992).
“What little we ...” refers to The Merck Manual of Diagnosis and Ther
apy, 15th ed., R. Berkow and A. Fletcher, eds., Merck Sharp and Dohme Re
search Laboratories, 1987, p. 1978. For more information on attention deficit
disorder, see P. Hauser, A. Zametkin, P. Martinez, B. Vitiello, J. Matochik,
A. Mixson, and B. Weinstraub, “Attention Deficit-Hyperactivity Disorder
in People with Generalized Resistance to Thyroid Hormone,” New England
Journal of Medicine 328 (14) :997-l 001 (1993).
“It has long . ..” mentions S. Porterfield, “Vulnerability of the Devel
oping Brain to Thyroid Abnormalities: Environmental Insults to the Thy
roid System,” Environmental Health Perspectives 102(2): 125-30 (1994),
1
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287
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S. Porterfield and S. Stein, “Thyroid Hormones and Neurological Develop
ment: Update 1994,” Endocrine Reviews 3(1)357-63 (1994); and S. Porter
field and C. Hendrich, “The Role of Thyroid Hormones in Prenatal and
Neonatal Neurological Development—Current Perspectives,” Endocrine
Reviews 14(l):94-106 (1993).
For more information concerning the paragraph starting “PCBs and
dioxin . . .see H. Pluim, J. de Vijlder, K. Olie, J. Kok, T. Vulsma, D. van
Tijn, J. van der Slikke, and J. Koppe, “Effects of Pre- and Postnatal Expo
sure to Chlorinated Dioxins and Furans on Human Neonatal Thyroid Hor
mone Concentrations," Environmental Health Perspectives 101 (6):504-508
(1993); D. Bombick, J. Jankun, K. Tullis, and F. Matsumura, “2,3,7,8Tetrachlorodibenzo-p-dioxin Causes Increases in Expression of c-erb-A and
Levels of Protein-Tyrosine Kinases in Selected Tissues of Responsive Mouse
Strains,” Proceedings of the National Academy of Sciences 85:4128-32
(1988); A. Brouwer, “Inhibition of Thyroid Hormone Transport in Plasma
of Rats by Polychlorinated Biphenyls,” Archives of Toxicology Supplements
13:440-45 (1989); A. Brouwer, E. Klasson-Wehler, M. Bokdam, D. Morse, and
W. Traag, “Competitive Inhibition of Thyroxin Binding to Transthyretin by
Monohydroxy Metabolites of 3,4,3',4'-Tetrachlorobiphenyl,” Chemosphere
20(7—9): 1257—62 (1990); D. Morse, H. Koeter, A. Smits van Prooijen, and
A. Brouwer, “Interference of Polychlorinated Biphenyls in Thyroid Hormone
Metabolism: Possible Neurotoxic Consequences in Fetal and Neonatal
Rats,” Chemosphere 25(1-2):165—68 (1992); and D. Ness et al., 1993, cited
in Chapter 6.
“Based on the . ..” refers to a conversation with Linda Birnbaum,
1994; and H. Tilson, J. Jacobson, and W. Rogan, “Polychlorinated
Biphenyls and the Developing Nervous System: Cross-Species Compar
isons,” Neurotoxicology and Teratology 12:239-48 (1990). This paper pre
sents an excellent review. The studies that Tilson and coauthors referred
to did not permit the researchers to separate the effects of exposure in the
womb from exposure via breast milk. However, the researchers later de
termined that the effects they were measuring were the result of prenatal
exposure.
“Much of our. . cites Y. Guo, G. Lambert, and C.-C. Hsu, “Growth
Abnormalities in the Population Exposed to PCBs and Dibenzofurans,” pa
per presented at Children’s Environmental Health Network Conference,
1994. See also M. Yu, C. Hsu, Y. Guo, T. Lai, S. Chen, and J. Luo, “Disor
dered Behavior in the Early-Born Taiwan Yucheng Children,” Chemosphere
29(9—11):2413—22 (1994); for further reading about the rice oil incidents,
see W. Rogan, B. Gl.iden, K. Hung, S. Koong, L. Shih, J. Taylor, Y. Wu,
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D. Yang, N. Ragan, and C.-C. Hsu, “Congenital Poisoning by Polychlori
nated Biphenyls and Their Contaminants in Taiwan,” Science 241:334-36,
(1988); and W. Rogan, “PCBs and Cola-Colored Babies: Japan, 1968, and
Taiwan, 1979,” Teratology 26:259-61 (1982).
The first study . . .” refers to J. Jacobson, S. Jacobson, P. Schwartz,
G. Fein, and J. Dowler, “Prenatal Exposure to an Environmental Toxin: A
Test of the Multiple Effects Model,” Developmental Psychology 20(4):523-32
(1984). There were 242 infants of fisheaters and 71 infants whose mothers
ate no Lake Michigan fish in the study. The figure on the value of the sports
fishing industry in the Great Lakes was taken from D. Talheim, “Economics
of Great Lakes Fisheries: A 1985 Assessment,” Special Economic Report,
Great Lakes Fishery Commission, Ann Arbor, Mich., 1987.
“The second study ...” refers to B. Gladen, W. Rogan, P. Hardy,
J. Thullen, J. Tirigelstad, and M. Tully, “Development After Exposure to
Polychlorinated Biphenyls and Dichlorodiphenyl Dichloroethene Transplacentally and Through Human Milk,” Journal of Pediatrics 113(6):991—95
(1988); and W. Rogan, B. Gladen, J. McKinney, N. Carreras, P. Hardy,
J. Thullen, J. Tinglestad, and M. Tully, “Neonatal Effects of Transplacental
Exposure to PCBs and DDE,” Journal of Pediatrics 109(2) .-335—41 (1986).
For more extensive information about the section that begins “At the
State University . . .,” see H. Daly, “The Evaluation of Behavioral Changes
Produced by Consumption of Environmentally Contaminated Fish,” in
The Vulnerable Brain and Environmental Risks: Vol. 1. Malnutrition and
Hazard Assessment, Chapter 7, R. Isaacson and K. Jensen, eds.. Plenum,
1992, pp. 151-71; H. Daly, “Laboratory Rat Experiments Show Consump
tion of Lake Ontario Salmon Causes Behavioral Changes: Support for
Wildlife and Human Research Results,” Journal of Great Lakes Research
19(4):784—88 (1993); and H. Daly, “Reward Reductions Found More Aver
sive by Rats Fed Environmentally Contaminated Salmon,” Neurotoxicology
and Teratology 13:449-53 (1991).
“In May 1995 .. .” refers to a paper presented by H. Daly at the 38th
Annual Conference of the International Association for Great Lakes Re
search (IAGLR), East Lansing, Michigan, and a May 27, 1995, press release
by the State University of New York, Oswego, pointing out that this “is the
first large-scale replication and extension of the Jacobsons’ Lake Michigan
Infant Cohort Study.” Only associations with the amount of fish eaten over
a lifetime were reported at this time. The statistical results of chemical
analysis on mother’s blood, placental blood, and breast milk will be released
in a series of future papers.
In 1991, Dr. Simon LeVay . . . refers to S. LeVay, “A Difference in
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Hypothalamic Structure Between Heterosexual and Homosexual Men,”
Science 253:1034-37, 1991; and S. LeVay, The Sexual Brain, MIT Press,
1993, p. 168.
