The foundation of our well-being interactions between endocrine, immune and nervous systems is being undermined by synthetic chemicals in the world's environment. We are living in a newly-made sea of hormone-like chemicals and similar toxic substances.
There is growing evidence that "hormone copycat" chemicals at levels found in our everyday environment are assaulting intricate biological systems. Human reproductive potential, the health of our children and the diversity of life on Earth is at risk.
Among at least 48 common chemicals known to have reproductive- and endocrine-disrupting effects are pesticides, including atrazine and endosulfan; industrial chemicals, including PCBs, dioxin, mercury, cadmium and hexachlorobenzene; and components of plastics, which can leach from consumer products. Chlorine is an essential ingredient in about half of these chemicals.
This report is about the effects on wildlife and people from environmental exposure to such chemicals. It is intended as a compendium for a general reader with a modest understanding of biology and environmental issues. Its objective is to summarize the latest research and point out emerging trends in scientific findings, as well as new questions being raised.
Our conclusions: Current industry practices and consumer habits pose unacceptable risks to life from exposure to toxic chemicals. Government regulations and industry testing of chemicals provide inadequate protection, particularly from risks of exposure to everyday combinations of environmental contaminants that can damage health.
Hormone-like chemicals' effects on life are difficult to predict; absolute cause-and-effect relationships are often impossible to prove. Some of the most disturbing evidence, however, comes from Earth's wild kingdom. Contaminant-related damage to a wide range of wildlife species appears to have common features:
Offspring of exposed populations suffer birth defects, reproductive abnormalities and poor survival. This report cites numerous examples of "feminized" or "demasculinized" populations.
Adults of exposed populations have impaired immune systems, resulting in decreased survival from attacks by disease and parasites.
Among the most bizarre trends cited in this report are discoveries of sexual anomalies in wildlife. Various forms of "inter-sex" features of male/female organs are being seen globally in marine snails, fish, alligators, turtles, fish-eating birds, marine mammals and bears.
Just as there are major global health problems in a wide variety of wildlife, we see similar trends in humans. In males, sperm counts are down, genital abnormalities in baby boys are up, cancer of the testicles and prostate gland are up. In females, breast cancer now strikes one in nine, with links to environmental chemicals increasingly implicated as a cause. Endometriosis is increasing; in recent primate studies this painful disease has been linked to dioxin exposure.
In children, problems of hyperactivity and aggressive behavior seem to be increasing and overall school performance seems to be decreasing. Human, wildlife and laboratory animal studies have established correlations between maternal exposure to environmental pollutants and these types of problems in offspring.
As humans in industrial countries such as the U.S. and Canada, all of us typically carry 30-50 parts per trillion (ppt) of dioxin-like pollutants in our bodies (as measured by "toxic equivalency factors," or TEFs, which add up the dioxin-like toxicity of dioxins, furans and PCBs). This is the same range of exposure believed to be affecting some wildlife populations. Our continuing exposure is in the order of 3-10 picograms per kilogram per day, which translates to about 0.2-0.6 ppt per day for a 140-pound person. However, a nursing infants' daily exposure may be 10-20 times higher than that rate.
There are at least five ways that environmental contaminants can disrupt vital functions of the endocrine system which includes the organs that produce hormones that control functions such as metabolism, sexual development and reproduction:
Some contaminants are similar enough in structure to hormones that they are able to bind to cellular receptors designed to be targets for natural hormones. This causes unpredictable and abnormal cell activity.
Other contaminants appear to block these binding sites so that hormones are unable to bind to them, thus impairing normal cell activity.
Some contaminants induce the creation of extra receptor sites in the cell. The consequence can be an amplification of the impact of hormones on cell activity.
Contaminants can interact directly and indirectly with natural hormones, changing the hormones' messages and thus altering cell activity.
The natural pattern of hormone synthesis can be disrupted by contaminants, resulting in an improper balance or quantity of circulating hormones.
The complexities of potential interactions with normal cell functions are remarkable. Natural hormones and hormone copycats have different effects on different parts of the body; can have different effects at different stages of development; can have different effects depending on nutritional health, age, genetic pre-disposition and even time of the year or the day that exposure occurs; can vary in their effects depending on the presence of other chemicals; and can vary greatly in effects among different species.
The way scientists identify chemical compounds and describe their effects can be confusing. Not all toxic chemicals behave as hormone copycats. In addition, some chemicals that act as hormone copycats may also produce cancers or other overt toxic reactions. The ways that hormone copycats can interrupt endocrine and other systems are difficult to decipher and separate, which is not surprising given the exquisite complexities of and interactions among endocrine, immune and nervous systems. The public must continue to be concerned about environmental pollutants that can be acutely toxic or cause cancer and other diseases; nevertheless, the magnitude of potential impacts of hormone copycats warrants special public attention.
Fetuses and newborns are particularly susceptible to hormone copycats. At these stages the systems that provide protection against foreign chemicals the liver enzyme system and the blood-brain barrier are not fully developed. Exposure to hormone-like chemicals early in embryonic or fetal life, for example, can lead to the development of major structural changes in the genital tract, including tumors and other abnormal cell growth. Damage done at this stage can be permanent and irreversible. Often the cause is difficult to determine because the parents may show no obvious adverse effects associated with exposure to hormone copycats, and the damage to the offspring may not reveal itself until maturity.
No component of the chain of life is safe from minute "water fleas" in backyard ponds to polar bears at the north end of the globe. The table on the next page shows the general trends during the last 50 years in uses of chlorinated organic chemicals and pesticides around the world. Note that peak use appears to have occurred in the 1960s and 1970s when today's generation of young adults was being born to parents who were exposed as adolescents. The second table summarizes general trends of pollution-related declines and abnormalities in the wildlife kingdom.
Many of these declines of bird, fish, reptile and mammal populations are correlated to exposures to pollutants capable of disrupting endocrine functions. Chemicals frequently blamed include PCBs, DDT and dioxins. Nevertheless, definitive links between specific chemicals and many wildlife maladies have not been proven because animals are exposed to so many chemicals.
