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#343 - Are Environmental Chemicals Causing Men To Lose Their Fundamental Masculinity, 23-Jun-1993

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

=====

[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;
estrogen; food safety; des; cattle; agriculture; beef; birth control;
birth control pill; ethinyl estradiol; heavy metals; chlorinated
hydrocarbons; chlorine; breast cancer;