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males receive extra doses of testosterone just prior to delivery, as the hormone circulates in the amniotic fluid. “The differences in hormone exposure caused by the positioning effect of the mice in the uterus were quite small, yet the behavioral and physiological effects were nonetheless significant,” writes Krimsky in Hormonal Chaos. “Some animals that experienced the positioning effect become more aggressive and territorial—the result of one-time exposures to additional estrogen (or testosterone) that seemed to have made imprints in their brains. These experiments revealed that even minute changes in the hormone exposure of the developing fetus during certain sensitive stages could result in measurable effects.”

Colborn, vom Saal, and other researchers began sharing data, “a unique cross-fertilization of scientific disciplines,” says Krimsky, which soon produced provocative results. Toxicologists were forced to rethink the dose-response paradigm and to consider the possibility that barely detectable doses of estrogenic chemicals could disrupt the functioning of the exquisitely sensitive, self-regulating endocrine system—a system that engages in “cross talk” with every other system in the body, including the nervous system. In July 1991, researchers from a number of different disciplines met at a seminal scientific meeting to discuss “Chemically Induced Alterations in Functional Development: The Wildlife/Human Connection” at the Wingspread Conference Center in Racine, Wisconsin. The consensus statement signed by twenty-one scientists at the meeting laid the groundwork for future research and marked the start of public debate on the subject of environmental estrogens.

This debate was given added impetus by Danish researcher Niels Skakkebaek and British researcher Richard Sharpe, who, working independently, had both identified spiking rates of male reproductive problems. Together, the two wrote a paper, published in the British medical journal The Lancet in 1993, linking fetal exposure to estrogens or estrogen mimics to declining sperm counts, sperm quality, and motility. The threads of the environmental estrogen hypothesis began coming together in the mid-nineties, as scientists in various disciplines who had been working separately began meeting and pooling their data. Funding agencies, too, began taking notice, and as more money became available to study the problem, generating more data, the environmental endocrine hypothesis achieved a greater degree of scientific legitimacy. “Additional research funds to study different components of the environmental endocrine hypothesis soon became available. Scientists in a variety of subfields of molecular and cellular biology, toxicology, and enviromental sciences, taking notice of the new funding opportunities, began to reorient their model systems to compete for a share of the newly available grant money,” writes Krim-sky. “Once it enters America’s network of biomedical and environmental funding streams and is incorporated within program requests for proposals, a scientific hypothesis gains new constituencies.”

As a result of this focused research program over the past decade, scientific understanding of the mechanisms by which estrogenic chemicals exert their effects has grown dramatically. Studies have shown that environmental estrogens may alter production of normal hormones, disrupt the transport of hormones, affect the metabolism of hormones, interfere with hormone signaling at the receptor level, or modify hormone-regulated gene transcription. Adverse effects include reproductive failure, developmental effects, immune system dysfunction, and cognitive and behavioral pathologies of various types. The types of chemicals that may produce these effects include pesticides, organocholorines, plasticizers, heavy metals, and plant estrogens. In Our Stolen Future, Theo Colborn and her coauthors list eighty-five chemicals known to be estrogen disrupters, many of them ubiquitious in the environment. We are living, scientists now say, “in a sea of estrogens.” Does this have any