For example, alligators in Florida's Lake Apopka don't reproduce well. Males have abnormally small phalluses. Pesticide pollution (DDE and dicofol) is blamed. Around the Great Lakes, bald eagle reproduction is low and an unusual number of baby eagles are born with crossed beaks. The parent eagles' diet of PCB-contaminated fish and birds appears to be the cause.
In other cases, combinations of pollutants in the food chain appear responsible. Beluga whales in the St. Lawrence River, swimming in the toxic chemicals discharged from the Great Lakes and from Qué bec rivers, are vanishing. They suffer from tumors and a variety of health ailments.
And in some cases, the causes are speculative or unknown, such as the wholesale disappearance of frogs and toads in the mountains of the western U.S. since the 1970s. There is recent evidence that pollution-caused thinning of the earth's ozone layer may be a cause. Other scientists suspect that air-borne pollutants, including pesticides that drift from farms, are a factor harming amphibian health, but the truth remains unproven.
Slowly, we are awaking from a state of denial. Hormone copycats are ubiquitous in pesticides, building materials, consumer products and environmental pollutants, and largely beyond our individual control. The reality of what is happening in the environment and the personal costs of pollution are dawning on us. These are not someone else's problems.
The average man today produces only half as much sperm as his grandfather did. He is far more likely to contract certain cancers, including prostate and testicular cancer. The average woman today is twice as likely to contract breast cancer as her grandmother. What will be the odds of these and other maladies afflicting our grandchildren?
The public's concern about cancer has guided policy decisions on pollutants, and to an extent, the resulting regulations have provided some protection from hormonal effects. The regulations are inadequate, however, because impacts on wildlife have been observed at levels of contamination far below those that cause cancer. The hormone-like potency of many of these contaminants is unknown.
Some solutions exist today. We recommend in this report that federal environmental and food safety laws be revised to contend with sublethal effects of long-term exposures to combinations of chemicals that impair endocrine, immune and nervous systems. Regional programs, such as the U.S. Environmental Protection Agency's proposed Great Lakes Water Quality Initiative, can help lead the way.
A phase-out of most uses of chlorine as an industrial feedstock has been recommended by the U.S.-Canada International Joint Commission in response to these problems. Recently, President Clinton, in his proposal for reauthorization of the Clean Water Act, recommended a study on reducing and eliminating chlorine in several industries.
Fundamental changes far beyond anything being seriously contemplated by government regulators are needed in chemical use and management on farms, in industries and in homes. For example, "integrated pest management" is a step toward reducing farmers' reliance on chemicals poisons on crops.
Bioassay tests that detect hormone-like characters of chemicals must be approved by federal agencies and adopted for everyday regulatory use. Chemicals that fail such bioassays should not be sold or used.
We recommend that decisions to phase out ("sunset") individual chemicals and classes of chemicals must be based on the weight-of-evidence, not on a judicial standard of guilt beyond reasonable doubt. The burden of proof must be on chemical makers and users to establish the safety of exposure to mixtures of chemicals in the environment prior to sale and use. Chlorine-based chemicals should be targeted first for sunsetting.
Finally, it is up to ordinary people to change public policies regarding chemical use, management and regulation. Not too long ago, for example, the pleasures of smoking were viewed as innocent and a sign of affluence and status. No longer.
That same change in our innocence about exposure to endocrine-disrupting chemicals is urgently needed. Unlike tobacco smoke, pollution doesn't always seem to vanish when the smoking stops. It often persists, building up in the environment and our food chain, and affects future generations.
We delay change at great peril. Warnings are clear from the wildlife kingdom and from scientists: "...Unless the environmental load of synthetic hormone disruptors is abated and controlled, large scale dysfunction at the population level is possible."
--Wingspread Statement (1991)
This Wingspread Statement warning came from a meeting of 21 experts from diverse disciplines from the U.S., Canada and Europe. Included were noted scientists in the fields of toxicology, wildlife population biology, epidemiology, psychiatry, anthropology and cell biology. The Statement was agreed upon by all the scientists present; each month evidence mounts in support of the scientists' unanimous conclusions.
A few of the scientists most closely monitoring wide-scale changes in wildlife and humans are starting to sound an alarm. We should listen to them carefully. Dr. Louis J. Guillette Jr. and his colleagues at the University of Florida, for example, have focused their wildlife toxicology research on alligator and turtle reproductive problems caused by exposure to pesticides.
How does Dr. Guillette view the global implications of the emerging research on effects from environmental pollutants? Here's wha t he recently said on the documentary, Assault on the Male, produced by BBC television and televised in 1994 by The Discovery Channel® :
Imagine if, for the last 50 years, we had sprayed the whole earth with a nerve gas. Would you be upset? Would I be upset? Yes, I think people would be screaming in the streets. Well, we've done that. We've released endocrine disruptors throughout the world that are having fundamental effects on the immune system and on the reproductive system. We have good data that show that wildlife and humans are being affected. Should we be upset? Yes, I think we should be fundamentally upset. I think we should be screaming in the streets.
-- Dr. Louis J. Guillette Jr.
Professor & Scientific Director
Biotechnologies for the Ecological, Evolutionary & Conservation Program
University of Florida - Gainesville
An invisible assault on life is underway. Human reproductive potential and the health of our children is at risk from our exposure to everyday chemicals.
We are living in a newly-made sea of estrogenic chemicals and similar toxic substances. There is growing evidence that risks from exposure to these exotic chemicals have been grossly underestimated. As a result, the foundation of our health interactions between endocrine, immune and nervous systems is being undermined by modern chemicals.
Some of the ecological havoc is being caused by now-discredited "miracle" chemicals, like the bug-killer DDT or the industrial chemical PCB. Such chemicals were used indiscriminately for decades until the 1970s. Then, as now, we embraced the benefits of pesticides, fungicides, plastics, building materials and cleaners without measuring their true long-term costs.
We are told the amounts of these toxicants entering our bodies are so tiny like a few grains of sand on the beach how can they hurt? Because of the exquisite complexities of life on Earth, however, they can and do hurt. Our bodies are designed to respond to natural hormones in the parts per quadrillion range. And now we are learning that "hormone copycat" chemicals exist at similar levels in our everyday environment and are assaulting our intricate biological systems.
