In 1941 the Food and Drug Administration approved the use of diethylstilbestrol (DES), the first synthetic chemical to be marketed as an estrogen and one of the first to be identified as a hormone disruptor—a chemical that mimics hormones. Although researchers knew that DES caused cancer and disrupted sexual development, doctors prescribed it for millions of women, initially for menopause and then for miscarriage, while farmers gave cattle the hormone to promote rapid weight gain. Its residues, and those of other chemicals, in the American food supply are changing the internal ecosystems of human, livestock, and wildlife bodies in increasingly troubling ways.
In this gripping exploration, Nancy Langston shows how these chemicals have penetrated into every aspect of our bodies and ecosystems, yet the U.S. government has largely failed to regulate them and has skillfully manipulated scientific uncertainty to delay regulation. Personally affected by endocrine disruptors, Langston argues that the FDA needs to institute proper regulation of these commonly produced synthetic chemicals.
In 1941 the Food and Drug Administration approved the use of diethylstilbestrol (DES), the first synthetic chemical to be marketed as an estrogen and one of the first to be identified as a hormone disruptor—a chemical that mimics hormones. Although researchers knew that DES caused cancer and disrupted sexual development, doctors prescribed it for millions of women, initially for menopause and then for miscarriage, while farmers gave cattle the hormone to promote rapid weight gain. Its residues, and those of other chemicals, in the American food supply are changing the internal ecosystems of human, livestock, and wildlife bodies in increasingly troubling ways.
In this gripping exploration, Nancy Langston shows how these chemicals have penetrated into every aspect of our bodies and ecosystems, yet the U.S. government has largely failed to regulate them and has skillfully manipulated scientific uncertainty to delay regulation. Personally affected by endocrine disruptors, Langston argues that the FDA needs to institute proper regulation of these commonly produced synthetic chemicals.
Toxic Bodies: Hormone Disruptors and the Legacy of DES
Toxic Bodies: Hormone Disruptors and the Legacy of DES
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Overview
In 1941 the Food and Drug Administration approved the use of diethylstilbestrol (DES), the first synthetic chemical to be marketed as an estrogen and one of the first to be identified as a hormone disruptor—a chemical that mimics hormones. Although researchers knew that DES caused cancer and disrupted sexual development, doctors prescribed it for millions of women, initially for menopause and then for miscarriage, while farmers gave cattle the hormone to promote rapid weight gain. Its residues, and those of other chemicals, in the American food supply are changing the internal ecosystems of human, livestock, and wildlife bodies in increasingly troubling ways.
In this gripping exploration, Nancy Langston shows how these chemicals have penetrated into every aspect of our bodies and ecosystems, yet the U.S. government has largely failed to regulate them and has skillfully manipulated scientific uncertainty to delay regulation. Personally affected by endocrine disruptors, Langston argues that the FDA needs to institute proper regulation of these commonly produced synthetic chemicals.
Product Details
| ISBN-13: | 9780300162998 |
|---|---|
| Publisher: | Yale University Press |
| Publication date: | 03/02/2010 |
| Sold by: | Barnes & Noble |
| Format: | eBook |
| File size: | 2 MB |
About the Author
Read an Excerpt
TOXIC BODIES
Hormone Disruptors and the Legacy of DES
By Nancy Langston
Yale UNIVERSITY PRESS
Copyright © 2010 Nancy LangstonAll rights reserved.
ISBN: 978-0-300-16299-8
Excerpt
CHAPTER 1
Disrupting Hormonal Signals
In March 2000, I joined an environmental justice field trip that met with women of Washington State's Shoalwater Bay Indian Tribe. One of the poorest tribes in the West, the Shoalwater were losing their tiny reservation to erosion and legal battles, and they were losing their future to a mysterious run of miscarriages. One woman after another described losing her fetus. They spoke to us of their grief, anger, sense of confusion, and fear that something in the water they drank or the fish they ate was killing their babies.
The U.S. Centers for Disease Control and Prevention claims that the miscarriages could simply be random events, or possibly the result of genetic flaws. Or they could stem from diet, poverty, alcohol, or drug abuse, all of which can contribute to miscarriages. Few tribal members are reassured, for women on the reservation have taken meticulous care of their health during their pregnancies, yet they still have high rates of pregnancy loss. Many people in the tribe fear that the culprit could be environmental. Farmers spread pesticides on cranberry bogs near the reservation, foresters spray herbicides on surrounding forests, and oysterers use chemicals in Willapa Bay to control parasites that threaten the oyster industry. Many of these chemicals have the potential to disrupt the actions of hormones that shape fetal development. Yet because fetal development is so complex and because synthetic chemicals are so difficult to monitor, no one can determine exactly what is harming the developing children.
