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attached: male estrogenics media coverage
as an attachment, reuters, A>P., Science News & the press release from this
story.
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Pollution from PCBs Keeps GE in Trouble With Pittsfield, Mass.
The Wall Street Journal, December 4, 1997, ppA1, A6.
The General Electric company used polychlorinated biphenyls
(PCBs) for many different uses for decades. These chemicals are
now causing an uproar in Pittsfield, Massachusetts.
PCBs were banned as a probable cause of cancer in 1976. In
Pittsfield, GE has been working to contain or remove the
chemicals at its 250-acre plant.
Tests done around the area indicate unsafe levels of PCBs.
One lot measured 20,000 parts per million and another 44,000 ppm.
The safe level for residential lots is no more than 2 parts per
million.
The rising number of homes found contaminated has alarmed
local residents. GE's capping proposals provoked outrage.
"No capping. Removal, removal, removal," said one man at a
recent town meeting. "My kids are playing out there. I don't want
them dying of cancer," said a housewife.
GE has agreed to move at least 30,000 tons of earth from
home sites in the area.
A state study showing low PCB levels in residents' blood has
helped the company but it still faces problems. Eighteen
homeowners have sued in federal court for damages from diminished
property values. The Massachusetts attorney general is
investigating claims that GE covered up internal memos that might
have shown the presence of PCBs in a donated landfill years
earlier. EPA is investigating similar issues.
GE executives claim the dangers of PCBs are exaggerated.
"This thing has been blown way out of proportion," said Stephen
Ramsey, GE's vice president for environmental programs.
One environmental regulator believes the company magnified
its problems by trying to manage the PCB problems by capping
them, which he considers only a quick inadequate fix for
residential properties. Ramsey contends that it's "a misperception
that it's a cheap, cheesy remedy that doesn't work."
The article details the recent history of the PCB problem in
Pittsfield including GE attempts to control the problem, EPA and
state level investigations into the company's actions and public
reaction.
Wednesday December 3 6:00 PM EST Estrogens Influence Male Fertility
NEW YORK (Reuters) -- Experts say estrogen, the 'female' hormone, may
strongly influence male fertility and help shape masculine growth and
behaviors.
"Estrogens may exert more widespread effects in the male and, remarkably,
they may even be essential for (male) fertility," said Dr. Richard Sharpe,
a fertility expert at the MRC Reproductive Biology Unit in Edinburgh,
Scotland.
Sharpe's commentary appears in this week's issue of the journal Nature,
which also includes an American study investigating the links between
estrogen and male fertility. (snip)
Scientists at the University of Illinois in Urbana, Illinois, focused on
the high concentrations of estrogen found in an area of the male
reproductive system known as the efferent ducts. These ducts serve as
pooling areas for sperm produced by the testes. The researchers say
estrogen present in these ducts seems to trigger the reabsorption of up to
90% of the fluid surrounding freshly produced sperm, "thereby increasing
the concentration of sperm" before its (eventual) ejaculation. (snip)
The Illinois findings run counter to recent speculation that the ingestion
of environmental pollutants mimicking the effects of estrogen may actually
lower male fertility. Sharpe theorizes that "under some circumstances,
estrogens may inhibit rather than promote (efferent duct) fluid
reabsorption."
SOURCE: Nature (1997;390:449-450, 509-512)
------------------------------
[CNN logo] [Health banner] [Taking the pulse of family
health & fitness]
NEW YORK (AP) -- Most people consider estrogen a
female hormone, but men make it too. A new study
suggests one reason why: Estrogen may help men
stay fertile by preventing a plumbing problem in
the reproductive system.
The study, done in mice, marks the first time
scientists have specified a detailed role for
estrogen in the male reproductive tract.
The topic is timely because of recent assertions
that some environmental chemicals may be reducing
sperm counts and otherwise harming male
reproductive health by disrupting hormonal
signaling. The new study, published in Thursday's
issue of the journal Nature, may help research
into the issue.
It also might help scientists develop a male
contraceptive, said the study's lead author, Rex
Hess of the University of Illinois.