Upon finishing this chapter the reader might want to see “Male Re
productive Health and Environmental Oestrogens,” editorial in Lancet
345:933-35 (1995); or R. Sharpe, “Another DDT Connection,” News and
Views article in Nature 375:538-39 (1995); and, as well, “Masculinity at
Risk,” Opinion article in Nature 375:522 (1995). See also A. Abell, E. Ernst,
and J. Bonde, “High Sperm Density Among Members of Organic Farmers'
Association,” Lancet 343:1498 (1994).
Chapter 11: BEYOND CANCER
The first paragraph refers to H. Burlington and V. Lindeman, 1950, cited in
Chapter 5.
“The study provided .. .,f leans on T. Dunlap, DDT: Scientists, Citizens,
and Public Policy, Princeton University Press, 1981, p. 70; and C. Bosso, Pesti
cides and Politics: The Life Cycle of a Public Issue, University of Pittsburgh
Press, 1987.
“By the 1960s . . Z’ refers to R. Carson, Silent Spring, Houghton Mif
flin, 1962.
For interesting reading about the 1972 decision to restrict the use of
DDT (as mentioned in the paragraph that opens “Cancer holds a special..
see U.S. Environmental Protection Agency I. F. and R. Docket 63, “Consoli
dated DDT Hearings: Opinion and Order of the Administrator,” Federal Reg
ister 37 (131):13369-76,July7,1972.
“The federal appeals ..refers to Environmental Defense Fund v. U.S.
Department of Health Education and Welfare, 1970, U.S. Court of Appeals,
District of Columbia Circuit.
“Some critics of EPA ...” refers to those who insist that low-dose ex
posure is tolerable; for example, P. Abelson, “Risk Assessments of LowLevel Exposures,” editorial in Science 265:1507 (1994).
“Those studying ...” mentions the complexity of feedback loops in
the endocrine system; for example, within one low range of exposure one
response may prevail—but as doses increase another response may set in,
with part of the impact being to shut down the first response.
“As EPA toxicologist Linda Birnbaum ...” refers again to her 1994 pa
per cited in Chapter 10. The Seveso studies by Bertazzi et al. were cited in
Chapter 7. An earlier study looked for birth defects in children and con-
290
NOTES
eluded that "although the data collected failed to demonstrate any increased
risk of birth defects associated with 2,3,7,8-tetrachlorodibenzo-p-dioxin, the
number of exposed pregnancies was not big enough to show a low and spe
cific teratogenic risk increase” (P. Mastroiacovo, A. Spagnolo, E. Marni,
L. Meazza, R. Bertollini, and G. Segni, "Birth Defects in the Seveso Area
After TCDD Contamination,” Journal of the American Medical Association
259(11):1668-72 [1988]).
"If we are . ..” gets into a discussion about the weight-of-evidence
approach to deal with difficult decisions concerning cause and effect. See
G. Fox, "Scientific Principles in Applying the Weight of Evidence” in
Applying Weight of Evidence: Issues and Practice, Canadian and U.S. In
ternational Joint Commission, June 1994; and G. Fox, "Practical Causal In
ference for Ecoepidemiologists,” Journal of Toxicology and Environmental
Health 33:359-73 (1991).
Chapter 12: DEFENDING OURSELVES
"Unfortunately, however, solutions ...” refers to findings like that of
S. Hooper et al., 1990, cited in Chapter 6. For the closing sentence of this
paragraph, see D. Patterson, Jr., G. Todd, W. Turner, V. Maggio, L. Alexan
der, and L. Needham, "Levels of Non-ortho-substituted (Coplanar), Monoand Di ortho-substituted Polychlorinated Biphenyls, Dibenzo-p-dioxins,
and Dibenzofurans in Human Serum and Adipose Tissue,” Environmental
Health Perspectives Supplements 102( 1): 195—204 (1994); and once again see
L. Birnbaum, 1994, cited in Chapter 10.
The following are only a few organizations that are structured to deal
with the vast questions that are emerging as more and more people want to
learn how to deal with synthetic chemicals in their environment:
1
Rachel Carson Council, 8940 Jones Mill Road, Chevy Chase, MD
20815; tel. 301-652-1877; fax 301-951-7179. Provides information re
garding pesticides and alternatives.
■ National Coalition Against the Misuse of Pesticides (NCAMP), 701
E Street, SE, Washington, DC 20003; tel. 202-541-5450; fax 202543-4791. Provides information regarding pesticide use.
■ American PIE (American Public Information on the Environment),
31 North Main Street, P.O. Box 460, Marlborough. CT 06447-0460;
tel. 800-320-APIE[2743]. Provides information about environmen
tally safe practices for home, office, and the outdoors. It can advise on
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topics ranging from drinking water safety to household waste to lawn
and garden practices.
■ Enviro-Health, 100 Capitola Drive, Suite 108, Durham, NC 27713;
tel. 800-NIEHS-94[643-4794]; fax 919-361-9408. This is the environ
mental health effects clearinghouse of the National Institute of Envi
ronmental Health Sciences (NIEHS), U.S. Department of Health and
Human Services. Topics include human health, general health, chemi
cal exposures, multiple chemical sensitivity, immunotoxicity, water and
air quality, NIEHS research, education and information, hazardous
waste, and more.
■ Pesticide Action Network (North America), 116 New Montgomery
Street, #810, San Francisco, CA 94105; tel. 415-541-9140; fax 415541-9253; gopher site: gopher.econet.ape.org provides information on
the global use of pesticides.
For further reading related to the section titled “Choose Your Food
Intelligently," we recommend H. Needleman and P. Landrigan, Raising
Healthy Children, Farrar, Straus, and Giroux, 1994; and A. Garland, The
Way We Grow, Berkley, 1993.
“Clean fish are ..." refers to health advisories for fish. The first U.S.
review of fish advisories was D. Zeitlin, “State-Issued Fish Consumption
Advisories: A National Perspective," for the National Oceanic and Atmos
pheric Administration, National Ocean Pollution Program Office, Wash
ington, D.C., 1990.
“Avoid animal fat..." leads into a discussion about persistent chemicals
building up in animal tissue. More and more laboratories are acquiring the
equipment and technology to detect “low levels" of chemicals in food prod
ucts, and as a result, new papers are appearing regularly in the scientific lit
erature. Surprisingly, it appears as though dioxin is being delivered to
millions daily through their favorite food, the hamburger.
An article that provides more food for thought concerning the para
graph starting “Researchers are only . . ." is K. Uvnas-Moberg, “The Gastroin
testinal Tract in Growth and Reproduction," Scientific American, July 1989,
pp. 78-83. The author states that the gastrointestinal tract “is the largest en
docrine gland in the body, and it has a significant role in the readjustment of
metabolism that accompanies pregnancy as well as fetal and infant growth."
In this and other writings the author notes that oxytocin levels increase in
women during pregnancy and breast feeding and thus increase their social
sensitivity and bonding. She also notes that an infant's weight doubles during
its first six months. A six-week-old baby, weighing about 9 pounds, drinks ap-
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proximately 22 ounces of milk a day. If the mother, weighing approximately
140 pounds, consumed a proportional amount of milk, she would drink about
10 quarts or 342 ounces a day. We should like to point out that this source of
high energy for the infant also provides the medium to transport high doses
of fat-soluble chemicals to the baby.