The expectant mothers of the Shoalwater tribe are being exposed to something, yet no one knows what. Their situation is extreme but not unique. Rich or poor, urban or rural, we are all breathing air that carries toxic dust from fertilizers, drinking water contaminated by plumes of toxins, eating food tainted with chemicals leached from plastic containers. The water that moves inside us is eventually the water that moves through the bodies of the Shoalwater women. It is the water that stagnates over the Superfund site behind my old house, and it is the water where fish swim, connecting one ecosystem to another, one species to another, and one body to another. Toxic chemicals have the potential to cross the boundaries between species and generations, altering the hormone systems that shape our internal ecosystems of health, as well as our relationships with the broader ecosystems around us.
New technologies and methods for the detection of synthetic chemicals, particularly endocrine disruptors, have drawn increasing attention toward the pervasive presence of industrial chemicals in our bodies. In July 2005, the Centers for Disease Control released its Third National Report on Human Exposure to Environmental Chemicals, revealing that synthetic chemicals permeate bodies and ecosystems. Many of these chemicals can interfere with the body's hormonal signaling system (called the endocrine system), and many are persistent, resisting the metabolic processes that bind and break down natural hormones.
In the 1980s the researcher Theo Colborn of the Conservation Foundation began documenting wildlife responses to pollutants in the Great Lakes. About one-fifth of U.S. industries and one-half of Canadian industries are located along the Great Lakes or tributary streams, making the region a microcosm for problems with pollutants in industrial society. Colborn found no shortage of wildlife problems in the area, but few consistent patterns. Some studies suggested elevated rates of cancer in certain species, others showed impaired fetal development, while still others found behavioral changes in wildlife.
Little seemed to tie these results together until Colborn learned of research by the biologist Frederick vom Saal showing that developing fetuses could be extraordinarily sensitive to tiny differences in fetal hormones. Vom Saal had noticed that female mice from the same litter showed dramatic differences in size and aggression. Because these mice were genetically identical, something other than genes was determining their differences. A female mouse's position in the womb turned out to powerfully influence her behavior when she reached adulthood. In the mother's uterus, females positioned next to their developing brothers were exposed to more androgens than those next to their sisters. In maturity, the mice located near their brothers were more aggressive and slower to mature, not because of genetic differences but because of tiny differences in prenatal hormones.
Vom Saal's work made Colborn wonder whether the effects she was seeing in Great Lakes species might be linked to fetal development. If exposure to tiny doses of hormones could lead to significant effects later in life for laboratory animals, might the same be true for wildlife? Could synthetic chemicals be disrupting the endocrine system in developing fetuses? Colborn hypothesized that certain chemicals in the Great Lakes were mimicking estrogen, thus influencing the action of steroid hormones on fetal development, leading to reproductive problems in adulthood.
The more researchers looked, the more they found that rivers and streams were laden with chemicals that had the potential to affect reproduction in wildlife. In the effluent of sewage plants, scientists found male carp and walleyes that were not making sperm but were instead producing high quantities of vitellogenin, an egg-yolk protein typically made by females. Other studies in the Great Lakes region found male white perch that had developed intersex characteristics. Students on a biology field trip in Florida noticed that every mosquitofish they found seemed to be a male, for each had a gonopodium—an anal fin that males use for copulation. But many of these apparent males turned out to be pregnant, and the students discovered that many of them were actually females that had developed gonopodia. As the biologist Mike Howell discovered, the problem was that wastes from pulp and paper mills were contaminated with chemicals that acted like testosterone. Around the world female killifish, sailfin mollys, blue-gill sunfish, American eels, and Swedish eelpouts had all become masculinized in streams that contained pulp-mill waste. Other fish species have become feminized by synthetic chemicals that mimic estrogen. In some western U.S. rivers, male Chinook salmon have developed female characteristics, while some male Atlantic cod and winter flounder have reduced testosterone levels, hampering reproduction.
Sexual transformations were not limited to fish. Once researchers began looking, they found signs of reproductive problems in numerous species. Male alligators exposed to DDT in Florida's Lake Apopka developed penises that were one-half to one-third the typical size, too small to function. Two-thirds of male Florida panthers had cryptorchidism, a hormonally related condition in which the testes do not descend. Prothonotary warblers in Alabama, sea turtles in Georgia, and mink and otters around the Great Lakes all showed reproductive changes. Male porpoises did not have enough testosterone to reproduce, while polar bears on the Arctic island of Svarlbard developed intersex characteristics. In one particularly disturbing example, Gerald A. LeBlanc of North Carolina State University in Raleigh found that more than a hundred species of marine snails were experiencing a condition known as imposex, a pollution-induced masculinization. Affected females could develop a malformed penis that blocked their release of eggs. Engorged by eggs that could not get out, many snails died.
