Adenomyosis

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Xenoestrogen Research Still Too Crude (Xenoestrogens Cause Adenomyosis)

 

Jury Still Out on Estrogen-Like Chemicals, Adenomyosis

Fri Feb 22, 2002 5:28 PM ET By Anne Harding

NEW YORK (Reuters Health)

SYNOPSIS: Current research methods are too crude to determine the risk of xenoestrogens that may cause cancer, reproductive malformations, and female diseases [ such as adenomyosis ]. Current research does not take into account synergistic activity of these chemicals nor long term storage in the fat.

While studies of a link between exposure to chemicals with estrogen-like effects and cancer in women have had murky results, current research methods may simply be too crude to detect any relationship, some experts on the issue believe.

And there is evidence from animal studies that prenatal exposure to these compounds--found in products ranging from cosmetics to pesticides--could have long-lasting effects, scientists reported recently at a seminar at the American Academy for the Advancement of Science's annual meeting in Boston, Massachusetts.

Such prenatal exposure could be behind increasing rates of testicular and breast cancer, the decline in male fertility and sperm quality, and an increase in the number of deformations of the male genital tract, said Dr. Ana Soto of Tufts University.

These chemicals, known collectively as environmental estrogens or xenoestrogens, are so called because they exert estrogen-like effects, causing breast cells to grow and increasing uterine tissue mass.

Xenoestrogens are virtually ubiquitous in the environment. There are 87,000 chemicals that "potentially could be of concern"--75,500 of which are used in industry, noted Kristen Fertuck, a graduate student at Michigan State who reported on methods for screening these chemicals for their cancer-causing potential.

While evidence is mounting that environmental estrogens do not cause breast cancer, Dr. Sheila Zahm of the Division of Cancer Epidemiology and Genetics at the National Cancer Institute noted, there are clues that these chemicals could increase the aggressiveness of existing breast tumors.

It's tough for scientists to accurately measure a woman's exposure to these chemicals, she added. Such measures usually involve looking for a particular chemical in blood samples. But Zahm pointed out that many agents may persist in the blood for only a short time while still doing harm.

While attention has focused on environmental estrogens, she noted, chemicals that disrupt the endocrine system in other ways should also be investigated. One such chemical is atrazine, she said, which is currently the number one herbicide or weed killer in use in the US.

Atrazine throws off the brain's control of the pituitary gland, she explained, which in turn disrupts ovarian function. The chemical is banned in seven European countries, Zahm pointed out. Two Italian studies, she added, found atrazine increased women's risk of two types of ovarian tumor fourfold and nearly threefold, respectively.

Soto reported on a technique she and her colleagues developed to provide a fuller picture of environmental estrogen exposure. Xenoestrogens tend to collect in fat, and to stay there. The method involves taking a fat tissue sample and measuring the level of natural estrogen and estrogen-like chemicals it contains. It's possible to separate out the natural hormone, she added, and thus use what's left over to gauge a woman's total xenoestrogen exposure.

Soto questioned whether research done to date--which has largely involved the amount of a single chemical found in the blood--is able to truly evaluate the risks of estrogen-like chemicals.

Soto also conducted studies in mice that showed exposing the animals to low levels of bisphenol A, a xenoestrogen released from the linings of metal cans, during pregnancy resulted in changes in their offspring. The in-utero-exposed animals entered puberty early, and the males had swollen prostates and decreased sperm counts. And the female animals had changes in mammary tissue similar to those seen in pregnant animals.

Dr. Retha Newbold of the National Institute for Environmental Health Sciences has been conducting research on the effects of DES in mice. DES, a very powerful artificial estrogen, was prescribed from 1945 to 1976 to prevent miscarriage, and resulted in reproductive malformations in female children of women exposed to the chemical.

Newbold is concerned, she said, that prenatal exposure to the many chemicals in the environment with estrogen-like effects could be harmful. She is currently testing a number of these chemicals in mice to gauge whether they do pose a risk.

While it is not likely that any particular chemical causes cancer per se, Newbold said, their effects nevertheless must be studied. Some chemicals could, she noted, cause problems in sensitive populations.

"We have to be worried about not exposure to one but to multiple agents," she told Reuters Health in an interview. "I don't want to be too quick to say 'no, there's nothing to worry about."'

She added, "It's going to take epidemiology combined with these animal studies to really make sense about what's going on."