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Emerging
science on the impacts of endocrine disruptors on people.
Our
Stolen Future reviews scientific studies of the impacts of
endocrine disruptors on human health through 1995 (hardback) and
1996 (paperback). The most detailed information available was
from studies of the daughters and sons of women who took diethylstilbestrol
(DES) during pregnancy. The impacts were devastating and included
severe reproductive tract deformities, declines in sperm count,
alterations in behavior and a greatly elevated risk of a rare
cancer. Several industrial accidents involving relatively high
exposures also provided concrete examples of human harm by endocrine
disruptors, with the most dramatic effects seen in children exposed
in the womb. Ongoing studies of human impacts at environmental
levels (exposures experienced by a significant portion of the
US population) were consistent with significant impacts (especially
neurological) but were insufficient to prove, with scientific
certainty, that harm had been caused by the mechanism of endocrine
disruption.
Research
has exploded since the book was published. Follow links below
to find brief summaries of key results. Some of these studies
describe advances in epidemiology specifically linked to endocrine
disruption. Others examine human health endpoints which, based
on animal studies, may have endocrine disruption as a causative
agent.
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Fetal
deaths are linked to exposure to pesticides during the
most sensitive period of fetal growth, pregnancy weeks 3-8.
This is the time period when major organ systems are forming.
Mothers living within a few miles of agricultural pesticide
use are vulnerable.
Hypospadias--a
birth defect of the penis--is occuring with increasing frequency
in the United States and other countries. This defect is
caused by developmental errors in the womb. It can be easily
and reliably produced in laboratory experiments with rodents
using endocrine disrupting chemicals.
Background
levels of PCBs accumulated by eating fish and other contaminated
food available in grocery markets can be sufficient to undermine
immune system protections against childhood diseases.
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Sperm
counts
may be holding steady in some places, but in others they
are declining.
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IQ
and reading ability of children exposed to modestly
elevated PCB levels in the womb are beneath their less-exposed
peers.
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Children
exposed to high levels of agricultural pesticides have difficulty
performing simple motor tasks.
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Important
broad trends
in the emerging science emphasize the ubiquity of exposure,
the extremely low levels at which impacts occur, the diversity
of hormonal systems affected, the ever expanding list of
chemicals involved, and the importance of focusing on life
long impacts of fetal exposure.
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Girls
in the United States are reaching puberty
at an increasingly early age. Animal
studies show that the age of sexual maturity is affected
by exposure to endocrine disruptors in the womb.
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The
evidence linking endocrine disruption and human
cancer remains highly plausible but uncertain. For
the most part, as affirmed by the National Academy of Sciences
report released in
August 1999, the necessary studies haven't been done.
- Human
epidemiological studies testing for associations between
endocrine disruptors and cancers typically focus on only
a handful of endocrine disruptors (usually DDT or its
metabolites, dioxin, and PCBs).
- For
the most part, they measure contamination in adults and
ask whether these are associated with cancer risks in
adulthood.
Negative
results from such studies tell you nothing about all the
other endocrine disruptors, hundreds if not thousands of
them, to which people are exposed daily. Nor do they reveal
anything about the role that developmental exposure may
play in increasing risk to adult cancers.
This
approach--adult exposures, adult risks---has only limited
merit for asking about cancers induced in adulthood,
specifically for the contaminants tested. Interactions among
contaminants may render the epidemiological studies virtually
impossible to interpret. And now there is evidence
for interactions among contaminants and infectious disease
agents. Only a handful of studies have considered possibilities
like this in relation to the origens of cancer. The difficulty
of these epidemiological hurdles means that the likelihood
of false negatives (statistical analysis indicating
there is no relationship when in fact there is) is very
high.
Some
strong evidence, however, is accumulating as studies become
more sophisticated and broaden the universe beyond the few
highly studied contaminants. More...
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