For more reading following the discussion in the paragraph starting
“Never assume a pesticide . . .,” see C. Clement and T. Colborn, “Herbi
cides and Fungicides: A Perspective on Potential Human Exposure/’ in
Chemically Induced Alterations in Sexual and Functional Development: The
Wildlife-Human Connection, T. Colborn and C. Clement, eds., Princeton
Scientific Publishing, 1992, pp. 347-64. The chapter cited reveals how little is
known about the pesticide (Dacthal or DCPA) most frequently found in
groundwater in the United States. Dacthal was discovered in trout and
whitefish tissue from Siskiwit Lake on Isle Royale in Lake Superior, evi
dence that this product volatilizes and moves on air currents as well. See
D. Swackhamer and R. Hites, “Occurrence and Bioaccumulation of
Organochlorine Compounds in Fishes from Siskiwit Lake, Isle Royale,
Lake Superior,” Environmental Science and Technology 22(5):543—48 (1988).
“Don’t be blase ...” discusses “inerts.” See a video narrated by Dr.
Mary O’Brien, “Inert Alert: Secret Poisons in Pesticides,” The Northwest
Coalition for Alternatives to Pesticides, 1991; available from S. Genasci,
P.O. Box 1393, Eugene, OR 97440. See also D. Krewski, J. Wargo, and
R. Rizek, “Risks of Dietary Exposure to Pesticides in Infants and Children,”
in Monitoring Dietary Intakes, I. Macdonald, ed., Springer-Verlag, 1991,
pp. 75-89. The authors point out that nearly three hundred pesticide active
ingredients used in commercial agricultural products are tolerated as food
residues under U.S. EPA regulations.
“Be aware that .. .” cites the results of a report by the Attorney Gen
eral of New York State, “Toxic Fairways: Risking Groundwater Contamina
tion from Pesticides on Long Island Golf Courses,” 1991.
For further reading about alternative production processes, we recom
mend P. Hawken. The Ecology of Commerce, Harper Business, 1993.
“Garden designers ...” discusses redesigning yards and lawns to reduce
chemical use. Once you have established a chemical-free yard, send to
American PIE for a set of lawn flags boasting that your lawn is “SAFE TO PLAY
ON.” American PIE’s address and phone number are given above in the cita
tions for this chapter.
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293
i
Chapter 13: LOOMINGS
l.'-'
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For the closing section of the paragraph starting “If currently regulated ...
see V. Bhatnagar, J. Patel, M. Variya, K. Venkaiah, M. Shah, and S. Kashyap,
“Levels of Organochlorine Insecticides in Human Blood from Ahmedabad
(Rural), India,” Bulletin of Environmental Contamination and Toxicology
48302-307 (1992).
The decline discussed in the paragraph starting “Why did the Scholas
tic ...” was described in a report of the Advisory Panel on the Scholastic Apti
tude Test Score Decline for the College Entrance Examination Board New
York, 1977.
“Consider, however ...” refers to B. Weiss, “The Scope and Promise
of Behavioral Toxicology,” in Behavioral Measures of Neurotoxicity: Report
of a Symposium, R. Russell, P. Flattau, and A. Pope, eds., National Research
Council, National Academy Press, 1990, pp. 395-413. The numbers of indi
viduals affected at the high and low ends of the IQ scale are based on the
assumption that the standard deviation of 15 holds after a 5-point popula
tion-wide IQ decrease.
“Other studies suggest ...” discusses the research of Fred vom Saal
and coworkers at the University of Missouri cited in earlier chapters and the
research of Dr. Warren Porter and coworkers, Zoology Department, Uni
versity of Wisconsin, Madison, in which they gave rats and mice free access
to water containing mixtures of pesticides and nutrients commonly found
in wells in Dane County; see W. Porter, S. Green, N. Debbink, and I. Carl
son, “Groundwater Pesticides: Interactive Effects of Low Concentrations of
Carbamates, Aldicarb and Methomyl, and the Triazine Metribuzin on Thy
roxine and Somatotropin Levels in White I^ats,” Journal of Toxicology and
Environmental Health 40:15-34 (1993).
Chapter 14; FLYING BLIND
The historical account of Midgely’s work and other aspects of the ozone his
tory leans on S. Cagin and P. Dray, Between Earth and Sky: How CFCs
Changed Our World and Endangered the Ozone Layer, Pantheon, 1993. We
also supplemented with our own research.
"Du Pont was ..mentions S. Rowland and M. Molina, "Stratospheric
Sink for Chlorofluoromethanes: Chlorine Atom-Catalyzed Destruction of
Ozone,” Nature, June 28, 1974. The authors are recent Nobel Prize winners.
.
294
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To our knowledge, endocrine disruption is not among the adverse health ef
fects associated with reduced ozone in the stratosphere.
The situation confronting . . cites a figure taken from a seminar
presented by Brad Leinhart, Chlorine Chemical Council, Chemical Manuacturer s Association, Massachusetts Institute of Technology, January 26
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INDEX
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Page numbers in boldface refer to illustrations.