Estrogen acts by binding to structures called
receptors in cells. There are at least two kinds
of estrogen receptors, and last year scientists
reported that male mice that lacked one kind were
infertile.
Using mice that lacked one of the estrogen
receptors, researchers found that tubes that
transport sperm and fluid in these mice fail to do
an important job: absorbing a lot of that fluid.
That absorption concentrates substances in the
fluid that help the sperm mature, and also
concentrates the sperm to ensure a large dose for
ejaculation.
Copyright 1997 The Associated Press. All rights
reserved. This material may not be published,
broadcast, rewritten, or redistributed.
[SCIENCE NEWS ONLINE]
[Rule][space] December 6, 1997 [space] [Rule]
Estrogen's Emerging Manly Alter Ego by J. Raloff
Estrogen is usually described as the animal kingdom's primary
female sex hormone. That's a gross oversimplification, however.
Even that quintessentially male preserve -- the sperm -- depends
on estrogen, scientists report this week. Without estrogen, males
are infertile.
The new study, by Rex A. Hess at the University of Illinois at
Urbana-Champaign and his colleagues, focuses on estrogen's role in
male reproductive function. Nevertheless, the researchers observe
that their findings also suggest a mechanism by which DDT and
other estrogen-mimicking pollutants (SN: 7/3/93, p. 10) could
wreak havoc on fertility. If these weak estrogens displace the
body's more potent natural ones, they might diminish estrogen
exposure -- and sperm activity (SN: 1/22/94, p. 56).
Hess and his colleagues study mutant mice. These animals were bred
to produce estrogen normally, but they lack the gene for an
estrogen receptor -- a protein that allows cells to take up the
hormone. As a result, the mice cannot respond to the estrogen in
their bodies.
Since this hormone plays a pivotal feminizing role in development,
the scientists expected that mutant females would develop
abnormally. "The big surprise," notes Patricia M. Saling, a
reproductive cell biologist at Duke University Medical Center in
Durham, N.C., was the finding 4 years ago that the males were
infertile. Since then, Hess and others have been probing why.
Last year, Mitch Eddy of the National Institute of Environmental
Health Sciences (NIEHS) in Research Triangle Park, N.C., and his
colleagues showed that although the mutant males initially make
sperm, their testes quickly degenerate. They traced the problem to
a backup of excess seminal fluid.
In the Dec. 4 Nature, Hess and his colleagues uncover the cause of
the backup. It's not overproduction of the secreted fluid, as many
had suspected. Instead, it's a drainage problem: The tubes running
from the testes to the epididymis, where sperm mature and acquire
the ability to fertilize eggs, are unable to drain off the excess
liquid.
Besides damaging the testes, this excess fluid "also results in a
very dilute ejaculate," notes Hess' colleague Kenneth S. Korach of
NIEHS, a developer of the mutant strain of mice. If sperm are not
packed densely in seminal fluid, fertility is impaired.
The tubes -- known as efferent ducts -- and the epididymis have
never been considered "dominant in terms of making or breaking
fertility," Saling says. The new study suggests otherwise. In
fact, she says, "if manipulating the epididymal environment can
lead to whopping amounts of infertility, this would suggest a new
organ to target in the development of [male] contraceptives."
Ineffective fluid removal may not explain all of the mutant males'
fertility problems, however. Eddy's team found that any sperm
produced fail to mature and become capable of fertilization. Yet
excess fluid might play a role here, too, speculates Richard M.
Sharpe of the Medical Research Council in Edinburgh. In a
commentary accompanying the Nature report, he says that ". . . the
abnormal amounts of fluid will effectively dilute [any maturing
agents] secreted within the epididymis."
What the new data clearly demonstrate, Korach states, is the
essential role of estrogen in male reproductive health. Indeed,
Sharpe adds, "Suddenly, the idea of 'male' and 'female' hormones
begins to look thin."
Hess' team argues that the new data also raise "further concern
over the potential direct effects of environmental estrogens on
male reproduction and reported declines in sperm counts."
After analyzing 61 studies, Danish scientists reported an apparent
downward trend in human sperm counts 5 years ago (SN: 1/22/94, p.
