RACHEL's Hazardous Waste News #343

=======================Electronic Edition========================

RACHEL’S HAZARDOUS WASTE NEWS #343
—June 24, 1993—
News and resources for environmental justice.
——
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org
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ARE ENVIRONMENTAL CHEMICALS CAUSING
MEN TO LOSE THEIR FUNDAMENTAL MASCULINITY?

Are environmental chemicals causing men to lose their masculine
characteristics?

A recent study in the BRITISH MEDICAL JOURNAL concludes that men
in western countries today have sperm counts less than half as
high as their grandfathers had at the same age.[1] In addition,
the occurrence of cancer of the testicles has increased 3-fold to
4-fold during the past 40 years; and various birth defects of the
male reproductive system have increased 2-fold to 4-fold during
the same period, including undescended testicles (a condition
called cryptorchidism) and a birth defect called hypospadias in
which the male urinary canal is open for a variable distance on
the underside of the penis.[2]

An article published last month in THE LANCET, another
prestigious British medical journal, asks whether these phenomena
can all be traced to the same cause, namely exposure of males
very early in life to female sex hormones (estrogens) or to
environmental chemicals that act like estrogens.[3]

This hypothesis is being taken seriously within the scientific
community; both SCIENCE magazine and C&EN [CHEMICAL & ENGINEERING
NEWS] reported on the publication of the LANCET article. [4,5]

The report on sperm counts, in the BRITISH MEDICAL JOURNAL,
examined 61 separate studies of sperm count in men in many
countries, including the U.S., and concluded that, among men in
western countries, there has been a 42 percent decrease in
average sperm count, from 113 million per milliliter (ml) to 66
million per ml, since 1940. (There are 4.5 milliliters in a
teaspoon.) Furthermore, the average volume of semen diminished
from 3.4 ml to 2.75 ml, a 20 percent loss since 1940. Thus the
average man has lost 53 percent of sperm production since 1940.

The researchers examined the possibility that sperm counting
methods have changed during the past 50 years, or that racial or
geographic factors might be at work. After careful analysis,
they concluded that the diminished sperm count in men is real, is
widespread throughout the industrialized western world, and
affects men of all races.

Some of these facts have been known to some medical researchers
for the better part of a decade, but only recently has the
explanation been offered that all these problems may be related
to male exposures to female hormones (estrogens) early in life.

The hypothesis put forth in THE LANCET last month suggests that
males are being exposed in the womb to female sex hormones that
permanently alter their sexual development, increase their risk
of having undescended testicles, hypospadias, and testicular
cancer, and reduce by half the average man’s ability to produce
sperm.

Five sources of increased estrogenic exposures to males in the
womb are being considered:

1) A modern diet may increase the levels of natural estrogen in
women. Fiber in the diet today is lower than it was 50 years ago.
(Fiber in the diet is basically anything that cannot be
digested.) Natural estrogens excreted in the bile are more
readily reabsorbed into the bloodstream when the lower intestine
contains little dietary fiber. Therefore, a fetus today may be
exposed to higher levels of the mother’s own natural estrogens,
compared to a fetus 50 years ago.

2) Some 3 to 4 million women were treated with a potent synthetic
hormone called diethylstilbestrol (commonly known as DES) from
1950 through 1970. Daughters of DES-treated women have an
increased risk of a rare vaginal cancer. The sons of DES-exposed
women have low sperm counts, and a higher-than-normal risk of
malformations of the reproductive tract such as hypospadias and
undescended testicles. Furthermore, all these effects can be
reproduced in the laboratory by exposing mice and rats to DES.
Thus there is compelling evidence, from humans and other animals,
that males exposed in the womb to female hormones can suffer
reproductive system damage, some of which only becomes apparent
after puberty in the form of reduced sperm count.

3) Synthetic estrogens, including DES, were fed to beef cattle
from the 1950s through the 1970s to make them grow more meat
faster. Such practices may have increased the quantity of
estrogens in meat-eating women and perhaps, as a contaminant, in
some water supplies.

4) The use of synthetic estrogens as a contraceptive pill has
increased greatly during the past 20 to 40 years. One such
compound, ethinyl estradiol, has been detected as a contaminant
in some water supplies, but the data are skimpy.

5) Another source of increased estrogens in women today is the
many synthetic organic chemicals and heavy metals that have been
released into the environment in massive quantities since world
war II. Some of these compounds, such as PCBs and dioxins, are
known to interfere powerfully in the reproductive system of fish,
birds, and mammals, including humans.[6] A single, tiny oral
dose [0.064 micrograms per kilogram of body weight] of dioxin on
day 15 of pregnancy in rats has no effect on the mother but
increases the likelihood of various reproductive disorders in
their male offspring: undescended testicles, smaller testicles,
reduced levels of male hormone circulating in their blood, and
reduced sperm count.[7] Here again, we see effects caused by
exposures in the womb, but which only become apparent after the
offspring mature. Many common industrial chemicals are weakly
estrogenic,[8] but they are now present in all our food and
water, and are stored in the fat tissues of our bodies, including
women’s breast milk. As one researcher observed, “Humans now
live in an environment that can be viewed as a virtual sea of
oestrogens.”[9] [Estrogens and oestrogens are the same thing,
only spelled differently.]

These findings and hypotheses add to the growing body of medical
knowledge indicating that many chemicals –especially chlorinated
hydrocarbons –mimic hormones and interfere with the endocrine
systems of fish, birds, wildlife and humans. Earlier studies
have linked chlorinated hydrocarbons to female breast cancer [see
RHWN #279, #334], and it is worth pointing out
that breast cancer
in women is associated with an increased likelihood of testicular
cancer in their sons. [10] Another well-established risk factor
for testicular cancer is undescended testicles. [11] Thus breast
cancer, testicular cancer, and defects of the male reproductive
system, including diminished sperm count, all seem linked.