Estrogen, for example, is one of the most powerful hormones controlling human life. As a supplementary drug, it is prescribed by doctors carefully and in finely-regulated doses. Yet, we might as well be sprinkling it on our cereal, mixing it with our vegetables and topping it on our kids' ice cream. Estrogenic pollutants are everywhere all the time.
This report is about the effects on wildlife and people from exposure to environmental chemicals, including many that can mimic the effects of estrogen. It is intended as a compendium for a general reader with a modest understanding of biology and environmental issues. Its objective is to summarize the latest research and point out emerging trends in scientific findings, as well as new questions being raised.
The mechanisms of this damage are only briefly explained here but enough, we hope, to provide a sense of the incredible complexities of biology, our rudimentary understanding of it and the myriad ways exotic chemicals can damage life.
For readers wanting more detail, a list of the studies used to prepare this report is included. We particularly recommend to readers Dr. Theo Colborn's 1992 book: Chemically-Induced Alterations in Sexual and Functional Development: The Wildlife/Human Connection.
Common chemicals in use today that can cause reproductive- and endocrine-disrupting effects include:
Atrazine a herbicide widely used on corn and other crops, estrogenic, with perhaps 100 million pounds spread annually in the U.S.
Endosulfan an insecticide widely used on vegetables, estrogenic, with at least 20 million of pounds per year currently used worldwide, including some 2 million pounds in the U.S.
Hexachlorobenzene a by-product in the production of pesticides and the burning of chlorine-containing substances.
Alkylphenols chemicals used in the production of polyvinyl chloride and polystyrene plastics, milk and food packaging, toiletries, spermicides and industrial detergents; estrogenic chemicals that can leach from plastics.
Bisphenol-A (BPA) a ubiquitous estrogenic chemical in the consumer world, known to leach from plastic containers into liquids. Used to make everything from plastic jugs for "purified" water to dishes used to heat baby food.
Our ignorance is profound. Yet we conduct our affairs with the naive faith that "surely someone would tell us if these chemicals were hurting us." In most cases, however, no one even monitors how much of these chemicals are produced or released into the environment. No one monitors human or wildlife exposure. No one today knows which of the thousands of chemicals, or which combinations of chemicals in our lives, are causing damage to people and wildlife. Chemicals generally are not tested for their estrogenic or other hormone-mimicking qualities, their abilities to damage offspring of exposed adults or their effects when mixed with other common pollutants. As a result, this chemical "who-dunnit" today has no tidy conclusion.
The problem is big, it is understated and it affects the lives and well-being of virtually everyone on Earth. No component of the chain of life is safe from minute "water fleas" in backyard ponds to polar bears at the north end of the globe.
Warning messages being sounded from the wildlife kingdom read like bad headlines from supermarket tabloids: Pollution causing short penises in alligators. Female bears, fish and snails grow penises; bear cubs born through odd organ. Effeminate male gulls created by pollution. Florida panthers face oblivion from undeveloped testes; pollution to blame. Pollution twists beaks of baby eagles. Unlike the tabloids, however, these sordid tales are true.
We have not listened soon enough or carefully enough to these messages. Now it appears we are beginning to pay, and the costs are consistent with what wild creatures have been trying to tell us for years. Now we face the prospect of major human population reproduction and health problems. Here are the trends in industrialized Western nations. Links to hormone copycats are likely.
Sperm production down 50% in men, on average, in the past 50 years. Sperm abnormalities are up; sperm quality is down. Average semen volume is down. If this trend continues, widespread human infertility will result.
Testicular cancer rates have tripled in the past 30 years. The disease is more common in young men.
Prostate cancer rates have at least doubled in the last decade.
Undescended testicles in baby boys the incidence has at least doubled in the last 30-40 years. Genital abnormalities also appear to be increasing.
Abnormally short penises now documented among adolescent boys whose mothers were exposed to high concentrations of PCBs prior to pregnancy.
Breast cancer now is epidemic. One in nine women in the U.S. and Canada will contract breast cancer in her lifetime, double the rate 50 years ago.
Endometriosis the incidence has dramatically increased; today, 10% of reproductive-age women are afflicted with this painful uterine disease.
Childhood problems declining school performance, increasing aggression and behavior problems in children are commonly reported. Possible linkages with environmental pollutants are intriguing, but unprovable.
There is no way we can know precisely how much damage we've caused. Much of the critical chemical exposure of today's children, for example, already happened when they were in the womb; we won't know for decades what that really means.
There are solutions. Some are outlined in this report. First, however, must come a public realization of the magnitude of the problem. Continued denial gets us nowhere.
We should be willing to initiate preventative or remedial action and to risk that the findings we accept as true may turn out to be untrue rather than to learn that we were not protective enough of human health and the planet Earth, the only place in the universe known to sustain life.
-- Dr. Glen A. Fox, Canadian Wildlife Service [1]
Some environmental pollutants are capable of mimicking the critical functions of natural hormones with dire and often unpredictable consequences to wildlife, people and their offspring. These "hormone copycats" threaten all living things, including people.
A powerful indictment regarding the risks of exposure to hormone copycats that are now common in the environment was issued by scientists in 1991. A meeting of 21 experts from diverse disciplines in the U.S., Canada and Europe was convened by Dr. Theo Colborn, senior scientist with the World Wildlife Fund. Included were noted scientists in the fields of toxicology, wildlife population biology, epidemiology, psychiatry, anthropology and cell biology.
The consensus statement that emerged from this unusual group, agreed upon by all the scientists present, has come to be known as the Wingspread Statement. Among the scientific experts' conclusions:
Many compounds introduced into the environment by human activity are capable of disrupting the endocrine system of animals, including fish, wildlife and humans. The consequences of such disruption can be profound because of the crucial role hormones play in controlling development.
We are certain [that]...many wildlife populations are already affected by these compounds... Humans may be at risk to the same environmental hazards as wildlife.