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Achromobacter bacteria, 96
Additive effects, 140, 220
Adenocarcinoma, 58
Adrenal glands, 32,70, 85
Africa, 136
Agent Orange, 113-14
Aggression, 30-37,64
and societal change, 232, 237
Agriculture, 151, 223, 224, 228-29
Aguilar, Alex, 8-9
AIDS, 62-63,147
Aldrin, 96
Alfalfa sprouts, 79
Algae, 95-96
Alkylphenols, 128-29,134,224
Allergies, 60
Alligators, 6, 150-53, 168, 189
American Fertility Society, 178
American Gynecological Society, 54
Androgen blockers, 84, 135,139,177
Androgen receptor, 83, 84,179
Anholt island, 7
Animal (s)
fat, avoiding, 214
feed and implants, 48
human fate connected with, 167
population declines, 147-66
See also specific animals
Animal studies
applied to humans, 59, 63-64, 86, 168-69,
171-72, 189
and DES, 62-64
and PCBs, 188-89
Anniston, Alabama, 91,104
Anorexia nervosa, 65
Antibiotic resistance, 230
Anxiety, 65
Apopka, Lake, 6,150,151,153, 189
Aquatic Toxicity Workshop, 16
Arctic, 101-2,107-9, 167
Aroclor-1254,91,92
Arthritis, 60, 61
Aryl hydrocarbon (Ah) receptor, 120
Atlantic Ocean, 160
Atrazine, 184, 213
Attention deficits, 189, 206, 208
Auger, Jacques, 175
Aulerich, Richard, 156
Australia, 114, 160, 162
Australian Veterinary Journal, 76
Autoimmune diseases, 63
Automobile manufacturing, 227-28
Baby formulas, soy-based, 82
Bacteria, 123
Baikal, Lake, 160, 167
__ ___________
1
296
Baker, Michael, 86
Bald eagles, 1-2, 14, 20, 23,25,99, 154-55
168
Baltic Sea, 18, 159, 160, 161, 167
Barcelona, University of, 8
Behavior abnormalities
in children, 186-94, 235
and DES, 63-66
and human society, 231, 235-38
and PCBs, 192-93
and prenatal hormones, 45-46
in wildlife, 10, 21, 22
Beland, Pierre, 142-45, 146, 147
Beluga whales, 142-47, 165
Bengtsson, Bengt-Erik, 17-18, 23
Bern, Howard, 58, 73-74, 110, 150, 170
Big Cypress swamp, 148
Big Spring, Texas, 93-94, 104
“Binding” chemical, 70
Biodiversity, 165
Biological mechanisms research, 224
Biomagnification, 26-28, 104-5
Birds, 20, 168
and DDT, 14
and hormone-disruptors, 164-65
male feminized, 21-22, 23, 153
migrations, 164-66
and sex differentiation, 42
water, decline, 224
Birnbaum, Linda, 84, 85, 188, 206
Birth control
natural plant, 78-79, 82
pills, 133
Birth defects, 26, 49-51, 115, 154-55
Bisexuality, 65, 195
Bisphenol-A, 130-31, 135, 185,217
Black River, 17
Bladder cancer, 144
Blood proteins, 140
Body fat
and breast milk, 146
chemicals in, 28, 168
DDE in, 139
and diet, 214
dioxin in, 113
and migratory birds, 165
PCBs in, 96, 98, 106—9, 187, 190-91
and pregnant women, 212
Bone-marrow cancer, 115
Booly (whale), 144-45, 146
Boston Globe, 52
Bowman Gray School of Medicine, Wake
Forest University, 77
Bradlow, H. Leon, 183-84
Brain
and DES, 62, 63-66
and dioxin, 116, 119, 120
INDEX
human, 187-94, 206-7
and nervous system, 32
and plant estrogens, 79-80
and prenatal hormones, 45-46
and receptors, 70
and sexual orientation, 195
and societal problems, 231-38
tumors, 33
Braungart, Michael, 226-27, 228
Breast, 33
and marijuana, 77-78
Breast cancer, 197
Carson and, 200, 201
and DES, 62,63
and dioxin, 115
and estrogen-induced growth studies
123-31, 140
increasing, 172, 182-86, 201
and plant estrogens, 80
and prenatal estrogen, 62
and synthetic chemicals, 84, 85
Breast milk
and beluga deformities, 145-46
contamination of, effects on humans
106-9,191
and decision to breast feed, 215-16
dioxin in,118
PCBs in, 92,106, 108-9, 156, 178, 187
PCBs in, and behavior problems, 188—94,
research on, 225
British Medical Journal, 172
Broley, Charles, 1
Broughton Island, Canada, 107-9
Brunel University, 131-32
Burlington, Howard, 69, 198, 199, 200 201
203
f
’
Cabbage family, 184
California, University of, 5, 21, 64 73 86
150
r ’
Canadian Institute for Research on Public
Policy, 13
Canadian Wildlife Service, 4, 20, 208
Cancer
and Agent Orange, 114
in beluga whales, 144
and DES, 52-54, 57-58, 60-63
and dioxin, 115,116-17
and estrogen metabolism, 183—86
focus on, vs. other negative effects, 19-20
198-203, 208-9
and Great Lakes, 15-26, 18-20
hormone-responsive, 172
human, and animal testing, 169
and plant estrogens, 80
and prenatal history, 57-58
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registries, 15, 18
and regulatory biases, 202
Cancer, 183
Cans, 134-35, 185
Carbon-based chemicals, 137-38
Carcinogens, 205
Caribou, 108
Carson, Rachel, 15, 51, 96, 167, 210, 230
Catfish, 17
Cell proliferation, 122-23
Cervical cancer, 62
Channel Islands, California, 5-6
Chapman, Sydney, 245
Cheese, 214
Chemical manufacturers, 219, 245
Chemical messengers, 29-46,70, 204
Chemicals (synthetic or man-made)
animals studies on, and humans, 168-69
and Arctic peoples, 107-8
cause and effect links, 196-97
debate over dangers of, 135-36
and fish cancer, 16-17
global contamination by, 240, 244
hormonal effects, 67
in humans, 106—9, 140-41
and immune system, 161-62
levels, regulating, 220
measurement, 226
number of, 18, 80-86, 137-41, 194
prenatal exposure, 57-58
receptor effects of, 72, 72-73, 84
reducing number of, 226-27
regulation of, 218-22
research on, 222-25
rethinking use of, 226-30, 239-49
safety data on, 18, 139, 140
threat to human health by, 170-97
timing of exposure, 50-51
See also Hormone disruptors; and specific
chemicals
Chicago, University of, 54, 59
Chickens, 4, 22
Children
protecting from exposure, 212-22
neglect and abuse, 237-38
Chloracne, 114-15
Chlordane, 24, 96, 102, 111. 153
Chlorinated compounds, 17, 138
Chlorine, 213
Chlorofluorocarbons (CFCs), 173, 218,
243-45, 248
Cholesterol, 85
Clark, Mertice, 35
Clean Water Act, 14
Clinical Endocrine Physiology, 23
Closed loop recycling, 228
('lover, 75-76, 78
297
o
Cod, 101-2
Coho salmon, 26
Colborn, Theo, 11-28,29,41, 110-12,170,
198,251
Columbia River, 154
Conservation Foundation, 12-13
Contraceptive creams, 129
Copenhagen, University of, 9, 173
Copepod, 101, 102
Coming lab tubes, 127-28
Costa Rica, 162, 163
Coumestrol, 79-80
Crayfish, 100
Crewes, David, 152
Crossed bill defect, 155
Cumulative exposure, 220
Cuyahoga River, 13-14,17
Dacthal, 213
Daly, Helen, 191-94, 214, 236-37
Darvill, Thomas, 191
DDE, 21, 233
