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No
aspect of the extensive scientific evidence considered in Our
Stolen Future commanded more media attention than the controversial
reports of declining sperm counts, launched by the 1992 paper by
Carlsen et
al. reporting 40% decline in sperm count over the second
half of the 20th century.
Animal
studies clearly demonstrated that in utero exposure to low
levels of endocrine disruptors at critical times in development
cause low sperm counts and other sperm maladies. Human studies document
exposure to these compounds. Data presented by Carlsen et al.
suggested that major declines were occurring in people.
All
of a sudden, endocrine disruption seemed less theoretical and more
concrete in its impacts--not just concrete... potentially catastrophic
if the decline was real and if it was continuing. Industry scientists
set out to undermine the validity of the Carlsen report, seizing
upon many virtually unavoidable
difficulties in retrospective studies of something as difficult
to measure in an unbiased way as human sperm density. At times the
New York Times seemed in collusion with this effort, via the biased
reporting of the reporter on that newspaper's staff who handled
the story.
Shortly
after Our Stolen Future went to press, a series of new
studies began to emerge revealing, it would appear, significant
geographic variation in sperm count and in sperm count trends. The
bottom line for the sperm story is that:
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Sperm
counts have decreased significantly in some areas and held
steady in others. There are no reports of significant increases
in sperm count. Mathematically this means there has been an
overall average decline. But more practically, it means that
there may be clues as to the causes of decline in the geographic
patterns.
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Sperm
count varies geographically. The variability among areas is
as large as the largest temporal declines. A large number
of studies are now underway, documenting these geographic
changes and looking for their causes. Research
published in 2003, for example, finds large differences
in the United States comparing men in the mid-West to men
on the coasts.
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There
is no agreed-upon explanation of why declines have taken place,
if they have, nor why there is geographic variation.
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Endocrine
disruption is one of the plausible explanations for the declines,
and for the geographic variation. This is particularly the
case because controlled experiments
with laboratory animals reveal endocrine disrupters decrease
sperm count when the male fetus is exposed at critical times
of development in the womb. Results show ways in which in
utero exposure to endocrine disruptors can both increase
and decrease adult
sperm count.
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Humans
are exposed quite commonly to substances, such as phthalates
and dioxin, that are known to cause sperm count declines in
experimental animals. Data
from the CDC released in September 2000 indicate that
within the US one of the subpopulations with highest exposures
may be women of child-bearing age. The mixture of exposures
varies significantly among areas and demographic groups.
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Serious
epidemiological work on phthalates is now underway. Studies
published in 2003 link phthalate levels to DNA damage in sperm
and to sub-optimal sperm
characteristics (sperm count, mobility and deformity).
Other links to low sperm count are also being found, including
exposures to certain PCB
congeners and to maternal
smoking during pregnancy.
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It
is not likely that there is a single cause of low sperm count.
The process of sperm formation can be disrupted at multiple
points, some in the developmental formation of the glands and
organs essential for sperm production, some in altering hormonal
sensitivity, and some in the ongoing process in adulthood of
spermatogenesis. Different agents are likely to attack different
parts of the chain of events that leads to the production of
healthy sperm. This reality will confound all but the most sophisticated
of epidemiological studies. Taking cues from animal experiments
will be essential. |
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