We estimate with confidence that...unless the environmental load of synthetic hormone disruptors is abated and controlled, large scale dysfunction at the population level is possible. The scope and potential hazard to wildlife and humans are great because of the probability of repeated and/or constant exposure to numerous synthetic chemicals that are known to be endocrine disruptors.
Timing of exposure to hormone copycats can be critical. A single exposure at a vulnerable moment for a developing embryo can cause damage. Long term exposure to relatively small amounts of certain contaminants also can cause damage.
"Bioaccumulative" chemicals, including many hormone copycats, can build up in the bodies of living creatures. Once these contaminants are incorporated into the tissues and fat of animals and humans, they can remain there indefinitely. The embryo, the most sensitive stage of life, can be damaged by chemicals the mother was exposed to weeks or years earlier.
The most significant source reported to-date of exposure by the general public to environmental pollutants is through consumption of contaminated fish. Any time a contaminated organism is eaten, the contaminants are passed on to the consumer. Thus, organisms at higher levels of the food chain, such as humans, are exposed to greater concentrations of contaminants and develop higher accumulations in their tissues. The effect of bioaccumulation is that by eating a single serving of moderately PCB-contaminated fish, for example, a human receives the equivalent quantity of PCBs as drinking several million gallons of water that the fish lived in.
Women are more prone to higher levels of accumulation of pollutants than men since they generally have a higher percentage of body fat, but everyone who consumes contaminated fish is at risk. Pregnant and lactating women are more likely to mobilize contaminants stored in fatty tissues, which can result in substantial fetal and neonatal (infant) exposure.
As humans in industrial countries such as the U.S. and Canada, all of us typically carry 30-50 ppt of dioxin-like pollutants in our bodies (as measured by "toxic equivalency factors," or TEFs, which add the dioxin-like toxicity of dioxin, furans and PCBs).[2] This is the same range of exposure believed to be affecting some wildlife populations. Our continuing exposure is in the order of 3-10 pg/kg/day, which translates to about 0.2-0.6 ppt per day for a 140-pound person. However, nursing infants may have 10-20 times higher daily exposure, relative to their weight.
When the subject of hormones is mentioned, many people conjure up images of adolescence and the profound changes of puberty. But the story goes much further. Hormones play an integral role in daily biological processes beginning in the earliest stages of fetal development and throughout our entire lifespan.
The endocrine system is the set of organs responsible for producing secretions (hormones) that travel through the bloodstream to target tissues or organs. The major organs of the endocrine system include the brain, sex organs, liver, pituitary gland, adrenal glands and the pancreas. Among the many functions performed by hormones are regulation of metabolism, response to stress and coordination of processes that occur over time, such as sexual development and reproduction. Some of the most familiar hormones are estradiol (natural estrogen), testosterone and epinephrine (commonly called "adrenaline").
The endocrine system is complex and works through a series of feed-back mechanisms between the central nervous system, the immune system and the various hormone producing organs.[3] The feed-back mechanisms act to control the levels of circulating hormones. The circulating hormones act as chemical signals to the various parts of the body where a certain cellular action is desired. This action is brought about by the hormone binding to receptors in the cell. Once the receptor has been bound (whether by a natural hormone or a chemical "copycat"), the cell's activity is altered. The change in cell activity may result in a shift in the cell's enzyme action or induce activity by specific genes. These genes in turn may produce enzymes that modify metabolism, proteins that build new cells or secretory materials.
Estrogen-like chemicals, such as diethylstilbestrol (DES), a drug formerly widely prescribed to pregnant women to help them maintain their pregnancies, and certain environmental pollutants, have the ability to bind and activate cellular estrogen receptors. To make matters worse, it appears as though plasma proteins that bind estrogen and thus control its ability to enter cells, do not bind synthetic compounds as well or at all. Consequently, synthetic estrogen-like molecules may be able to enter cells more readily than natural estrogens.
DES shows a slightly higher affinity than estradiol for estrogen-binding sites; it is still unclear, however, what the relative affinities are for the environmental pollutants. The possible combination of greater access and greater affinity increases the likelihood of detrimental effects.
There are at least five mechanisms by which environmental contaminants are able to disrupt vital functions of the endocrine system:
Some contaminants are similar enough in structure to hormones that they are able to bind to cellular receptors designed to be targets for natural hormones. This causes unpredictable and abnormal cell activity.
Other contaminants appear to block these binding sites so that hormones are unable to bind to them, thus impairing normal cell activity.
Some contaminants induce the creation of extra receptor sites in the cell. The consequence can be an amplification of the impact of hormones on cell activity.
Contaminants can interact directly and indirectly with natural hormones, changing the hormones' messages and thus altering cell activity.
The natural pattern of hormone synthesis can be disrupted by contaminants, resulting in an improper balance or quantity of circulating hormones.
Studies have indicated that environmental contaminants are able to trigger the mixed function oxidase system (MFO), which is responsible for the production of enzymes involved in the biosynthesis of sex steroids. In addition, the MFO produces enzymes that influence the synthesis of new hormones and the breakdown of hormones. These three enzyme activities control the level of sex hormones circulating in the body. By inducing the MFO to produce the controlling enzymes, contaminants are able to drastically alter the level of sex hormones in the body.
The exact effect of hormone exposure, both natural and unnatural, is greatly dependent on factors such as species, age and gender. Generally, the offspring of exposed adults are the most vulnerable to these effects.
Fetuses and newborns are uniquely susceptible to environmental contaminants. At these stages the systems that have protective functions the liver enzyme system and the blood-brain barrier are not fully developed. Exposure to estrogenic chemicals early in embryonic or fetal life, for example, can lead to the development of major structural changes in the genital tract, including tumors and other abnormal cell growth. Damage done at this stage can be permanent and irreversible. Often the cause of this damage is difficult to determine because the parents may show no obvious adverse effect, and the damage to the offspring may not reveal itself until maturity.
