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---February 17, 1994---
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For the past 3 or 4 years, evidence has been accumulating that many industrial chemicals (including many common plastics, pesticides, and by-products of combustion) mimic hormones. These hormone mimickers disrupt reproduction and development in humans and in many other species of mammals, birds, and fish. A growing body of evidence also indicates that these same chemicals may cause some of the most common and fastest-increasing cancers: breast cancer in women, and cancers of the testicles and prostate in men.

The American Chemical Society [ACS] recently affirmed the following phenomena: [1]

** Sperm count in men worldwide has dropped to 50% of what it was 50 years ago.

** The incidence of testicular cancer has tripled in some countries in the last 50 years and prostate cancer has doubled.

** Endometriosis--the growth outside the uterus of cells that normally line the uterus--which was "formerly a rare condition, now afflicts 5 million American women," the ACS said.

** In 1960, a woman's chance of developing breast cancer during her lifetime was one in 20. Today the chances are one in nine.

** Female common terns (sea birds) are sharing nests near a PCB-contaminated site in New Bedford Harbor, Mass., an unnatural female-female pairing.

** Young male alligators in pesticide-contaminated lakes in Florida are growing up with penises so small that they are "sexually incompetent."

In January, the federal National Institute of Environmental Health Sciences [NIEHS] convened a meeting of 300 scientists who presented papers on estrogens and estrogen mimickers in the environment. Many of those scientists think there's probably a connection between diminished sperm counts, increasing endometriosis, female-to-female pairing in birds, sexually incompetent alligators, and breast cancer in women. The connection is poorly understood, they say, but the common link is probably chemicals dumped into the environment that mimic, or interfere with, hormones.

Slowly, mainstream scientific thinking has been coming to grips with this accumulating bad news. First the American Chemical Society began to write about it. [2] Then the National Institute of Environmental Health Sciences [NIEHS], a division of the U.S. National Institutes of Health, started writing about it. [3] And this month the JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION (JAMA) broke the story for its readers: "Estrogen and [chemical] agents that mimic it appear to be more pervasive and problematic then ever suspected," JAMA said February 9th. [4]

Estrogen is usually considered a female hormone, but males produce estrogen too, in small amounts. In the developing fetus, in both humans and animals, a specific ratio of estrogen to androgens (male hormones) must be maintained for proper sexual differentiation to occur; in other words, for a male to become a male and a female to become a female --regardless of the species --a certain balance of male and female hormones must be present in the mother between the time of fertilization and the time of birth or hatching.

If the hormone balance is disturbed, the offspring will be born with two sets of partially developed sex organs (intersex), or with a single set that is incompletely or improperly developed. Diminished sperm count, or future cancer, may be set at this early stage.

All plants and animals are composed of cells --tiny bags of fluid that work cooperatively together to carry out metabolism (extraction of energy from nutrients) to maintain life. The human body is composed of roughly 50 trillion individual cells that all cooperate and communicate with each other. Hormones are chemical messengers, essential to the body's healthy cooperation and internal communication. Hormones are present at very low levels (parts per billion or even parts per trillion), and often for only short periods of time, yet they have very powerful, long-lasting effects on growth, development, and metabolism.

The female hormone, estrogen, and chemicals that mimic estrogen, operate inside cells by fitting themselves into "estrogen receptors" (proteins) the way a key fits into a lock. Once the key is in the lock, the key-and-lock together can move into the nucleus of a cell and attach to the DNA, releasing messenger RNA which then causes a cascade of changes in cells, tissues, and organs throughout the body.

No, the story of estrogen mimickers is not simple. Some estrogen mimics fit into the lock wrong, filling up the space that the "correct" key would have used, thus interfering with natural estrogens; these are called estrogen antagonists. Some estrogen mimickers fit into locks that weren't ever intended to have an estrogen fitted into them. The amount of natural estrogen in the mother is usually much greater than the amount of estrogen mimickers. However most natural estrogens are bound up by sex-hormone-binding proteins in the blood stream, which are not able to bind estrogen mimickers. This increases the effective dose of the mimickers. The many ways estrogen mimickers can cause problems are just now beginning to be appreciated.

"The structural diversity of estrogenic chemicals is enormous," says John A. McLachlan, chief of the reproductive and developmental toxicology laboratory at NIEHS, according to JAMA.

In other words, you cannot simply observe a molecule and tell, by its chemical structure, whether it will act as an estrogen mimic or not.

"Compounds with widely different structure bind to estrogen receptors even though they bear no obvious structural resemblance" to estrogen, says John A. Katzenellenbogen, professor of chemistry at University of Illinois.