and alligators and turtles, 152-53
as androgen blocker, 139
and bald eagles, 154
and breast cancer, 184, 201
and fish, 214
and Florida panthers, 149
as hormone disruptor, 83-86, 111
DDT, 151
animal testing of, 169
ban enacted, 14, 201, 233
and behavior, 237
and beluga whales, 144
and birth defects, 155
and breast cancer, 184,201
chemical structure of, 69, 71
continued use of, 136-39
discovered, 68-69
dosages, 111
early warnings ignored, 198-201
estrogen mimicked by, 69,74-76
and fish, 17, 157
and Florida panthers, 149
and herring gulls, 5, 100
history of, 243, 244, 245
as hormone disruptor, 67, 80, 81,83-86
in humans, 90, 106,136-37
and immune system, 161
and male birds, 21
persistence of, 96, 98
regulation of, 219, 242
and polar bears, 88
and seals, 102
tolerance levels in food, 202
widespread use of, 200, 233
and wildlife abnormalities, 24
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De Guise, Sylvain, 143, 144, 147
Delaney clause, 202
Denmark, 9-10, 175
Depression, 65-66
Design Tex, 228
Detergents, 129, 134, 185,224
Developing countries, 138, 223
DFD (designed for disassembly), 227-28
Dicofol, 6, 151-53
Dieckmann, William, 54
Dieldrin, 3, 24, 96, 153,233
Diethylstilbestrol (DES)
and animal vs. human studies, 169
and birds, 4, 150
and brain and behavior, 63-65
chemical structure of, 69, 71
damage caused by, 110
effect across species, 74
and female offspring, 62
history of, 48-67
as hormone mimic, 68-76, 81, 84
and humans, 253-54
and immune system, 62-63, 162
in livestock, 48
low doses harmful, 169-70
and male offspring, 58-61
rat studies, 47, 49
and sexual orientation, 65, 195
synthesized and marketed, 48-49
and tubal pregnancies, 180-81
Dioxin (2,3,7, 8-TCDD), 111-21, 139
ban on, 114
and birds, 4-5, 100, 155
and brain and behavior, 187-88
in breast milk, 107
dosages, 111, 112, 117
effects of, 113-21, 139, 206
and endometriosis, 181
and fish, 157-58,214
as hormone disruptor, 81, 139
and humans, 171
persistence of, 96
and rats, 112
Disease model, 206-7
Distemper virus, 7-9, 160-62
Distributors, 221
DNA, 17, 120, 203-4, 205
Dodds, Edward Charles, 48, 68, 69, 72-73
Dolphins, 8—9, 160
Dosages (dose-response curve)
bisphenol-A, 131
dioxin, 115, 117, 118
low \ s. high, and hormone disruptors,
169-70, 197, 205-7
synthetic chemicals, 111
and research and regulation, 225
Double-crested cormorant, 14
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INDEX
Duke University Medical Center, 59
Dunn, Thelma, 57
Du Pont company, 244
Dust, 94
Dutch National Institute of Public Health
and Environmental Protection, 161
Eco-epidemiology, 208
Ectopic pregnancy, 56-57, 62, 181
Educational problems, 235-36
Eels, 100-101
Egypt, 138
Electrical transformers, 92-94, 137
Electron capture detector, 243-44
Emory University, 79
Endocrine glands, 32, 33
Endocrine system
and animal studies and humans, 169-70
and bird behavior, 23-24
chemicals’ effects on, not studied, 139
and dioxin dosage, 115, 117-18
disruption of, by chemicals, 110
and doses, 169-70
and evolution, 74
of Great Lakes salmon, 158-59
number of chemicals disrupting, 81, 85
and receptors, 71-72, 74
regulated by hormones, 32-33, 33
and wasting syndrome, 25
and wildlife offspring, 26-28
Endometrial cancer, 184
Endometriosis, 172, 181
Endosulfan, 184
Endrin, 96
England, 2, 7, 10, 167, 175
Environmental Defense Fund, 202
Environmental Health Perspectives, 187
Environmental Protection Agency (EPA), 83,
84, 114,116-17,119,135,149,177,
188, 202,205,206,214,217
Enzymes, 86
Epidemiology. 205. 206. 208, 225
Epididymis, 44. 58, 60, 61
Erie, Lake, 13, 14, 158
Estradiol, 40, 149
across species, 74
and estrogen receptors, 70—71,73
human metabolism of, 183-84
vs. plant estrogens, 80
Estrogen
and brain and behavior, 63-64
and breast cancer, 123. 135, 140. 182-86. 201
and cancer. 62. 80
chemical structure of, 69, 71
and DDT, 21-22
and dioxin, 117
fetus protected from natural, 73
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INDEX
and Florida panthers, 149
human vs. animal, 66, 168
and human male reproductive problems,
176-77
and immune system, 62
manmade synthesized, as DES, 48
metabolism, and cancer, 183-84
natural vs. “weak” synthetic, 74
and newborn mice, 57-58
and ovaries, 32
prenatal exposure to, 37-40,47-48
synthetic chemicals that act like, 68-75
See also Diethylstilbestrol (DES);
Estrogen mimics; Hormone disruptors
Estrogen mimics
and blood proteins, 140
and breast cancer, 140, 183
broad effects of, 135
in canned foods, 134-35
and human male infertility, 176-79, 207
in humans, 141
vs. other hormone disruptors, 84-86
in plants, 76-80, 81
in plastics and detergents, 128-35
and prostate cancer, 179-80
-responsive tumors, 182-84
synthetic chemicals, 81-82
See also DDT; Diethylstilbestrol (DES);
Hormone disruptors
Estrogen receptor, 70—75, 71, 84
and breast cancer, 182-83
and plant estrogens, 80
Ethynylestradiol, 133
Everglades, 148
Evolution, 74, 80, 123,167-68
Facemire, Charles, 148-49
Fallopian tubes, 180
Family breakdown, 237-38
Feldman, David, 130, 131
Females
and aggression, 30-32, 34
and dioxin, 116, 119
and masculine behavior, 64-66
and prenatal hormones, 43-45
reproductive organs, 33
and reproductive problems in, 180-86
Feminized males, 23, 44-45, 77, 80, 119,
149, 172
Fennel, 78, 82
Fertility, 68-86, 197
and chemicals, 80-86
and DES daughters, 58, 62
and DES sons, 59, 60
and dioxin, 118, 120-21
and hormone disruptors, 112, 121, 209
in human females, 180-86
299
in human males, 172-79, 233-34
and PCBs, 92
and plants, 76-80, 82
in wildlife, 10, 88, 89,148
Fetus, 66, 86
estrogen receptors, 73-74, 140
Finkbine, Sherri, 51
Fish
avoiding contaminated, 213-14
cancer, in Great Lakes, 12, 16-17, 19
children of mothers who ate Great Lakes,
24, 190-94
decline of, 26,157-58
sexual confusion problems, in England,
131-35
testes size, 18, 23
Flea-control products, 217
Florida, 1,6,10, 167
Game and Freshwater Fish Commission,
150,151
Florida, University of, 6, 150, 151
Florida panther, 148-50, 165, 168
Flutamide, 139
Follicle-stimulating hormone, 177
Food additives, 202
Food and Drug Administration, 51, 54, 221
