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  September/October 1999 Features:
Cancer, Inc.
Rachel's Daughter
The Estrogen Connection
Signs of the Wild
Manta Dance
 
  Departments:
Letters
Inside Sierra
Ways & Means
Good Going
Hearth & Home
Lay of the Land
Home Front
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Last Words
 

Sierra Magazine
The Estrogen Connection

How synthetic chemicals may increase breast cancer

by Sharon Batt and Liza Gross

Breast cancer kills more women between the ages of 35 and 50 than any other disease. These women belong to the first generation exposed to synthetic chemicals and poisons on a wide scale, from the moment of conception. Roughly 200 of these chemicals can be detected in the average person's body fat. Many of them mimic a woman's naturally occurring estrogen, which means they can affect the normal production and metabolism of estrogen. And that means they share an alarming characteristic with some of the known risk factors for breast cancer. Like "delayed" or no childbirth, early menstruation, and late menopause, they increase a woman's lifetime exposure to estrogen.

Although the jury is still out on whether a high-fat diet increases risk, Dr. Samuel Epstein, a professor of occupational and environmental medicine at the University of Illinois, insists the culprit is not the fat but what's in the fat: hormones, pesticides, and industrial pollutants. Cancer researchers at Tufts University discovered in 1991 that chemical ingredients in some everyday plastics act like estrogens, as do certain PCBs, pesticides, and ingredients called surfactants, which help paints, detergents, and insecticides stick to surfaces. In 1994 British scientists found that trace amounts of surfactants can stimulate the growth of breast cancer cells.

It turns out that estrogen, like cholesterol, can be good or bad. "Things in plant products, such as soy and broccoli, promote good estrogens that appear protective against breast cancer," says Dr. Devra Lee Davis, an epidemiologist at the World Resources Institute. "In contrast many synthetic organic estrogens, such as those in some plastics, fuels, and pesticides, appear to increase risk." Davis calls "foreign" substances found in pesticides and plastics "xenoestrogens." They're fat-soluble and collect in tissues with high fat content, where they bioaccumulate—that is, concentrate as they move up the food chain—until they settle in human fatty tissue, including breast tissue. As we age, certain harmful xenoestrogens like organochlorines concentrate in our fat, Davis says. "Fat has been called the body's natural hazardous-waste site."

Because extended exposure to estrogen increases breast cancer risk, she explains, long-term exposure to synthetic endocrine-disrupting chemicals that accumulate in breast tissue might also promote the disease. Skeptics contend that synthetic chemicals are much weaker than the body's own estrogen and couldn't possibly play a role. But unlike a woman's own estrogen, synthetic varieties are not easily metabolized and excreted—some can linger in the body for decades. And they may have a much more potent effect on a fetus or young child, whose still-developing body interprets chemical signals much differently than an adult's.

This theory challenges the traditional notion that a substance must directly damage a gene to cause cancer. Davis and other scientists now believe that because hormones are the chemical messengers that switch genes on and off, agents that interfere with those signals can also create genetic damage. Also being challenged is the old saw that "the dose makes the poison." Increasing evidence suggests that when you're exposed to a chemical is at least as important as the amount you're exposed to. The timing of exposure is especially significant with breast cancer because the breast goes through so many changes over a woman's lifetime. A six-week-old fetus that's just growing breast cells, a girl going through puberty whose breasts are just budding, a menstruating woman whose breast cells are rapidly dividing, may all be far more vulnerable to the effects of chemicals than the adult male whom scientists have traditionally studied when they set tolerance levels.

Industry groups claim that because none of these theories have been conclusively proven, there's no basis for regulation. What would give us that proof? Deliberately exposing one group of people to suspected carcinogens and comparing the results to an unexposed group. This type of experiment is obviously unethical, yet we're essentially conducting uncontrolled human experiments—because there is no unexposed population—by allowing the deliberate release of known and suspected carcinogens into our environment. Good public policies can be made in advance of absolute proof, Davis says, citing the precautionary principle: where there are indications of significant risks to public health, we must act to diminish those risks even in the absence of scientific certainty. (For more on the precautionary principle, see www.wri.org.) Waiting for decisive proof, she says, amounts to playing Russian roulette with women's lives.


More Resources on breast cancer research and treatment.

Sharon Batt, a breast cancer survivor, is the author of Patient No More: The Politics of Breast Cancer. Liza Gross is Sierra's copy editor.

(C) 2000 Sierra Club. Reproduction of this article is not permitted without permission. Contact sierra.magazine@sierraclub.org for more information.


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