56). Since then, others have challenged their assessment, arguing
that the data -- collected in different regions, over different
times, and using different criteria -- are not comparable.
Not so, concludes a major reanalysis.
"I think we were the only group that actually got all of the
original data," says Shanna H. Swan of the California Department
of Health Services in Emeryville. Her group analyzed the data
using a series of alternative statistical techniques to see if the
decline originally reported was an artifact of the way the data
had been analyzed.
In the just-published November Environmental Health Perspectives,
Swan's team reports that all its analyses show a decline in sperm
counts since 1970 for men in Western countries. Indeed, Swan
observes, the statistical representations that best fit the data
detected an even stronger drop than the Danes had reported.
The new declines average more than 1 percent annually -- or about
1.5 million sperm per milliliter per year in the United States and
3 million sperm per milliliter per year in Europe.
[Image] [Image] [Image]
References:
Eddy, E.M., et al. 1996. Targeted disruption of the estrogen
receptor gene in male mice causes alteration of spermatogenesis
and infertility. Endocrinology 137(November):4796.
Hess, R.A., et al. 1997. A role for oestrogens in the male
reproductive system. Nature 390(Dec. 4):509.
Sharpe, R.M. 1997. Do males rely on female hormones? Nature
390(Dec. 4).
Swan, S.H., E.P. Elkin, and L. Fenster. 1997. Have sperm densities
declined? A reanalysis of global trend data. Environmental Health
Perspectives 105(November):1228.
Further Readings:
Fackelmann, K. 1996. Study finds no decline in sperm counts.
Science News 149(June 8):365.
Raloff, J. 1997. Roller-coaster sperm counts-and births. Science
News 151(April 5):212.
______. 1997. Radical prostates. Science News 151(Feb. 22):126.
______. 1997. A new breadth to estrogen's bisexuality. Science
News 151(Feb. 22):116.
______. 1995. A two-decade drop in sperm counts. Science News
147(Feb. 25):127.
______. 1994. That feminine touch. Science News 145(Jan. 22):56.
______. 1993. EcoCancers. Science News 144(July 3):10.
Sources:
Kenneth S. Korach Receptor Biology Section
Laboratory of Reproductive and Developmental Toxicology
National Institute of Environmental Health Sciences
National Institutes of Health
Research Triangle Park, NC 27709-2233
Patricia Saling Duke University Medical Center
P.O. Box 3648 Durham, NC 27710
Richard M. Sharpe Medical Research Council
Reproductive Biology Unit 37 Chalmers Street
Edinburgh EH3 9EW United Kingdom
Shanna H. Swan Reproductive Epidemiology Section
California Department of Health Services
5900 Hollis Street, Suite E
Emeryville, CA 94608-2008
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Embargoed For Release: 3 December 1997 at 14:00:00 ET US
Contact: Jim Barlow b-james3@uiuc.edu 217-333-5802 U. of Illinois at
Urbana-Champaign Estrogen Linked To Sperm Count, Male Fertility
CHAMPAIGN, Ill. -- Testosterone may be the hormone that makes the man, but
it is estrogen -- the so-called 'female' hormone -- that gives sperm its
reproductive punch, a team of researchers report in Thursday's (Dec. 4)
issue of the journal Nature.
Estrogen is vital to male fertility -- specifically to sperm count. That
discovery, coupled with the debate over declining sperm counts worldwide,
means "we must be concerned about the potential for environmental chemicals
to influence male reproductive function," said Rex A. Hess, a professor of
veterinary biosciences at the University of Illinois and principal author
of the Nature report.
"If there is a normal function for estrogen in the male, and that function
is required for normal fertility, then it is logical to hypothesize that
chemicals that interfere with estrogen receptors may interfere with
fertility," Hess said. "Until now, there has been no known function for
estrogen in the male. We have had nothing to focus on. Now we can ask the
question: Does this chemical or that chemical interfere?"