By the 1990s, researchers had noticed that not only wildlife species were showing difficulties with reproductive health; increasing numbers of people were as well. As with panthers, the incidence of cryptorchidism in British men has increased, doubling in two decades. Since 1970, boys in the United States have become increasingly likely to develop severe hypospadias, a birth defect of the penis. Testicular cancer has increased in many industrialized countries; in Denmark it has more than tripled since World War II, while in the United States incidence increased by 51 percent between 1973 and 1995. Similar increases have occurred in other Scandinavian countries and Scotland. Since the 1950s, sperm counts in some regions have declined significantly worldwide. Men in many industrial nations are showing increases in prostate cancer; a 1999 review found that men in the United States in 1994 had a much greater risk of being diagnosed with prostate cancer than their fathers had. Much of the increase in the number of diagnosed cases is probably the result of better screening tests, but researchers are nonetheless concerned that actual incidence may also be increasing for unexplained reasons. Across the United States and Puerto Rico girls appear to be developing breasts at a younger age, and other signs of early puberty have also become apparent. Epidemiological research on women's reproductive health has found an increase in the incidence of infertility, endometriosis, fibroids, breast cancer, and ovarian cancer since synthetic chemical production began to boom in the 1950s.
What, if anything, connects all these problems with reproductive health? Many researchers now believe that these changes stem from disruptions of hormones by synthetic chemicals, particularly during vulnerable stages of fetal development. Hormones are chemical signals that regulate communication among cells and organs, orchestrating a complex process of fetal development that relies upon precise dosage and timing. Anything that scrambles the messages from hormone-signaling systems can alter patterns of development and health, just as scrambling airplane radio systems can alter flight patterns. The plane might not crash, but the static can disrupt the signals necessary for clear communication. The consequences may sometimes be minor, such as when the plane is in midflight at a steady altitude, but at other times—during take-o and landing, for instance—scrambled messages create havoc. Similarly, when synthetic chemicals alter hormone-signaling systems, adults might be resilient to the changes, but fetuses and young children can experience permanent transformations.
Ever since endocrine-disrupting chemicals were first commercially produced in the 1940s, their hormonal mechanisms of action have posed novel challenges for scientists and regulatory agencies seeking to protect public health, because they do not easily fit within traditional risk paradigms. Toxicologists based their paradigms of risk on natural toxins that caused acute poisoning at high doses. As the environmental scientist John Peterson Myers writes, "Traditional toxicants are thought to work by starting a process (or stopping one) by overwhelming the body's defense system. Up to some level of contamination, the body can defend itself against chemical assaults." Chemicals that disrupt hormone systems act in a variety of ways, however, usually by changing signals that direct complex processes with intricate feedback loops.
Even today, a popular Yale University Web site for poisons teaches that "the dose makes the poison." All toxins, this Web site states, are dose dependent: "The toxic effect of a substance increases as the exposure (or dose) to the susceptible biological system increases. For all chemicals there is a dose response curve, or a range of doses that result in a graded effect between the extremes of no effect and 100 percent response (toxic effect). All chemical substances will exhibit a toxic effect given a large enough dose. If the dose is low enough even a highly toxic substance will cease to cause a harmful effect." Endocrine disruptors, however, violate every aspect of this definition of risk. Instead of being dose dependent, with a threshold below which the chemical is safe, endocrine disruptors typically demonstrate the following properties:
Dose: Their effects are often not dose dependent. Classic natural toxins such as poisonous mushrooms typically show a dose-response curve, with larger doses leading to more harmful effects than smaller doses (often in a linear relation: twice as much toxin leads to twice the effect). In contrast, endocrine disruptors may show greater effects at lower doses, depending on the timing of exposure rather than the dose alone.
Threshold: Natural toxins usually have a threshold of safety, or what is called a "no observable adverse effect level." At some point, for example, a sample of a poisonous mushroom will be so tiny that a person would not be harmed by it. In contrast, endocrine disruptors often lack this threshold. Even a single molecule diluted in a trillion molecules of water may have potential activity. These biological effects occur at doses that are orders of magnitude lower than current dose limits for other toxins.
Age: Effects often do not correlate to the size or weight of the exposed individual, as is usual with traditional toxins. A large person should be able to eat more of a poisonous mushroom than a small person before feeling the harmful effects, but the effects of endocrine disruptors are rarely so predictable. Age rather than size is often the critical factor. Infants and developing fetuses are most at risk, while adults can often show entirely different effects.
Timing: Endocrine disruptors often have effects that are not apparent immediately after exposure. Unlike natural toxins, which usually show effects almost at once, endocrine disruptors may not show effects for decades. A person who was exposed to synthetic endocrine disruptors such as DES in the womb might show no harm at birth but might develop cancer or reproductive problems at puberty.