Food web, 26,106-8,154,156
Food, Drug, and Cosmetic Act, 202
Foods(s), 135,138,213-16,223-24
Forensic research, 223-24
Formononetin, 76
Fox, Glen, 20-22, 23,208
Freedom of Information Act, 136
Friedman, Rick, 59-60
Friedman, Sachi, 60
Frog declines, 162-64,224
Fruits and vegetables, 214-15, 228-29
Fry, Michael, 21-22, 23, 111, 153, 170
Fungicides, 85, 135, 216
Furans, 113, 155,181,189
Gaia hypothesis, 243
Galef, Bennett, 35
Gallbladder cancer, 115
“Gay gulls” phenomenon, 23
General Electric, 92
Genes
expression, 40, 120, 204
vs. hormones, 30,204, 211
Genetic drift, 158
Genetic engineering, 241
Genital abnormalities
and DES, 58-62,66
and dioxin, 120
in humans, 9-10,44-45, 171
in rats, 47-48
in wildlife. 10, 145, 151-52
300
INDEX
GE Plastics Company, 130-31
Gilbertson, Mike, 4-5, 20, 208
Golden toad, 163
Goldstein, Andrea Schwartz, 56-57
Goldstein, Paul, 56, 57
Golf courses, 218
Granada, University of, 134-35
Grant Chemical Company, 48
Graves’ disease, 63
Gray, Earl, 83-84, 85, 86, 110, 119-20, 135,
139, 149, 170, 177,216
Great Lakes, 3-6, 10, 154-59, 167
PCBs in, 95-96,98, 100, 102,104
research review on, 12-28
studies of children of mothers who ate fish
in, 190-94,214
Greenland Sea, 101, 102, 104
Gross, Timothy, 151
Growth factors, 122-23
Guelph, University of, 158
Guillette, Lou, 6, 150-51
Gulf Stream, 101
Guo, Yue-Liang L., 189
Habituation assessment, 194
Hamsters, 119-20
Handwashing, 216
Haney, Arthur “Hap,” 59
Harshbarger, John, 16
Harvard Medical School, 55
Hashimoto’s thyroiditis, 63
Health data systems, 222
Heptachlor, 96
Herbicides, 213
Herbst, Arthur, 5 5
Hermaphrodites (“intersex” individuals), 83,
132-35,145,152
Herring gulls, 4-6, 12, 14, 15, 20-23, 26, 27,
99-100, 158
Hertzler, David, 192
Hessel0 island, 7
“High affinity,” 70
Hines, Melissa, 64, 170
Hippocampus, 33
Hippocrates. 78
Ho, Shuk Mei, 179
Hodgkin’s disease, 114
Homosexuality, 65, 194-95
Hormone blockers, 72, 78, 83
Hormone disruptors (synthetic)
and animal population declines, 147-66
animal studies, and humans, 169-70
avoiding, 212-18
and biomagnification, 26-28
and breast cancer, 182-86
and brain and behavior, 187-94
DDT and kepone as, 67
debate over dangers of, 135-36
DES as, 47-49, 51-67
dioxin as, 115, 117-21
early warning signs ignored, 198-201
and fertility problems in females, 180-82
going beyond cancer risks to regulate,
203-9
dosages, 111-12,169-70
hazards of, 82-86
and homosexuality, 194-95
how estrogen is mimicked by, 68-75, 71
how to solve problem of, 210-30
number of, 80-82, 137-41
PCBs as, 89
“persistent,” 89
in plastics and cleaners, 127-35
and prostate, 179-80, 185-86
proving cause and effect, 196-97
regulating, 218-22
research on, 139, 222-25
and social problems, 231-38
and sperm counts, 172-79
threat of, to humans, 140-41, 170-97
and trade secrets, 136
“weak,” 73-74, 139
Hormone mimics, 72, 73-75
natural, vs. synthetic, 81-82
in plants, 76-78
Hormone receptors, 70-72, 72
Hormones, 32-33
in alligators, 151-52
and brain and behavior, 23-24,26,29-46,64
defined, 32
effect of low levels, 40-41, 86
and endocrine glands, 33
prenatal, 30-48
See also Hormone disruptors
Household cleaners, 129
Household pesticides, 217
Huggett, Cynthia, 35
Hughes, Claude, 76-78, 81, 82
Humans
applicability of animal studies to, 49, 51,
59, 86,167-72,189
body fat. contaminants in, 106
brain and behavior problems. 22-23.
64-66, 186-94
breast milk contaminants in, 25
cancer studies, 18-19
changing relationship with Earth, 168,
239-40, 247-49
children, 206
DDT in, 136-37
and DES, 47-67
dioxin exposure, 112
exposure to hormone disruptors, 139
female reproductive problems, 180-86
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INDEX
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fertility problems, 10, 172-75
and food chain, 106-9
health and Great Lakes, 15, 18-19, 24
male sperm count declines, 9-10, 121,
172-80, 207, 208, 231-34, 240, 241,
246-47
PCBs in, 92,137
potential, erosion of, 232, 235
prenatal exposure, 38, 58
prostate problems, 179-80
sexual orientation, 194-95
society, and chemicals, 231-38
threat to, of persistent chemicals, 168-97
Hungary, 175
Hunt, George and Molly, 5
Huron, Lake, 157
Hyperactivity, 186, 235
Hyperreactivity, 193
Hypospadia, 171, 176
Hypothalamus, 32, 33,70
Iceland, 101
Illinois, University of, 187
Immune system
of Arctic peoples, 107
connected with other body systems, 32
and DDT, 89
and DES exposure, 62-63
and dioxin, 116
and endometriosis, 181
and prenatal estrogen, 62-63
wildlife, 147,148,160-64
Imprinting, 183
India, 233
Indole-3-carbinol, 184
Industrial processes, 227-28
“Inert” ingredients, 217
Infertility treatments, 179
Institute for Analytical Chemistry,
University of Stockholm, 90
Intelligence (IQ), 24,189-91, 204, 235-36
International agreements, 218-19
International Joint Commission, 208
Inuit people, 107—8, 196, 240
Inverted U response curve, 169-70
Irish Sea, 7
Jacobson, Sandra and Joseph, 24, 190, 191,
193,194,214
Jensen, Soren, 90-91
Journal of Obstetrics and Gynecology, 48
Journal of the American Cancer Institute, 57
Kansas, University of, 45
Karpiuk, Peter, 35
Kattegat Strait, 7
Kelce, William, 83-84
!
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301
Kelsey, Frances, 51
Kepone, 80-81, 67, 184
Kidney, 33
Kinsey surveys, 64-65
Kongs0ya Island, Norway, 87, 105
Labeling, 221
Lahvis, Caret, 161
Lake trout, 25-26, 27,98-99,157, 190
Lancet, 176
Landseer, Sir Edwin, 2
Laparoscopy, 181
Latin America, 136
Lawns, 216-17, 229
Lead,235
Learning disabilities, 186-88, 197, 208
and society, 232, 235,238
Leatherland, John, 158
LeVay, Simon, 195
Life, 51
Lindane, 24, 96, 137, 139, 219, 233
Lindeman, Verlus Frank, 69, 198, 199, 200,
201,203
Liroff, Rich, 15-16
Liver problems, 201
Long-term effects, delayed, 66
Lonky, Edward, 191
Lordosis, 45, 119
Los Angeles County Natural History
Museum, 5
Lovelock, James, 243-44
Low birth weights, 190
Luteinizing hormone, 77
Mably, Tom, 118-19
McCall’s, 60
McCarthy, Raymond, 244
Macdonald, Sheila, 156
McDonough, William, 226-27, 228
McLachlan, John, 58, 59, 66, 69-71, 73, 81,
110, 170
McMaster University, 35
Maine, 154
