The Precautionary Approach to Endocrine Disrupting Chemicals by Sheldon Krimsky

Sheldon Krimsky is a professor of urban and environmental policy at Tufts University in Massachusetts

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.

Legal Imperative

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 Dose Makes the Poison

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.

Reduction ad Absurdum

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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