The Riddle of Gender - Deborah Rudacille [147]
Another body of research is beginning to provide support to DES sons who believe that their gender and/or reproductive anomalies may have been caused by prenatal exposure to an endogenous estrogen. In 2001, researcher Niels Skakkebaek and colleagues published an article in the journal Human Reproduction providing evidence of the link between exposure to estrogenic chemicals ubiquitous in the environment and a condition that the researchers have termed “testicular dysgenesis syndrome.” Epidemiologie evidence from around the world has shown a rise in testicular cancer, low and declining sperm quality, reproductive tract abnormalities, and abnormal sexual differentiation in humans—a collection of effects that the authors attribute to prenatal exposure to chemicals that disrupt endocrine signaling. Such chemicals (collectively termed “endocrine disrupters” or EDCs) have become the target of major research programs in Europe and the United States. DDT, a potent endocrine disrupter, was banned in the United States following publication, in 1962, of Rachel Carson’s book Silent Spring, but many other chemicals in heavy use today also bind to hormone receptors, producing well-documented reproductive and other abnormalities in wildlife and laboratory animals. The publication of the book Our Stolen Future sounded the alarm in 1996 with its argument that some man-made chemicals disrupted chemical signaling in the body, creating myriad negative health effects. Subsequent studies have reinforced the environmental endocrine hypothesis advanced by the book’s authors: Theo Colborn, Dianne Dumanoski, and John Peterson Myers. Evidence has been steadily accumulating that the effects of endocrine-disrupting chemicals are not confined to wildlife. In fact, as the Skakkebaek article makes clear, many of the same effects are increasingly being observed in humans.
In April 2002, the U.S. National Institute of Environmental Health Sciences and the World Health Organization released a joint document that concluded that “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.”
The environmental endocrine hypothesis was germinated in 1979, when researcher John McLachlan, at that time working in the Laboratory of Reproductive and Developmental Toxicology at the National Institute of Environmental Health Sciences, in Research Triangle Park, North Carolina, organized the first symposium on the effects of estrogenic chemicals in the environment. McLachlan had been studying DES since 1971 and he was using DES as a model for investigating the effects of DDT, on the basis of similarities in their chemical structure. At the 1979 meeting on “Endocrines in the Environment,” McLachlan and Retha R. Newbold presented data showing the effects of DES on the genital tract development of a mouse model. McLachlan and Newbold linked the effects of DES to those of industrial chemicals including bisphenol A, widely used in the production of plastics, and other environmental chemicals that exhibited estrogenic effects— essentially “tricking” the body into responding to them as estrogens. Bisphenol A (BPA) was developed in the laboratory of none other than Sir Charles Dodds, the man who developed DES.