Male(s)
aggression, 38-39
and alkylphenols, 134
and DES, 58-61,64-66
and dioxin, 112, 119
feminized, 23, 44-45,77, 80, 119, 149, 172
and hormone blockers, 83, 135
hormones, 135, 149
and PCBs, 178, 189
and prenatal hormones, 37-39, 42-45, 64
reproductive organs, 33
reproductive problems, 172-79
Mammary glands, 62
Xhmomet Bird Observaton . 164
302
INDEX
Marijuana, 77-78
Martineau, Daniel, 143-44, 147
Masculinized females, 64, 79-80, 172
Mason, Chris, 156-57
Massachusetts, 6
Massachusetts General Hospital, 52, 54-55, 57
Mather, Joseph, Sr., 191
Mating behavior, 118, 119, 120, 232
Mayer, Jean, 127
Meat, and dioxin, 214
Medical College of Georgia, 187
Mediterranean Sea, 8—9, 10, 160
Memorial Sloan-Kettering Cancer Center, 61
Menstrual cycle, 71
Mental retardation, 187, 189
Mercury, 144, 148, 149, 157, 235
Metabolism, 32
Methoxychlor, 21,120, 137, 237
Mexico, Gulf of, 160
Mice, laboratory
behavior, and PCBs, 188
and DES, 58-59, 62-63, 66
and hormones, 29-31, 33-46
and humans, 168-69, 172
newborn estrogen, 57-58
and “weak” estrogens, 74
Michigan, Lake, 3-4,95-96,98-99
Michigan State University, 3-4, 156
Microwave cooking, 215
Midgley, Thomas, Jr., 243
Milan, University of, 115
Milk production, 48,77-78. See also Breast
milk
Mink, 3-4,14, 20, 26,155-57
Miscarriages, 54, 62, 181-82
Missouri, University of, 29, 34
Molina, Mario, 244
Monsanto Chemical Company, 89, 91
Montreal, University of, 143, 144
Montreal Protocol of 1987,218
Moore, Robert, 117-19, 120-21
Motor abilities, 189,191
Muir, John, 168
Muller, Paul, 68, 69, 244
Mullerian ducts, 42-43, 58-59
Multiple myeloma, 115
Muskrats, 156
Myers, John Pet.erson “Pete,” 111, 164-65,
170,251
Mysid, 27,98
Narwhals, 108
National Academy of Sciences, 114
National Audubon Society, 1
National Cancer Institute, 57, 180, 185, 201
National Institute of Child Health and
Human Development, 181
National Institute of Environmental Health
Sciences, 58, 69-70, 181
National Institutes of Health, 118
Natural killer cells, 63, 161
Nature, 244
Nerve cells, 187
Nervous system, 32
Ness, Daniel, 187
Neurological hazards, 186-94, 214
New England journal of Medicine, 52, 55
New Scientist, 90
New York, State University of, 191
New Yorker, 51
New York University Women’s Health
Study, 184
Nixon, Richard, 201
Non-Hodgkin’s lymphoma, 114
Nonoxynol-9, 129
Nonylphenols, 134, 185,217
p-nonylphenol, 128-31
North Carolina State University, 35,78, 191
Northeast/Mid-Atlantic Study, 185
North Sea, 7, 160
Northwestern University Medical School, 47,49
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Office of Technology Assessment, 12
Oil refineries, 93-94
Olea, Fdtima, 135
Olea, Nicolas, 135
Ontario, Lake, 4-5, 22, 27,99,157,191,
192-94,214,237
Oregon, 157
Organic produce, 215
Organochlorines, 18, 161,213
Orkney Islands, 7
“Orphan” receptors, 70, 115, 120, 155
Oslo Fjord, 7
Osterhaus, Albert, 7, 161
Oswego River, 192, 194
Otters, 2-3,20, 26, 156-57, 168
Ovaries, 146,151
cancer of, 63, 172
and hormones, 32, 33,47
Ovulation, 77,79-80
Ozone layer, 163, 173, 218, 240, 241, 244,
",45 "’47
Pancreas, 32, 33
Paracelsus-, 205
Parathyroid, 32, 33
Parental behavior, 15, 22, 232, 237-38
PCBs (polychlorinated biphenyls), 88-109,139
banned by U.S., 91
biomagnification of, 27
in body fat, 89
and brain and behavior problems, 186-94,
206-7
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INDEX
and breast cancer, 184, 185, 201
discovery of, 89-90
dosages, 111
effects on parents and children, 191, 193—
194
and endometriosis, 181
and fertility, 88-89
in humans, 24,90, 106-9, 137
and immune system, 161
and learning disabilities, 235
and miscarriages, 182
number of, 81
PCB-118, 187
PCB-153,91-103,187
persistence of, 96-98
rat studies, 118, 191-93
and regulations, 219, 233
and sperm damage, 178
widespread contamination by, 90-105,
104, 105
and wildlife declines, 3-4, 9, 24, 26, 144,
146, 149, 154-61,214
Penguins, 92
Penis, 33, 45, 57, 59,151, 171, 189
Percival, Franklin, 151
“Persistent” chemicals, 89, 96, 113, 137, 211
Perth, Australia, 75-76
Peru, 165
Pesticides
avoiding exposure to, 213-18
and cancer, 184, 200—1
difficulty of getting information on, 136
hormones mimicked by, 68-69
increasing production of, 138-39
labels, 217
nonylphenol in, 129, 134
persistence of, 98
regulation, 202-3, 222, 241-42
research on, 223
resistance, 230
rethinking use of, 228-30, 247, 248
and wildlife abnormalities, 3, 24, 151-53,
164-65
Peterson, Richard, 112, 117-18, 119, 120,
170
Pheromones, 34-35
Phobic neurosis, 65
Phocomelia, 50
Phoenix, Charles, 45
Phthalates, 224
Phytoplankton, 27
Pineal body, 33
Pittsfield, Massachusetts, 92-93
Pituitary, 32, 33, 62, 177
Placental barrier, 49-50, 66
Plante, Richard, 143
Plant estrogens, 76-82
303
Plastics
assessing risks of, 246-47
avoiding, 213, 215
as hormone disruptors, 127-35, 139, 185
recycling, 228
research on, 223-24
widespread use of, 234
Polar bears, 87-89,91,92,95, 102-5, 108,
168,214
Polyaromatic hydrocarbons (PAHs), 17
Polycarbonate, 130-31
Polystyrene, 128
Polyvinyl chloride (PVC), 128-29
Pomegranate, 78-79, 82
Porterfield, Susan, 187-88
Poskanzer, David, 55
Pregnant women, 48, 140, 211-22
Prenatal development
and brain, 187-88
and breast cancer, 183
and cancer, 57-58
and DES, 53-54
and dioxin, 118-19
and hormones, 33-34, 39-40
and mating and reproduction, 35
and sperm counts, 176-77
Proceedings of the Society of Experimental
Biology and Medicine, 198
Progesterone, 181-82
Progesterone blockers, 78
Prolactin, 77-78
Prostate, 33, 197
cancer, 62, 80
enlargement, 179
and prenatal development, 44
problems, in humans, 172, 179-80, 183,
185-86
size, 38
Psychiatric disorders, 65-66
Puget Sound, 6
Pyranol, 92, 93
Pyrimidine carbinol family, 85
Quail eggs, 22
Queen Anne’s lace, 78, 82
Racine, Wisconsin, 95, 97
Rat studies
and brain and behavior, 188, 191-92
DES, 47-49, 57
and dioxin, 112, 118-21
and hormone disruptors, 83-84, 86
and humans, 86, 172
and nonylphenol, 129
and plant estrogens, 79-80
and prostate problems. 179-80
and sperm counts, 178
304
Receptors, 70-73, 72, 85, 206
Recycling, 228
Redesign, 248-49
Redesigning the American Lawn, 229
