the environment and gynecological diseases. Research investigating these links has had mixed results. Now several new studies are adding to the evidence that some estrogenmimicking pesticides and industrial chemicals may increase women’s risk of uterine and ovarian diseases—helping to solidify a theory that emerged two decades ago. “Our studies are beginning to corroborate the idea that environmental estrogen may be associated with endometriosis,” said Germaine Buck-Louis, director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development’s epidemiology division in Maryland. Back in 1993, a connection between endometriosis and environmental chemicals was discovered. Rhesus monkeys fed food contaminated with dioxins—hormone-disrupting pollutants created by waste incinerators and other industries—developed endometriosis 10 years later. Endometriosis, when uterine tissue grows in the ovaries or other parts of the body, often causes pelvic pain and infertility. An estimated 10 to 20 percent of reproductiveage women in the United States suffer from it, according to the Endometriosis Foundation of America. In a major new study, two groups of women in the Salt Lake City and San Francisco areas—one group with pelvic pain and the other with no symptoms—were more likely to be diagnosed with endometriosis if they had high blood levels of the estrogenlike pesticide hexachlorocyclohexane (HCH) than women with low levels. HCH has been banned as a crop pesticide in the United States but it builds up and persists in the environment, so it remains in some food supplies. Calling the research “revolutionary,” Buck-Louis said that finding the link in both groups of women “is a pretty strong signal” that the connection between endometriosis and the pesticide is real. Also, women in the same group with the highest level of a sunscreen chemical, benzophenone, in their urine had a 19 percent higher risk of endometriosis than women with the lowest levels, according to research published in Environmental Science and Technology. And in Italy, women had endometriosis more often if they had higher levels of two banned chlorinated chemicals that can disrupt hormones—polychlorinated biphenyls (PCBs) or residue of the insecticide DDT, according to a 2009 study of 158 women. Recent research has uncovered links to other gynecological problems, too. Women in Greece diagnosed with polycystic ovary syndrome (PCOS)—which causes irregular menstrual periods, infertility, weight gain and excessive hair growth—were more likely
to have higher blood levels of the estrogenmimicking chemical bisphenol A than women without the disease, according to a study published last year. “It’s certainly plausible that any outside source that alters estrogen levels, even slightly, could contribute to gynecological diseases,” said Dr. Megan Schwarzman, a family physician at San Francisco General Hospital and an environmental health scientist at the University of California, Berkeley. Exposure to many hormone-disrupting chemicals starts in the womb, and some scientists suspect the timing may be important in determining reproductive disease risk later in life. “We know from animal models that there are critical periods during early development when cells are rapidly dividing and forming the circuitry through which cells will communicate with each other to form various tissues of the body,” said Retha Newbold, a reproductive biologist at the National Institute of Environmental Health Sciences in North Carolina. “When chemicals alter this set-up, the changes may not be reversible.” Future generations of females may be at risk, too, according to new animal research by Washington State University scientists. Female rats exposed in the womb to high doses of several chemicals—including pesticides and plasticizers—developed cysts resembling human polycystic ovarian syndrome and premature menopause, according to the study published in PLoS One in July. Those changes were passed down through three generations—great-granddaughters of the exposed rats also developed cysts and other ovarian problems, even though they were not directly exposed. Seeking to learn how the chemicals were able to harm future generations, the Washington State researchers examined the DNA of the ones whose mothers were exposed to vinclozolin, an estrogenic fungicide commonly used in the wine industry. They found that the chemical had reprogrammed genes as the rat fetuses developed. Other chemicals in the study that had the multigenerational effects were dioxins, a pesticide mixture including permethrin and DEET and a plastic mixture including BPA and two widely used phthalates. “What we are seeing in animal models is sobering,” said John McLachlan, a biomedical scientist at Tulane University in New Orleans. The gene mechanisms responsible for transmitting such harmful effects across generations are essentially the same in humans, he said. In the case of uterine fibroids, the body’s natural estrogens turn genes on and off in the smooth muscle of the uterus that allow the tumors to grow, according to research by McLachlan and col18 leagues. They are now investigating
“ Our studies are beginning
to corroborate the idea that environmental estrogen may be associated with endometriosis ” -Germaine Buck-Louis
16 | AUGUST 15–21, 2012 | BOISEweekly
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