=======================Electronic Edition========================
RACHEL’S HAZARDOUS WASTE NEWS #377
—February 17, 1994—
News and resources for environmental justice.
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SCIENTISTS PRETENDING
For the past 3 or 4 years, evidence has been accumulating that
many industrial chemicals (including many common plastics,
pesticides, and by-products of combustion) mimic hormones. These
hormone mimickers disrupt reproduction and development in humans
and in many other species of mammals, birds, and fish. A growing
body of evidence also indicates that these same chemicals may
cause some of the most common and fastest-increasing cancers:
breast cancer in women, and cancers of the testicles and prostate
in men.
The American Chemical Society [ACS] recently affirmed the
following phenomena: [1]
** Sperm count in men worldwide has dropped to 50% of what it was
50 years ago.
** The incidence of testicular cancer has tripled in some
countries in the last 50 years and prostate cancer has doubled.
** Endometriosis–the growth outside the uterus of cells that
normally line the uterus–which was “formerly a rare condition,
now afflicts 5 million American women,” the ACS said.
** In 1960, a woman’s chance of developing breast cancer during
her lifetime was one in 20. Today the chances are one in nine.
** Female common terns (sea birds) are sharing nests near a
PCB-contaminated site in New Bedford Harbor, Mass., an unnatural
female-female pairing.
** Young male alligators in pesticide-contaminated lakes in
Florida are growing up with penises so small that they are
“sexually incompetent.”
In January, the federal National Institute of Environmental
Health Sciences [NIEHS] convened a meeting of 300 scientists who
presented papers on estrogens and estrogen mimickers in the
environment. Many of those scientists think there’s probably a
connection between diminished sperm counts, increasing
endometriosis, female-to-female pairing in birds, sexually
incompetent alligators, and breast cancer in women. The
connection is poorly understood, they say, but the common link is
probably chemicals dumped into the environment that mimic, or
interfere with, hormones.
Slowly, mainstream scientific thinking has been coming to grips
with this accumulating bad news. First the American Chemical
Society began to write about it. [2] Then the National Institute
of Environmental Health Sciences [NIEHS], a division of the U.S.
National Institutes of Health, started writing about it. [3] And
this month the JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION (JAMA)
broke the story for its readers: “Estrogen and [chemical] agents
that mimic it appear to be more pervasive and problematic then
ever suspected,” JAMA said February 9th. [4]
Estrogen is usually considered a female hormone, but males
produce estrogen too, in small amounts. In the developing fetus,
in both humans and animals, a specific ratio of estrogen to
androgens (male hormones) must be maintained for proper sexual
differentiation to occur; in other words, for a male to become a
male and a female to become a female –regardless of the species
–a certain balance of male and female hormones must be present
in the mother between the time of fertilization and the time of
birth or hatching.
If the hormone balance is disturbed, the offspring will be born
with two sets of partially developed sex organs (intersex), or
with a single set that is incompletely or improperly developed.
Diminished sperm count, or future cancer, may be set at this
early stage.
All plants and animals are composed of cells –tiny bags of fluid
that work cooperatively together to carry out metabolism
(extraction of energy from nutrients) to maintain life. The
human body is composed of roughly 50 trillion individual cells
that all cooperate and communicate with each other. Hormones are
chemical messengers, essential to the body’s healthy cooperation
and internal communication. Hormones are present at very low
levels (parts per billion or even parts per trillion), and often
for only short periods of time, yet they have very powerful,
long-lasting effects on growth, development, and metabolism.
The female hormone, estrogen, and chemicals that mimic estrogen,
operate inside cells by fitting themselves into “estrogen
receptors” (proteins) the way a key fits into a lock. Once the
key is in the lock, the key-and-lock together can move into the
nucleus of a cell and attach to the DNA, releasing messenger RNA
which then causes a cascade of changes in cells, tissues, and
organs throughout the body.
No, the story of estrogen mimickers is not simple. Some estrogen
mimics fit into the lock wrong, filling up the space that the
“correct” key would have used, thus interfering with natural
estrogens; these are called estrogen antagonists. Some estrogen
mimickers fit into locks that weren’t ever intended to have an
estrogen fitted into them. The amount of natural estrogen in the
mother is usually much greater than the amount of estrogen
mimickers. However most natural estrogens are bound up by
sex-hormone-binding proteins in the blood stream, which are not
able to bind estrogen mimickers. This increases the effective
dose of the mimickers. The many ways estrogen mimickers can
cause problems are just now beginning to be appreciated.
“The structural diversity of estrogenic chemicals is enormous,”
