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Sheldon Krimsky is a professor of urban and environmental policy at Tufts University in Massachusetts
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As the debate rages over the exact mechanism of endocrine disruption, policy-
driven mandates are forging new alliances in the scientific community.
The debate over the endocrine disruption hypothesis represents more than just
another disagreement in the scientific community. It has opened the door to a
new way of thinking about the onset of uninherited diseases, the nature of
scientific investigation, and the role of scientific knowledge in the
policymaking process. In the past ten years, discoveries that have helped to
build the environmental endocrine hypothesis are already having a quiet
revolution in science and policy by influencing the way we think about chemical
risks.
In part, the revolution has been sparked by a new approach to environmental
policy forged in Europe: the precautionary principle. The term "precautionary
approach" was introduced during the 1987 Second International Conference on the
North Sea to declare an obligation to control the most dangerous substances
even before a definitive causal link had been established between the chemicals
and health or environmental effects. This principle represents a radical
departure from traditional approaches to risk assessment.
In the United States, the precautionary principle has emerged as the driving
force behind new legislative mandates aimed at reducing public health risks
from exposure to harmful environmental contaminants, even before the scientific
community has reached consensus on the exact mechanism that may cause adverse
effects in humans.
Two new laws passed by Congress in 1996, the Food Quality Protection Act and
the Amendment to the Safe Drinking Water Act, mandate the U.S. Environmental
Protection Agency (EPA) to develop a screening and testing program for
endocrine disrupting chemicals. These laws stipulate that the potential for
harm of endocrine disrupting chemicals be assessed not just on a case by case
basis. Rather, the cumulative, additive, or synergistic effects must also be
determined. It's a tall order, considering that the state of the science is
still in its infancy, and it is questionable whether EPA will be able to meet
its legislative deadline given the magnitude of its task.
In fact, it was only in 1991 that Theo Colburn organized the interdisciplinary
Wingspread Workshop in Racine, Wisconsin, at which researchers from diverse
specialties came to an agreement on the fundamental hypothesis that linked
persistent organic chemicals in the environment to abnormal reproductive and
developmental effects associated with the endocrine dysfunction of wildlife.
Though researchers agree that field and laboratory studies of animals provide
compelling evidence of such a link, the scientific community remains sharply
divided on whether organic chemicals are responsible for increases in certain
human cancers, diseases of the human reproductive system, the immune system,
and the thyroid gland. Nonetheless, scientists have known for at least two
decades that the synthetic hormone DES (diethylstilbestrol), prescribed to
pregnant women in the 1940s, 50s, and 60s, proved to be a time bomb for the
fetuses of those women. It was not the mothers, but instead their offspring,
who suffered abnormalities of the reproductive system. This inadvertent
experiment led researchers to examine the complex mechanism that binds foreign
agents to hormone receptors.
The endocrine disruption hypothesis has also unleashed a revolution in toxicity
theory. The traditional canon that *the dose makes the poison* has proven
inadequate in explaining the complex workings of the endocrine system. The
endocrine system involves a myriad of chemical messengers and feedback loops.
New evidence from animal studies shows that there may be adverse effects at
small doses that are not observed when the animal is exposed to larger
doses.
In addition, the developing fetus is highly sensitive to hormonal changes
during development. Effects of chemical exposure during fetal development may
not show up until maturity, as in the case of DES.
It is ironic that just as the human genome project promises to map every one of
the estimated 100,000 genes an exercise in reductionist research, the endocrine
disruption hypothesis ,has broken new ground in cooperative research. While
most of the emphasis placed on discoveries from the human genome project are on
inherited traits, genetic mutations, and polymorphisms, the environmental
endocrine hypothesis is pointing to a new direction of research to account for
human disease.
Though much scientific research can only be conducted at the molecular or
cellular level, other areas can be studied only at the level of the entire
organism. While the tendency in science is toward an ever finer structure of
specialization, the hypothesis that chemicals ubiquitous in our environment may
be masquerading as endogenous hormones has created a new demand for integrative
biological studies, multidisciplinary workshops, and creative
collaborations.
While some critics may hesitate to endorse the endocrine disruption hypothesis
until all the evidence is in, recent policy mandates have helped forge new
alliances in the scientific community. In short, policy-driven,
multidisciplinary collaborations will bring together scientists interested in
childhood diseases, developmental disorders, and abnormalities in wildlife on a
new joint venture in scientific inquiry.
Krimsky's essay "The Precautionary Approach to Endocrine Disrupting Chemicals"
will appear in the Fall 1998 issue of FORUM for Applied Research and Public
Policy.
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