Diminished sperm count alone is a potentially serious matter.
Many animals produce up to 1400 times as much sperm as is needed
for fertility. In contrast, the average human male produces only
2 to 4 times as much sperm as is needed for fertility. [12]
Humans don’t have much sperm to spare. A 50 percent reduction in
human sperm count may thus diminish human fertility and could
therefore take away from men the one thing they indisputably do
well: help women propagate the species.
–Peter Montague, Ph.D.

===============
[1] Elisabeth Carlsen and others, “Evidence for decreasing
quality of semen during past 50 years,” BRITISH MEDICAL JOURNAL
Vol. 305 (1992), pgs. 609-613.

[2] A. Giwercman and N.E. Skakkebaek, “The human testis–an organ
at risk?” INTERNATIONAL JOURNAL OF ANDROLOGY Vol. 15 (1992), pgs.
373-175. And: A. Osterlind, “Diverging trends in incidence and
mortality of testicular cancer in Denmark, 1943-1982,” BRITISH
JOURNAL OF CANCER Vol. 53 (1986), pgs. 501-505.

[3] Richard M. Sharpe and Niels E. Skakkebaek, “Are oestrogens
involved in falling sperm counts and disorders of the male
reproductive tract?” THE LANCET Vol. 341 (May 29, 1993), pgs.
1392-1395. And see: R. M. Sharpe, “Declining sperm counts in men
–is there an endocrine cause?” JOURNAL OF ENDOCRINOLOGY, Vol.
136 (1993), pgs. 357-360.

[4] Constance Holdren, “The Hazards of Estrogens,” SCIENCE Vol.
260 (May 28, 1993), pgs. 1238-1239.

[5] “Estrogenic Chemicals May Lower Sperm Counts,” C&EN [CHEMICAL
& ENGINEERING NEWS] June 7, 1993, pg. 28.

[6] Glen A. Fox, “Epidemiological and Pathobiological Evidence
of Contaminant-Induced Alternations in Sexual Development of
Free-Living Wildlife,” in Theo Colborn and Coralie Clement,
CHEMICALLY-INDUCED ALTERATIONS IN SEXUAL AND FUNCTIONAL
DEVELOPMENT: THE WILDLIFE/HUMAN CONNECTION (Princeton, N.J.:
Princeton Scientific Publishing Co., 1992), pgs. 147-158. And:
Peter J.H. Reijnders and Sophie M.J.M. Brasseur, “Xenobiotic
Induced Hormonal and Associated Developmental Disorders in
Marine Organisms and Related Effects in Humans,” in Theo Colborn
and Coralie Clement, CHEMICALLY-INDUCED ALTERATIONS IN SEXUAL
AND FUNCTIONAL DEVELOPMENT: THE WILDLIFE/HUMAN CONNECTION
(Princeton, N.J.: Princeton Scientific Publishing Co., 1992),
pgs. 159-174.

[7] Thomas A. Mably and others, “IN UTERO and Lactational
Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-P-dioxin. 3.
Effects on Spermatogenesis and Reproductive Capability.”
TOXICOLOGY AND APPLIED PHARMACOLOGY Vol. 114 (May, 1992), pgs.
118-126.

[8] Theo Colborn and Coralie Clement, CHEMICALLY-INDUCED
ALTERATIONS IN SEXUAL AND FUNCTIONAL DEVELOPMENT: THE
WILDLIFE/HUMAN CONNECTION (Princeton, N.J.: Princeton Scientific
Publishing Co., 1992), pgs. 1-2, list the following chemicals
“known to disrupt the endocrine system:” DDT and its degradation
products [DDE and DDD], DEHP (di(2-ethylhexyl)phthalate),
dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane and
other hexachlorocyclohexane congeners [forms], methoxychlor,
octachlorostyrene, synthetic pyrethroids, triazine herbicides,
EBDC fungicides, certain PCB congeners [forms], 2,3,7,8-TCDD and
other dioxins, 2,3,7,8-TCDF and other furans, cadmium, lead,
mercury, tributyltin and other organo-tin compounds, alkyl
phenols (non-biodegradable detergents and anti-oxidants present
in modified polystyrene and PVCs), styrene dimers and trimers,
soy products, and laboratory animal and pet food products.”

[9] Richard M. Sharpe and Niels E. Skakkebaek, cited above in
footnote 3, quoting B. Field and others, “Reproductive Effects of
Environmental Agents,” SEMINARS IN REPRODUCTIVE ENDOCRINOLOGY,
Vol. 8 (1990), pgs. 44-54.

[10] A. R. Moss and others, “Hormonal risk factors in testicular
cancer; a case control study,” AMERICAN JOURNAL OF EPIDEMIOLOGY
Vol. 124 (1986), pgs. 39-52.

[11] M.B. Jackson and others, “The Epidemiology of
Cryptorchidism,” HORMONE RESEARCH Vol. 30 (1988), pgs. 153-156.

[12] Peter K. Working, “Male Reproductive Toxicology: Comparison
of the Human to Animal Models,” ENVIRONMENTAL HEALTH PERSPECTIVES
Vol. 77 (1988), pgs. 37-44.

Descriptor terms: sperm count; fertility; cancer; birth defects;
statistics; undescended testicles; cryptorchidism; hypospadias;
estrogens; food safety; des; diethylstilbestrol; cattle;
agriculture; beef; contraceptives; birth control; the pill;
ethinyl estradiol; metals; chlorinated hydrocarbons; chlorine;
breast cancer;

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