says John A. McLachlan, chief of the reproductive and
developmental toxicology laboratory at NIEHS, according to JAMA.
In other words, you cannot simply observe a molecule and tell, by
its chemical structure, whether it will act as an estrogen mimic
or not.
“Compounds with widely different structure bind to estrogen
receptors even though they bear no obvious structural
resemblance” to estrogen, says John A. Katzenellenbogen,
professor of chemistry at University of Illinois.
Examples of estrogen mimickers are DDT and its breakdown
by-product DDE; Kepone; dieldrin; dicofol; methoxychlor; some
PCBs; 3,9-dihydrooxybenz[a]anthracene; and alkyl phenols from
penta-to nonylphenol, as well as bisphenol-A (the building block
of polycarbonate plastics) which is used in many common
detergents, toiletries, lubricants, and spermicides. Many
estrogen mimickers are persistent (they resist breaking down in
the environment) and highly soluble in fat (causing them to
accumulate in the bodies of fish, birds, and mammals, including
humans). Many of them cross the placental barrier and pass from
the mother to the developing fetus.
It is not simple to distinguish estrogens from non-estrogens.
“Historically, we think of the receptor as a switch,” turning on
or off the body’s reactions. But it is not that simple, says
George M. Stancel, head of the department of pharmacology at
University of Texas Medical School. Estrogen-like chemicals can
form “many molecular configurations” that can “act in differing
ways,” Stancel told JAMA. The same chemical can also act
differently in different tissues, Stancel said.
To complicate the picture further, some cells appear to have
estrogen receptors on their surface, rather than inside. So
“even if compounds do not manage to get inside cells, they may
still be estrogenic,” says Cheryl Watson, associate professor of
biological chemistry at the University of Texas Medical Branch at
Galveston.
Finally, JAMA reported that estrogenic chemicals have a
cumulative effect. David Feldman, professor of medicine and
endocrinology at Stanford University, says, “The cumulative
effect may be much greater than any individual molecule.” Ana M.
Soto at Tufts University combined 10 estrogen mimickers, each at
one-tenth of the dose required to produce a minimal response; she
found that the combination produced an estrogenic response.
This last bit of information has far-reaching implications for
the regulation of chemicals. For 50 years the U.S. has regulated
chemicals one by one, by conducting laboratory experiments on
animals, and by experimenting on workers. If rats or workers get
sick, then a particular chemical may be regulated to a level 10
times (or 100 times) lower than the lowest amount that caused an
observable effect.
If chemicals at low (“safe”) levels combine to produce an effect,
this means that chemicals will have to be regulated in
combination. “Testing mixtures is right on the mark” says George
M. Stancel, at University of Texas Medical School. Kenneth
Olden, head of NIEHS, agrees. “[W]e cannot ignore this milieu we
live in that has all these estrogens. We have polluted our
environment. It is polluted. Now we have to allocate resources
to sort out the different effects of agents and learn whether
they are synergistic, additive, inhibitory, or antagonistic. We
don’t know,” Olden says, meaning we must try to learn whether
chemicals in various combinations are weaker or stronger than
each chemical alone.
But these are scientists pretending. Pretending that science can
do something it cannot actually do. There is not sufficient money
to study the full effects of individual chemicals, much less
combinations of chemicals.
Scientists can pretend that they can discern “safe” levels of
hundreds of different chemicals, all acting in combination. They
can pretend that they can understand all the ill effects of
multiple hormone mimickers on each type of cell, each tissue and
each organ at every stage of development from conception to
birth, through youth and puberty and into maturity, in each of
the thousands of affected species. They can pretend to know
these things, but they cannot ever actually know them. They are
just pretending.
Scientists can pretend, but in so doing they perform a great
disservice, preventing decision-makers from seeing what really
needs to be done: we need to abandon the practice of
chemical-by-chemical regulation. We need to regulate whole
CLASSES of chemicals. And the dangerous classes need to be
phased out and banned. Zero discharge. Pollution prevention.
These are the keys to sustainability and survival.
                
                
                
                
    
–Peter Montague, Ph.D.
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[1] Bette Hileman, “Environmental Estrogens Linked to
Reproductive Abnormalities, Cancer,” C&EN [CHEMICAL & ENGINEERING
NEWS] January 31, 1994, pgs. 19-23.
Descriptor terms: endocrine disruptors; estrogen; androgens;
hormones; wildlife; endocrine system; reproductive system; niehs;
national institutes of health; national institute of
environmental health sciences; nih; american medical association;
ddt; dde; pesticides; plastics; dicofol; methoxychlor; pcbs;
polychlorinated biphenyls; alkyl phenols; bisphenol-a;
polycarbonate plastics; detergents; toiletries; lubricants;
spermicides; pentaphenol; nonylphenol;
3,9-dihydrooxybenz[a]anthracene;