Early in their existence, vertebrate embryos exhibit neither male nor female traits. The presence or absence of a Y-chromosome generally signals whether an embryo is to be male or female. Sexual differentiation of all other aspects of masculinization and feminization results from the effects of androgens (male hormones) or estrogens on the embryo.[4]
In mammals, males typically begin differentiation of the sex organs earlier than females. Shortly after differentiation, male embryos secrete testosterone at a high rate, which serves to initiate the process of masculinization (and defeminization) of the accessory reproductive organs, external genitalia and enzyme systems in other tissues such as liver, kidney and brain. In the absence of a Y-chromosome and testosterone, normal female development occurs.
In addition to regulating sexual differentiation during fetal development, sex hormones play a role in the organization of specific areas of the brain. Less is known about this action, but studies have shown a correlation between levels of estrogen and brain morphology, as well as with sexual behavior in male rats and mice. The brain and central nervous system continue development throughout the fetal stage and early natal period making them particularly susceptible to chemical exposure.
Depending on the level and timing of exposure of the fetus to hormone copycats, the impairments may not be recognizable at birth. Consequences, especially tumors or other abnormal cell growth, may not manifest themselves until adolescence, adulthood or even late in life. The detrimental effects seen in the offspring of women exposed to the estrogenic drug DES, for example, include decreased fertility, malformed genital ducts, rare reproductive cancers, depressed immune function and possibly effects on behavior and intelligence.[5,6] Various studies suggest that prenatal DES exposure increases the likelihood of major depressive disorders, as well as bisexual activity and interest in adult women.[7] One study, for example, looked at 12 pairs of sisters; 42% of the DES-exposed group, versus 8% of the unexposed sisters indicated a life-long bisexual orientation.
The studies done on individuals exposed to DES, when considered in light of the animal studies, provide compelling evidence of the dangers to human health effects from environmental exposures to estrogenic chemicals and other hormone copycats.
The complexities of potential effects and mechanisms for action are remarkable. Natural hormones and hormone copycats have different effects on different parts of the body; can have different effects at different stages of development; can have different effects depending on nutritional health, age, genetic disposition and even time of the year or the day that exposure occurs; vary in their effects with the presence of other chemicals; and vary greatly in effects among different species.
PCBs, for example, can produce either estrogenic or antiestrogenic effects.[8] These common chemicals can affect reproductive organs directly, or indirectly affect reproductive function through changing pituitary gland secretions. Cumulative small PCB doses can be more damaging than single, larger doses. Predicting effects is confounded further by the complexity of PCB mixtures in the environment.
Hormone copycats' effects on life are difficult to predict; absolute cause-and-effect relationships are often impossible to prove. Science seldom can provide definitive answers, but it can provide evidence of risks we all face. Some of the most disturbing evidence comes from Earth's wild kingdom.
Wild creatures are exposed to innumerable combinations of toxic chemicals. Myriad opportunities exist for these mixtures to disrupt health and development. Organisms are especially vulnerable to reproductive assaults by pollutants in the early phases in their existence. Contaminant-related damage to a wide range of wildlife species appears to have common features:
Offspring of exposed populations suffer birth defects, reproductive abnormalities and poor survival. This report cites numerous examples of "feminized" or "demasculinized" populations and other sexual anomalies.
Adults of exposed populations have impaired immune systems, resulting in decreased survival from attacks by disease and parasites.
Following is a summary of the most recent scientific findings regarding effects on wildlife. In addition to the specific studies cited, an increasing number of general summaries also are appearing in print and film.[10,11,12,13,14,15,16,17]
Any kid with a magnifying glass has watched tiny "water fleas," common in fresh water ponds and lakes, scurrying about their mysterious business. These Daphnia, a cornerstone of many ecosystems, are vulnerable to effects by hormone copycats.[18,19] The actual extent and significance of the effects, however, are unknown.
Insecticides, such as carbaryl (Sevin), at very low concentrations (5 ppb) reduce Daphnia productivity by about 15%. Other damaging effects, including increased energy demands, also may occur from synergistic interactions with other pollutants and with the odors given off in water by Daphnia's natural predators. There is some evidence that the proportion of males in Daphnia populations has declined since the 1940s, when estrogen-mimicking organic chemicals first were widely distributed in the environment.
Stresses cause by hormone copycats on this fundamental link in the natural food chain are disturbing. When Daphnia decline, the entire ecosystem suffers. They eat algae, so lower Daphnia numbers may increase algal growths and reduce water clarity and quality. Fish that eat Daphnia may decline, as may bigger fish and all other wildlife that depend on the little fish for food. And that affects people.
Every component of the Earth's marine ecosystem has been damaged by toxic chemicals and many links to hormone copycats have been identified. (References [20,21], summarize numerous studies noted here and include citations for original publications.) For example, copepods minute crustaceans similar to Daphnia in ecological importance can have egg production lowered by exposure to PCBs and other exotic chemicals. Along the Scottish coastline, 93% of the copepods near a major sewage discharge show combined male and female ("intersex") features.
Starfish reproduction is disrupted by cadmium and PCBs. The chemicals significantly reduce levels of progesterone and testosterone. Exact impacts are not understood, but probably adversely affect egg production. Deformities in starfish embryo development also are caused by cadmium, PCBs and crude oil.
Female marine snails that have male genitalia are now common; globally, at least 45 species have been affected.
Such pseudohermaphroditic marine snails are sterile because the male organs cover the genital pores, preventing eggs from being discharged. Mortality among females is increased, and some local populations are nearing extinction. The primary cause is tributyltin (TBT) compounds leached from marine anti-fouling paints that are used on ships, boats and fish farm nets. Incredibly low concentrations of tin less than 1 ng/ can cause this "imposex" condition. Oysters and other bivalves also are affected by TBT. The condition in the long-lived snails is nonreversible, even when pollution is removed.
Other species affected include mud snails on the Connecticut shoreline of Long Island; dogwhelk on both sides of the North Atlantic, Alaska, British Columbia and New Zealand; and other snails in Singapore, Malaysia and Indonesia. In addition, embryos of sea urchins are damaged by cadmium and PCB pollution, although the mechanisms producing the effects are not clear.