Examples of estrogen mimickers are DDT and its breakdown by-product DDE; Kepone; dieldrin; dicofol; methoxychlor; some PCBs; 3,9-dihydrooxybenz[a]anthracene; and alkyl phenols from penta-to nonylphenol, as well as bisphenol-A (the building block of polycarbonate plastics) which is used in many common detergents, toiletries, lubricants, and spermicides. Many estrogen mimickers are persistent (they resist breaking down in the environment) and highly soluble in fat (causing them to accumulate in the bodies of fish, birds, and mammals, including humans). Many of them cross the placental barrier and pass from the mother to the developing fetus.

It is not simple to distinguish estrogens from non-estrogens. "Historically, we think of the receptor as a switch," turning on or off the body's reactions. But it is not that simple, says George M. Stancel, head of the department of pharmacology at University of Texas Medical School. Estrogen-like chemicals can form "many molecular configurations" that can "act in differing ways," Stancel told JAMA. The same chemical can also act differently in different tissues, Stancel said.

To complicate the picture further, some cells appear to have estrogen receptors on their surface, rather than inside. So "even if compounds do not manage to get inside cells, they may still be estrogenic," says Cheryl Watson, associate professor of biological chemistry at the University of Texas Medical Branch at Galveston.

Finally, JAMA reported that estrogenic chemicals have a cumulative effect. David Feldman, professor of medicine and endocrinology at Stanford University, says, "The cumulative effect may be much greater than any individual molecule." Ana M. Soto at Tufts University combined 10 estrogen mimickers, each at one-tenth of the dose required to produce a minimal response; she found that the combination produced an estrogenic response.

This last bit of information has far-reaching implications for the regulation of chemicals. For 50 years the U.S. has regulated chemicals one by one, by conducting laboratory experiments on animals, and by experimenting on workers. If rats or workers get sick, then a particular chemical may be regulated to a level 10 times (or 100 times) lower than the lowest amount that caused an observable effect.

If chemicals at low ("safe") levels combine to produce an effect, this means that chemicals will have to be regulated in combination. "Testing mixtures is right on the mark" says George M. Stancel, at University of Texas Medical School. Kenneth Olden, head of NIEHS, agrees. "[W]e cannot ignore this milieu we live in that has all these estrogens. We have polluted our environment. It is polluted. Now we have to allocate resources to sort out the different effects of agents and learn whether they are synergistic, additive, inhibitory, or antagonistic. We don't know," Olden says, meaning we must try to learn whether chemicals in various combinations are weaker or stronger than each chemical alone.

But these are scientists pretending. Pretending that science can do something it cannot actually do. There is not sufficient money to study the full effects of individual chemicals, much less combinations of chemicals.

Scientists can pretend that they can discern "safe" levels of hundreds of different chemicals, all acting in combination. They can pretend that they can understand all the ill effects of multiple hormone mimickers on each type of cell, each tissue and each organ at every stage of development from conception to birth, through youth and puberty and into maturity, in each of the thousands of affected species. They can pretend to know these things, but they cannot ever actually know them. They are just pretending.

Scientists can pretend, but in so doing they perform a great disservice, preventing decision-makers from seeing what really needs to be done: we need to abandon the practice of chemical-by-chemical regulation. We need to regulate whole CLASSES of chemicals. And the dangerous classes need to be phased out and banned. Zero discharge. Pollution prevention. These are the keys to sustainability and survival.
                                                                         --Peter Montague, Ph.D.
[1] Bette Hileman, "Environmental Estrogens Linked to Reproductive Abnormalities, Cancer," C&EN [CHEMICAL & ENGINEERING NEWS] January 31, 1994, pgs. 19-23.

[2] Bette Hileman, "Concerns Broaden over Chlorine and Chlorinated Hydrocarbons," C&EN [CHEMICAL & ENGINEERING NEWS] April 19, 1993, pgs. 11-20.

[3] Theo Colborn, Frederick S. vom Saal, and Ana M. Soto, "Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 101 No. 5 (October 1993), pgs. 378-384.

[4] Paul Cotton, "Environmental Estrogenic Agents Area of Concern," JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Vol. 271 (February 9, 1994), pgs. 414, 416.

Descriptor terms: endocrine disruptors; estrogen; androgens; hormones; wildlife; endocrine system; reproductive system; niehs; national institutes of health; national institute of environmental health sciences; nih; american medical association; ddt; dde; pesticides; plastics; dicofol; methoxychlor; pcbs; polychlorinated biphenyls; alkyl phenols; bisphenol-a; polycarbonate plastics; detergents; toiletries; lubricants; spermicides; pentaphenol; nonylphenol; 3,9-dihydrooxybenz[a]anthracene;

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