Potential environmental influence on fertility, such as exposure to
pesticides and industrial chemicals, has sparked controversy since 1992,
when Copenhagen University researchers concluded that sperm counts were
declining around the world. In late November, a team led by Shanna Swan of
the California Department of Public Health reached a similar conclusion
after reconsidering the data from the 61 studies used in the Copenhagen
findings.
The Nature paper focuses on the regulatory role of estrogen-induced fluid
reabsorption during the transfer of sperm in fluid from the testis through
the efferent ductules -- a series of small tubes that act like kidneys,
producing concentrated semen instead of urine -- to the epididymis, where
sperm mature and are stored.
"We have found that estrogen regulates fluid reabsorption in the efferent
ductules of the male," Hess said. "It is important for the uptake of water,
ions and proteins from the fluid that carries the sperm. The efferent
ductules are responsible for reabsorbing nearly 90 percent of the water
from this fluid. Without the reabsorption, the sperm remain diluted and
therefore incapable of normal maturation in the epididymis."
The paper is part of three collaborative studies done over seven years on
male estrogen -- funded in part by the U.S. Department of Agriculture and
the U. of I.-- by a team that includes Janice Bahr, a professor of
physiology, molecular biologist David Bunick and Hess.
In another study, published in the December issue of the Journal of
Andrology, the researchers report that the number of genes that express
estrogen receptors in the efferent ductules of rats -- when operating
normally -- is 3.5 times greater than the estrogen receptor message in the
female reproductive tract.
"This means you have a target for estrogen, and there are plenty of targets
for the estrogen to bind to," Hess said. "It was surprising to find the
protein in such a high concentration. We knew it would be there, but
finding so much was unexpected."
The Nature findings resulted from studies of estrogen function in the
reproductive tracts of mice, including genetically produced mice whose
estrogen receptors are non-functional. As in humans, the mice used in the
research had similarities in their estrogen, estrogen receptors and
efferent ductules.
Hess, Bahr and Bunick reported in the 1994 Proceedings of the Estrogens in
the Environment, that they had found a new source of potential estrogen
synthesis in males, in the germ cells of the testis and sperm in the
epididymis of mice, rats and chickens. Similar findings have been made in
black bears.
When estrogen receptors are knocked out, the fluid "accumulates at the site
of production " just as happens when you get a blocked waste pipe and run
the tap," writes Richard M. Sharpe of the Medical Research Council
Reproductive Biology Unit in Edinburgh, Scotland, in an accompanying "News
and Views" article on Hess' findings. "This build-up progressively impairs
sperm production because of the increased fluid pressure within the
testis."
In 1993, Sharpe theorized that declines in sperm counts might be occurring
because of a complex interference with hormones involving the hypothalamus
in the brain and the pituitary gland during development of the testis.
Now that the research has provided the first recognized physiological
function for estrogen in males, Hess said, the next step in the research is
to determine the biochemical action. "We have known that estrogen is
present in the male, and in high concentrations in the seminal fluids, but
we did not know why it was there," he said. "Now we can focus on the
function of fluid reabsorption and on what genes are regulated by the
estrogen."
"Estrogen is not only important in the female for fertility, but it also
exerts its influence on the male, from birth to death," Hess said. "We can
now say that this female hormone is intimately involved in regulating
fertility in the male, because if you block the estrogen receptor's
function as we've shown here, you will have infertility. It is very likely
that this will be a similar finding in humans."
Coauthors of the Nature paper are Hess, Bunick and Bahr, along with Ki-Ho
Lee of the U. of I. department of veterinary biosciences; Julia A. Taylor
and Dennis B. Lubahn of the departments of biochemistry and child health at
the University of Missouri at Columbia; and Kenneth S. Korach of the
National Institutes of Health National Institute of Environmental Health
Sciences at Research Triangle Park, N.C.
Coauthors of the paper in the Journal of Andrology are Hess, Bunick,
Lubahn, Bahr, Daniel H. Gist of the department of biological sciences at
the University of Cincinnati, Amy Farrell and Paul S. Cooke of the U. of I.
department of veterinary biosciences, and Geoffrey L. Greene of the Ben May
Institute for Cancer Research at the University of Chicago.