Links between chemical exposures and reproductive impairment in marine fishes are difficult to assess. Many species are migratory, produce millions of eggs and may be subjected to over-fishing. Endocrine effects are complex. The seas contain mixtures of chemicals, complicating attempts to establish cause-and-effect relationships.
Yet, we do know that the early life stages of fish are more sensitive than adult fish to the lethal effects of dioxins, furans, PCBs [22] and presumably certain other toxic chemicals. Some of the congeners of these chemicals are more potent in killing young fish than their toxicity in mammals would predict.
Similar to trends in water birds and freshwater fish, exposure to estrogenic pollutants has been shown to impair reproduction in marine fish. For example, white croaker in San Pedro Bay in southern California, site of a former DDT manufacturing plant, are less fertile and less productive than normal. DDT continues to contaminate the food web, and the fishes' ovaries and estradiol levels are affected by exposure to the environmental estrogens. Scientists conclude:
Multigenerational contaminant effects compounded by over-fishing may have led to the dramatic population declines observed in many southern California fishes since the 1940's after DDT manufacture commenced in San Pedro.[23]
Atlantic croaker also are susceptible to reproductive impairment due to toxic pollutants. Lead, cadmium, benzo[a]pyrene and PCBs can cause decreases in testosterone or estradiol levels, and decreased ovarian growth in this species. [21]
Aromatic hydrocarbons, PCBs and possibly other contaminants in a heavily contaminated area depress ovarian development and estradiol levels in blood of female English sole. Endocrine disruptions from pollutants have been documented in other marine fish, including Atlantic cod and winter flounder. European flounder at an oil spill site had ovarian follicles that failed to mature. [21]
The infamous 1989 crude oil spill from the Exxon Valdez in Prince William Sound, Alaska, contaminated herring spawning, rearing and feeding areas. Herring are a critical link in the area's food chain and constitute a multi-million dollar commercial fishery. Genetic damage and severe larval herring malformations, including skeletal curvatures and other defects, were observed in oiled locations.[24] Exposed adult herring were less able to resist disease and parasites.
Fish living downstream from pulp and paper mills in North America and Scandinavia have been shown to develop numerous reproductive and developmental abnormalities. The damages presumably are caused by exposure to an unidentified androgenic chemical (i.e., acting like male hormones) in the complex mix of hundreds of pollutants present in mill effluent, even after secondary treatment of wastes.
On the one hand, some populations have exhibited underdevelopment of sexual characteristics. For example, downstream of a Canadian bleached kraft mill on Lake Superior, suckers have lower than normal levels of steroid sex hormones in their blood, take longer to mature, develop smaller gonads and other sex characteristics and are less fertile.[25] The reduced levels of circulating hormones affecting the fishes' endocrine systems correlate with the developmental and reproductive changes observed in both whi te suckers and lake whitefish populations. Similar impacts on the physiology of perch downstream from a Scandinavian pulp mill have been documented.
On the other hand, some populations have exhibited overdevelopment of sexual characteristics and organs.
Startling sex changes termed "environmentally induced sex inversion" occur in mosquitofish as far as four miles downstream from pulp and paper mills in Florida.[26] Females become masculinized, commonly developing male sexual organs, called the "gonopodium," and sometimes attempt to mate with normal females "i.e., chasing the control females with gonopodial swinging and thrusting, in vain attempts at fertilization." [27]
Scientists generally agree that some androgen-like compound in the mill effluent, likely the microbial degradation products of tree resin sterols, causes this pseudohermaphroditism in the mosquitofish. From the same polluted Florida waters, American eels have been found to sexually mature at a juvenile stage, developing secondary sexual characteristics (eye enlargement and gonadal development) earlier than normal. Biologists have concluded that successful migration by affected males to the Sargasso Sea, where the eels reproduce, would be unlikely.[26]
Such permanent sex change phenomena have also been observed in mosquitofish in Italy, where 60% of the females in one location were masculinized. Effluent from a pharmaceutical manufacturer was the suspected cause.
Lake trout, the only salmonid native to the Great Lakes, were nearly wiped out throughout most of the Great Lakes due to over-fishing, habitat destruction, accidental introductions of predatory sea lamprey from the Atlantic Ocean and long-term exposures to environmental pollutants. [28] More than 35 years ago, researchers in upstate New York proved that lake trout reproduction was severely affected by DDT.[29]
For decades, lake trout have been exposed to dioxins and dioxin-like PCBs, and to a host of other toxic chemicals. Lake trout eggs are extremely sensitive to pollution. Embryonic mortality in lake trout correlates with levels of PCBs in eggs and the adults.[30]
In Lake Ontario, which has received the highest dioxin contamination of the five Great Lakes since the 1930s, lake trout were extirpated during the 1960s and early 1970s. This likely was the period of peak contamination of the lake by dioxin-like pollutants. Biologists are starting to suspect that this timing was not a coincidence, even though other factors in addition to dioxin-like pollutants also must have played a role in wiping out the lake trout and slowing their recovery (e.g., predation by sea lamprey, overfishing, degradation of habitat). Studies are underway to better understand the links between toxic pollutants and lake trout reproductive success.
Scientists also are starting to question the historic role of toxic chemicals in the demise of other native Great Lakes fishes, such as lake herring and lake whitefish. Lake Ontario's deepwater sculpin became extinct somewhere in the late 1950s or early 1960s. This is the same time period when chemical plants dramatically increased their dumping of dioxins and other toxic wastes along the Niagara River (e.g., Love Canal), just upstream from Lake Ontario.
Pacific salmon, introduced into the Great Lakes 30 years ago and restocked annually, are the center-piece of a spectacular sport fishery. Yet these beautiful fish are laced with various mixtures and levels of toxic pollutants, including pesticides and industrial chemicals. Less well-known by anglers, the salmon also have serious reproductive problems. Few anglers express interest, because virtually all the salmon are reared in hatcheries. But like the miner's canary, the silvery coho salmon and chinook salmon of the Great Lakes are sentinels of a bad environment.
