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In
a scientifically comprehensive and cautious global assessment of
the state of endocrine disruption science, the World Health Organization
and the US National Institute of Environmental Health Sciences conclude
that the breadth of evidence from laboratory, wildlife and human
studies justifies concerns about the possible human health impacts
of endocrine disruptors.
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"Overall,
the biological plausibility of possible damage to certain human
functions (particularly, reproductive and developing systems)
from exposure to EDCs seems strong when viewed against the background
of known influences of endogenous and exogenous hormones on
many of these processes. Furthermore, the evidence of adverse
outcomes in wildlife and laboratory animals exposed to EDCs
substantiates human concerns. The changes in human health
trends in some areas (for some outcomes) are also sufficient
to warrant concern and make this area a high research priority,
but non-EDC mechanisms also need to be explored." (emphasis
added) [Chap 1.7] |
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The
report acknowledges considerable scientific uncertainty, particularly
in establishing definitive causal links between known exposures
to endocrine-disrupting chemicals in people and endocrine-mediated
adverse health effects.
For
example,
- even
though specific contaminants are known, via animal experiments,
to act as endocrine disruptors;
- and
even though people are known to be exposed to these compounds;
- and
even though the types of health effects expected on the basis
of animal experiments are occurring in people;
there
is no scientific evidence proving in people that effect is caused
by the contaminant acting through an endocrine pathway.
This
is an appropriate high level of scientific skepticism for research.
There may be other pathways, not endocrine-mediated, that are the
means by which the contaminant is having an effect.
And
thus on this basis, the assessment concludes that while it is plausible
that endocrine disruption is the cause of the health effects, it
is not scientifically proven.
While
such caution is warranted with respect to the scientific understanding
of the core mechanisms involved, UK toxicologist Gwynne Lyons argues
that this sort of residual uncertainty should not prevent public
health measures being taken: "It is worth remembering that
epidemiological research in 1952 demonstrated that smoking caused
lung cancer, but the probable causal mechanism was not found until
1996, and even this is still not universally accepted."
Lyon's
also cites DDT as another good example of the delay between evidence
of effect and proof of the mechanism. According to Lyons, "The
IPCS report acknowledges that DDT, via its degradation product,
caused eggshell thinning, leading to broken eggs and other adverse
reproductive effects in several bird species. However, as the report
states, “[the] mechanism of eggshell-thinning has never been
completely deduced” and there are several hypotheses. Therefore,
the report highlights that “it cannot be stated with certainty
that it is indeed a result of endocrine disruption”. However,
what really matters from a regulatory point of view is the end-result
of the exposure, not whether the mechanism of action is known with
certainty.
Lyon's
concludes that it would be "totally unacceptable for regulation
of chemicals of concern to have to wait until the precise mechanism
of action was known."
The
report also observes (Chapter 1.2):
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- Exposure
to EDCs during the period when programming of
the endocrine system is in progress may result in a permanent
change of function or sensitivity to stimulatory/inhibitory
signals.
- Exposure
in adulthood may be compensated for by normal homeostatic
mechanisms and may therefore not result in any significant
or detectable effects. [added: which is why regulatory
testing has been misled by decades of focus upon adult organisms]
- Exposure
to the same level of an endocrine signal during different
life history stages or during different seasons may produce
different effects.
- Because
of cross talk between different components of the endocrine
systems, effects may occur unpredictably in endocrine target
tissues other than the system predicted to be affected.
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