“Red leg” infection in frogs, 163
Regulation
and cancer bias, 202
improving, 218-22, 241-42, 256
research on, 224-25
Reihman, Jacqueline, 191
Reijnders, Peter J. H., 159-60, 170
Reproductive problems
cancer and,201
Carson on, 200
danger of rising, 209
and DES, 57, 62, 66
and DDT ignored, 198-201
and dioxin, 117, 118-20
and hormone disruptors, 23-24
and human females, 180-86
and human males, 172-80
and marijuana, 77
mice studies on, 30-46
and societal change, 232
in wildlife, 10, 145-47, 151-54,158-63
Research, 222-25
Rheumatic fever, 63
Rheumatoid arthritis, 63
Riddle, John M., 78-79
Ringer, Robert, 156
Risk assessment, 209, 219, 245-46
Rochester, University of, 236
Roosters, 69,75,198-200
Root River, 96
Rowland, Sherwood, 244
Ruckelshaus, William, 201
Sager, Dorothea, 118, 178
Saguenay River, 144
St. Lawrence National Institute of
Ecotox icology, 142-43
St. Lawrence River, 142-47
Salmon, 100, 102, 158-59
eating contaminated, 190, 192-94,214
Same-sex nests, 26
Sanderlings, 164-65
San Nicolas Island, 5
Sargasso Sea, 100, 101, 104
Schantz, Susan, 187
Schreiber, Ralph, 5
Schwartz, Andrea, 52, 53, 55-56
Schwartz, David, 52
Schwartz, Eva, 52-53, 55-56
Schwartz, Michael, 52
Science, 5, 37, 59, 195
Science Advisory Board of the International
Joint Commission, 15-16
INDEX
Scotch Bonnet Island, Canada, 99
Scotland, 7
Scottish Medical Research Council,
Reproductive Biology Unit, 174, 176
Sculpin, 157-58
Seals, 7, 89, 102-3, 108, 146, 159-61, 168
Seminal vesicles, 44
Sertoli cells, 177
Seveso, Italy, 114-15, 206
Sex steroid binding globulin, 73
Sexual behavior, 119, 120, 195
Sexual Brain, The (LeVay), 195
Sexual development, 83
and DDT, 199
and PCBs, 189
in salmon, 158-59
wildlife/human connection, 252-59
Sexual differentiation, 41-46, 195
and dioxin, 119
and plant estrogens, 79-80
Sexual orientation, 64-65, 194-95, 197
Sharpe, Richard, 176, 178
Sheep infertility, 75-76
Silent Spring (Carson), 15, 51, 96, 167, 200,
201,230
Skagerrak Strait, 7
Skakkebaek, Niels, 9,172-76
Skunks, 100
Smelt, 27,98
Smith, George van Siclen, 53
Smith, Olive Watkins, 53
Soft-tissue sarcoma, 114, 115
Sonnenschein, Carlos, 122-31, 134, 135, 140,
185
Soto, Ana, 122-31,134,135, 140. 170, 178,
185
Soybeans, 80, 82
Sperm
declining human, 9-10, 121, 172-79,
207-8,231-34, 240-41, 246-47
and DES, 58, 59, 60, 61
and dioxin, 116, 118, 119, 121
Florida panther, 148
and kepone, 80-81
and PCBs, 92
and sex differentiation, 41-42, 44
Sperm whale, 92
Stanford University School of Medicine,
130
Stebbins, Robert, 162-63
Steroid hormones, 69, 85-86, 216
Stevens, Nettie Marie, 41
Strang Cornell Cancer Research Laboratory,
183-84
Stress, 36-37,214,237
Stress hormones, 85
Striped bass, 92
I
INDEX
I
Sumpter, John, 131-34, 140
Sunflower seeds and oil, 79
Superior, Lake, 154, 157
Svalbard archipelago, 87-88, 91, 102-5,
104
Swann Chemical Company, 89
Sweden, 157, 175
Swedish Environmental Protection Board,
17-18
Syracuse University, 69, 198, 199
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Taiwan cooking oil, 189-90
Taiwan Department of Occupational and
Environmental Health, 189
Takasugi, Noboro, 57
Tarzan, Texas, 94
Technology, consequences of, 241-49
Termites, 229
Terns, 6,12, 22, 26
Territoriality, 237, 238
Testes, underdeveloped, 59
Testicles
cancer of, 9, 59-61, 172, 173, 175, 176,
207, 208
and DES, 58-59
and dicofol, 151
and dioxin, 118
and hormones, 32
and marijuana, 77
and sexual differentiation, 44
undescended, 59-61, 148, 149, 171,
175-76, 207
Testis, 33
Testosterone
and aggression, 30-32, 39
and alligators, 151-52
blockers, 149
chemical structure of, 69, 71
and dioxin, 118
and Florida panthers, 149
and marijuana, 77
and masculinity, 37, 39
prenatal, and behavior, 40-41
and sexual differentiation, 44-45
synthetic chemicals disrupting, 81, 83,
85-86
Testosterone receptors, 38
Texas, University of, 152, 183
Textile industry, 228
T4 (hormone), 187
Thalidomide, 49-51, 62
T-helper cells, 62-63, 161
Thymus, 32, 33
Thyroid, 32, 33,46
chemicals disrupting, 81, 85
and neurological problems, 186-94,
*^35
■
■
305
and receptors, 70, 187
and wildlife, 148, 158
Time lag, and DES, 53-54
Times Beach, Missouri, 115-16
Timing of exposure, 50^-51, 62, 206, 207
Tobacco industry, 196
Top predators, 26
Tower Chemical Company, 6, 150-51
Toxaphene, 96, 98,102
Toxicology, 205
Toxic Release Inventory, 221-22
Toys, 218
Trade secrets, 136, 217, 221, 234
Transgenerational effects, 139, 171, 192-94,
207, 223
Transthyretin, 187
Tubal pregnancies, 180-81
Tufts Medical School, 122, 134, 135, 179
Tumors, 144
Turtles, 26, 74, 152, 153, 168
Ulfelder, Howard, 55
Ultraviolet radiation, 97, 163, 245
U. S. Congress, 114
U. S. Fish and Wildlife Service, 17, 148, 150,
151, 154, 155
Uterus, 33, 47, 56-57,71,89
cancer, 62,63, 115, 172
Vaccination failure, 107
Vagina, 33, 47
cancer of, 52, 54-55, 57-58, 62
Vandenbergh, John, 35, 36
Vas deferens, 44
Vertebrates, 74, 168
Vietnam war, 113-14
Vinclozolin, 83, 84, 120
Viruses, 16-17
Vitellogenin, 132-33, 134
Vom Saal, Frederick, 29-31, 33-34, 36-37,
39-41,45,48, 111, 141, 169-70, 183,
237
Wadden Zee, 159, 160
W. Alton Jones Foundation, 111-12
Waste, 227
Wasting syndrome, 12,25, 154-55
Water, 212-13, 215, 237
Water flea, 97-98
Wayne State University, 24, 190
“Weak” estrogens, 73-74, 139, 140
Weiss, Bernard, 236
Western gull, 5-6, 21
Whales, 160, 168
White-tailed sea eagle, 20
Whitten, Patricia, 79-80, 170
Wiig, Oystein, 88
306
INDEX
Wildlife
abnormal behavior, 10, 21, 22
and DDT, 201
/human connection, 252-59
immigration, 153-54
population declines, 147-66
Wilson, Edmund Beecher, 41
Wingspread Statement, 150, 170-71, 251-60
Wisconsin, University of, 112, 117, 118, 178
Wolffian ducts, 42-44
“Wombmate” effect, 34-41, 35
Woodruff, Lake, 152
Woodward, Allan, 151
X Chromosome, 41-42
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Yale University, 229
Y chromosomes, 41-42, 43
Yeast receptor studies, 130
Yellowstone National Park, 154
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Zooplankton, 27
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Position: 1288 (4 views)