Goiters vastly enlarged thyroid glands are found in 100% of the salmon analyzed in the last two decades, according to researchers at Ontario's University of Guelph.[31] This indicates a disturbed endocrine system. Also, some stocks of young male salmon (jacks) begin to mature earlier than normal at a rate ten times greater than salmon from the Pacific Northwest, yet they never reach full maturity.
Great Lakes salmon eggs have unusually low thyroid hormone content and suffer high embryo mortality and deformities (such as twisted spines, double heads, clubbed tails and missing eyes). Adult salmon in the Great Lakes seldom develop the normal secondary sexual characteristics of Pacific salmon, such as the prominent hooked jaw ("kype") of spawning males.
Salmon populations in the Great Lakes have been devastated since 1988 due to bacterial kidney disease (BKD). In addition, a mysterious ailment is killing young coho salmon in hatcheries around Lake Michigan, which will mean a 60% cut in stocking in 1995. [32] The causes are unknown. Meanwhile, a multi-billion dollar sport fishery is in trouble.
None of these problems in Great Lakes salmon have been definitively linked to a specific water pollutant. Nevertheless, Dr. John F. Leatherland, the scientist most familiar with the salmon goiter epidemic, concludes that the 100% incidence of goiter "provides the most convincing evidence of a biologically active environmental factor affecting the function of the endocrine system in Great Lakes fish... Most evidence points to the omnipresence of a goitrogen(s) in the Great Lakes."
Leatherland's studies suggest that the pollutants associated with thyroid disruptions in mammals, such as PCBs, are not causing the similar problems in salmon. The true cause remains a mystery. Yet he concludes that "the possibility of an indirect relationship between thyroid dysfunction and gonadal function, via impaired steroid hormone synthesis, etc., cannot be discounted." [33]
Regarding the lake trout's poor recovery, Leatherland adds that this is "continuing evidence of developmental problems that are probably related to environmental toxicants."
Directly downstream from the Great Lakes, millions of fish in polluted waters of the St. Lawrence River are going blind, according to press reports.[34] Fish are affected downstream from Qué bec City for some 80 miles. In one especially hard-hit area, two-thirds of the walleye, 80% of the whitefish and 90% of the long-nosed suckers have been blinded.
The blinding is caused by a microscopic parasite, but scientists believe that the fishes' normal immune systems have been weakened, allowing the infestations. The problems appear to be spreading upstream, and blind fish now are being discovered near Montré al. The link between pollution and the immune system breakdowns has not been firmly established, but no traces of the parasite have been found in nearby unpolluted tributaries of the St. Lawrence River.
Amphibians across the globe--frogs, toads, salamanders and their relatives--are disappearing at a catastrophic rate. There is general agreement that the problem is human-caused. This stress on ecosystems causing amphibian extinctions is a warning: can non-amphibian species escape, can we be safe from whatever is silencing the amphibian world?
There is no agreement among scientists regarding the specific causes or the role of hormone-mimicking pollutants. We do know that amphibians' immune systems are being damaged by something that is making them more susceptible to diseases that they normally could resist. In many cases, the cause of death appears to be a bacterial infection called "red-leg," so-named because of hemorrhages that occur under the skin of the diseased amphibians. But why have certain species suddenly become susceptible to "red-leg?" That is the question baffling scientists.
Mountain populations in the western U.S. are being hard hit; in particular, the Rockies in Colorado and Wyoming, the Cascades in Oregon and the Sierra Nevada in California have suffered extinctions or serious declines of many amphibian species.[35-38]
In the seemingly-pristine wilderness of Yellowstone and Grand Teton National Parks, for example, western toads are declining. Developmental defects occur at some sites. Other amphibians at the same sites, however, do not appear to be affected. In Colorado's Rockies, entire mountain ranges and drainage basins are being hit. Widespread extinctions started in 1974.
A likely explanation is a combination of increasingly acidic rain and snowfall, plus exposure to other environmental pollutants, such as heavy metals or pesticides, according to Professor Cynthia Carey at the University of Colorado. The environmental stresses may act together synergistically, with the worst effects occurring in cold mountain climates where amphibians already are near limits of their abilities to withstand stresses on their immune systems.
Budget-stretched scientists have been unable to test layers of pond mud to see if some new toxic pollutant started showing up back in 1974, says Carey. But she suspects it is cadmium pollution that is killing off the Wyoming toad, now nearly extinct. Cadmium can suppress the immune system and it also can cause reproductive damage.[39]
Recent studies in the Pacific Northwest suggest that increasing ultraviolet radiation from a thinning of the Earth's ozone layer could be reducing amphibian reproduction by lowering the hatching success of eggs, especially at high altitudes.
Hormone copycats blowing north and east on winds from Mexico and the western states could be one factor in the decline of amphibians, some scientists suspect. For now, however, the evidence remains circumstantial regarding the role of various pollutants in the global decline of amphibians.
Despite millions of years of evolution, alligators are finding themselves unadapted for the insidious attack by estrogenic chemicals of our 20th century. Primitive and powerful, bull alligators are being emasculated by invisible traces of pesticides in their bodies.[40,41]
On Lake Apopka, Florida's fourth largest lake, astonished scientists have recently discovered an ecological disaster. Fewer than one in five alligator eggs hatch. Half the surviving baby alligators die within ten days. Males that survive are demasculinized. Even when normal appearing, they are full of female hormones.
But the most striking anomaly: the majority of male alligators living in Lake Apopka have abnormally small phalluses just one-half to one-third the normal size.
The source of this poisoning by estrogenic chemicals is a 1980 spill of the pesticide Kelthane, a mixture of dicofol and DDT, according to Professor Louis J. Guillette Jr., at the University of Florida. Guillette works with a team of environmental toxicologists that is still struggling to understand the extent of the problem in Florida and elsewhere. Today the lake waters test clean, but the persistent pesticides remain locked in animals' bodies and lake sediments, endlessly recirculating in the food chain.
Guillette says they don't yet know the impact on older alligators, which can weigh up to 600 pounds and live to 60 years. "It's somewhat difficult to get an 11-foot male to give you a semen sample. He really doesn't want to be with you!" Guillette deadpans. He believes that alligators' sex problems aren't limited to Lake Apopka. Because of widespread development and chemical spraying in Florida, Guillette estimates that one-fourth of all the Sunshine State's alligators may be abnormal due to exposure to estrogenic chemicals.