Researchers detected many of these patterns in the 1930s and 1940s during their initial investigations of diethylstilbestrol. While many scientists believed that these unexpected patterns indicated a need for extra caution, industry advocates dismissed the possibility that the new chemicals might be causing harm because the observed effects violated standard beliefs about toxicology. Yet these unusual effects all derive from the ways hormones typically function.
A review of some basic principles about the body's hormone system (known as the endocrine system) can help us make sense of the ways synthetic chemicals can act as endocrine disruptors. These principles will frame my argument about why regulators struggled to respond to the risks of many synthetic chemicals. To explore them I shall focus on one group of hormones critical for sexual development in both males and females: the estrogens, which include estradiol, estrone, and estriol.
Estrogens are steroid hormones: that is, they are fat-soluble and derived from cholesterol. Estrogen can be made in several locations within the body, but the ovaries are the most important production site in women of reproductive age. After the ovaries secrete estradiol, the molecules travel through the bloodstream until they encounter cells with specific receptor proteins that fit the hormone. Each hormone has a unique shape that fits the shape of particular receptor proteins at the target cell. Imagine the hormone as a key and the receptor protein as the lock. Only if the key fits can the door be unlocked. After estradiol binds to a matching receptor protein, it triggers a change in the shape of that protein, forming a new molecule called a hormone-receptor complex. The hormone-receptor complex enters the cell's nucleus and binds to its DNA, triggering a cascade of events in the cell, such as signaling the DNA to express particular genes, make particular proteins, or develop particular tissues. One familiar result is the instruction to breast cells to begin replicating during puberty. Even a tiny amount of estradiol that binds with the correct receptor can trigger the signaling cascade, with far-reaching effects such as breast growth.
Estrogen receptors are abundant in our bodies: in breast cells, the uterus, the ovaries, bone cells, hair cells, blood vessels, liver, kidneys, eyes, and even the prostate. Some hormone receptors for estrogens are unique, allowing only a single configuration of a molecule to fit. Other receptors are less specific, and many different chemicals can bind to them. A synthetic chemical that binds to an estrogen receptor might trigger cellular processes, effectively acting as an estrogen in the body. Other synthetic chemicals might bind to an estrogen receptor with antagonistic effects, blocking the binding of the body's own (endogenous) hormones. The PCBs in the Fox River, for example, can function as anti-estrogens by binding to a particular estrogen receptor and then preventing that receptor from binding to the body's endogenous estrogens.
While hormones are critical for life, too much of a given hormone can lead to havoc. Depending on timing, excess estrogens might stimulate the replication of cancer cells, signal tumors in a woman's uterus to grow, and transform patterns of sexual development. Because the levels of a particular hormone needed by a body can change from moment to moment, a complex suite of interconnected feedback systems governs hormone activity. This may regulate hormone synthesis within glands, control hormone release into the bloodstream, affect hormone uptake by target receptors, and alter the ways hormones bind to proteins so they can be broken down and removed from the body.
Negative feedback systems function like a thermostat, maintaining homeostasis, or internal balance. When temperatures go up, the thermostat shuts the furnace o, and when the temperature drops low enough, the thermostat signals the furnace to turn back on. Similarly, when levels of the body's estrogens drop below a certain amount, an organ called the hypothalamus secretes gonadotropin-releasing hormone, which travels to another organ in the body (the anterior pituitary gland), which then secretes yet another hormone called follicle-stimulating hormone, which makes its way back to the ovaries and stimulates more estrogen production. Blood estrogen levels eventually rise high enough that the hypothalamus stops secreting its gonadotropin-releasing hormone, thus stopping the secretion of follicle-stimulating hormone from the pituitary gland, and that in turn stops the production of estrogen from the ovaries. Feedback systems potentially enable small amounts of hormones to create larger effects than high doses, because high doses can shut down hormone synthesis.
(Continues...)
Excerpted from TOXIC BODIES by Nancy Langston. Copyright © 2010 by Nancy Langston. Excerpted by permission of Yale UNIVERSITY PRESS.
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Table of Contents
Contents
Preface.................... vii
Acknowledgments.................... xv
CHAPTER 1. Disrupting Hormonal Signals.................... 1
CHAPTER 2. Before World War II: Chemicals, Risk, and Regulation............ 17
CHAPTER 3. Help for Women over Forty.................... 28
CHAPTER 4. Bigger, Stronger Babies with Diethylstilbestrol................. 48
CHAPTER 5. Modern Meat: Hormones in Livestock.................... 61
CHAPTER 6. Growing Concerns.................... 83
CHAPTER 7. Assessing New Risks.................... 112
CHAPTER 8. Sexual Development and a New Ecology of Health.................. 134
CHAPTER 9. Precaution and the Lessons of History.................... 152
Notes.................... 167
Bibliography.................... 195
Index.................... 223