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 a new animal study 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 multi-generational 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, 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 on and off genes in the smooth muscle of the uterus that allow the tumors to grow, according to research by McLachlan and colleagues. They are now investigating whether estrogen-mimicking chemicals in the environment affect these same genes.
The danger of estrogen-like chemicals already has been well-documented with DES, or diethylstilbestrol, a drug that was prescribed to millions of women at risk of miscarriages between 1940 and 1971. Daughters and granddaughters of the pregnant women who took the potent estrogenic drug had an increased risk of endometriosis, uterine fibroids and rare reproductive cancers.
But pesticides, sunscreen ingredients and PCBs are less potent hormone mimics than DES. The effects on women’s health are not as clear.
Some studies have found no connection between women’s exposure to environmental chemicals and gynecological diseases. For instance, among several hundred women in Italy highly exposed to dioxins from a 1976 factory explosion, UC Berkeley scientists found no significant increase in endometriosis linked to their contaminant levels. And in Japan, there was no increased rate of the disease among 139 infertile women with higher exposures to hormone-disrupting compounds including PCBs and dioxins, according to a 2005 study.
Newbold said because decades can pass between exposure during fetal development or early childhood and the manifestation of the disease in adult life, it can be difficult to nail down a link.
“Only recently are studies starting to focus on developmental risk factors in relation to adult disease,” she said.
Endometriosis and fibroids are referred to as “benign uterine diseases,” characterized mostly by painful periods, according to McLachlan. “Because these growths are not life-threatening or malignant, traditionally, these diseases haven’t garnered the attention they should,” he said.