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.