Meanwhile, despite the alarming message from Lake Apopka's alligators, catfish farms on the same lake continue to harvest tons of fish for human consumption.
Red-bellied sliders (turtles) on Lake Apopka are reproducing more successfully than the alligators. Scientists aren't surprised because alligators are higher on the food chain than the sliders. Alligators eat meat, so are exposed to higher concentrations of bioaccumulative pesticides. Sliders, on the other hand, eat plants.
Nevertheless, even the turtles are showing effects, says Guillette. Few males are being born, with nearly one in five turtles having "intersex" features.
The gender of turtles (and many other reptiles) normally is determined by temperature during egg incubation; temperature affects enzyme activity and hormone receptors. Below 27 C, slider eggs produce all males. Above 30 C, all females. Eggs in the laboratory exposed to sex hormones (or certain congeners of PCBs) will produce all males, all females, or baby turtles with intersex features, depending on the chemical. This exposure disrupts the normal temperature-controlled determination of gender, significantly alters embryonic development and reduces reproductive success.[41,42]
The global survival of marine green turtles is at risk, due to fatal tumors known as "fibropapillomatosis" (GTFP). Populations of loggerhead turtles and olive ridley turtles may also be affected.[43] Field studies suggest a positive association between the disease and coastal habitats that have been contaminated by agricultural and urban runoff. Scientists therefore suspect that environmental pollutants are compromising the turtles' immune systems, making them susceptible to GTFP.
Populations of double-crested cormorants, snaky black birds that dive for fish, crashed by 80% on the Great Lakes during the 1960s. Cormorants had stopped breeding in most areas by the early 1970s. The problem was widespread environmental contamination by DDT, a potent estrogenic pesticide that converts to DDE in the environment. The DDT/DDE levels in the birds caused eggshell thinning.[44]
Yet even as populations rebounded following restrictions on DDT in 1972, cormorant chicks with birth defects started showing up. Deformed beaks are most apparent. As with similar reproductive problems of other water birds on the Great Lakes, researchers believe nearly all the damage is caused by certain dioxins, furans and PCBs.[45] Apparently, the high environmental levels of DDE in earlier years masked the effects of these dioxin-like compounds. Now that DDE is low enough so that eggs at least can hatch, the reproductive effects of other toxic chemicals are evident.
The most convincing evidence of the toxic role of certain ("planar") types of PCBs comes from tests done at Michigan State University.[46] Researchers extracted liquid from cormorant eggs. The extracts then were used to dose rat liver cells that produce special enzyme reactions in the presence of these toxic chemicals a sort of biochemical detective kit (H4IIE bioassay). The results showed a clear correlation between the amount of dioxin-like PCBs in eggs and hatching success in respective cormorant colonies.
Green Bay on Lake Michigan has the highest rate of cormorant bill defects (52 per 10,000 chicks, 1979 through 1987), up to 87 times the rate of defects expected based on normal cormorant reproduction.[47] The incidents of bill defects on Green Bay are not limited to cormorants. Biologists also discovered abnormalities in Forsters' terns, common terns, Caspian terns, ring-billed gulls, herring gulls and a Virginia rail.
Similar bill defects also have been detected in these species and locations: double-crested cormorant Gulf of St. Lawrence (1970), Boston Harbor (1988), Manitoba (1981 & 1988), British Columbia (1989); pelagic cormorant San Francisco (1981); Brandt's cormorant San Francisco (1984); and several related species at locations in Europe.
Most people wouldn't know an ibis from an ibex. They should, however, because these heron-like wading birds are sending us a message about our current unwitting importation of DDT.
Wildlife biologists have discovered that DDE levels in white-faced ibis in the Great Basin are not declining.[48,49] This bucks a general trend of decreasing DDE levels in wildlife since the pesticide DDT was restricted in the U.S. around 1972. Ibis nesting at Carson Lake, Nevada, still are showing the classic symptoms of DDE exposure: thin and weak eggshells and reduced productivity in 40% of the area's nesting population.
Good circumstantial evidence leads biologists to conclude that the ibis are accumulating the DDE from food they eat on their wintering range in inland Mexico. This agricultural region apparently still is actively using DDT. If the ibis are importing this estrogenic pesticide in their bodies before they migrate north, what about the 2 million metric tons of produce the U.S. imports each year from Mexico? (A recent U.S. government study of imported Mexican produce found residues of unregistered pesticides, which are made in the U.S. and exported to Mexico, on less than one percent of the samples; however, the study did not look for DDT/DDE residues.[50]) And what are the effects on the other wildlife and the people who live in areas of Central America where DDT apparently still is being sprayed?
DDT continues to plague wildlife elsewhere in the U.S. as well, suggesting that the so-called "ban" on DDT is illusionary. For example, black-crowned night herons of the intermountain western U.S., bald eagles in Oregon's lower Columbia River region (also contaminated with PCBs and dioxin) and water birds (especially green-backed herons and anhingas) in Mississippi's Yazoo National Wildlife Refuge [51] continue to show DDE-associated eggshell thinning and reduced productivity. DDE levels throughout the Great Lakes Ecosystem stopped declining around 1983, with associated effects still being felt throughout the food chain.
Great blue herons, feeding on fish, frogs and other creatures near a pulp and paper mill in British Columbia (Crofton on Vancouver Island), provide evidence of the endocrine effects of toxic chemicals in pulp and paper mill wastes.[52-54] These waters of the Georgia Strait receive wastes from the greatest concentration of pulp and paper mills in Canada.
In 1987 and 1988, one colony closest to the British Columbia mill failed to produce any fledglings. Parent herons behaved oddly, paying poor attention to their nests. Dioxin levels correlated with the observed effects in the herons. Dioxin interferes with the endocrine system, even though it does not directly mimic estrogen behavior. Nevertheless, other unidentified substances may also be responsible for the damages, such as steroids derived from plant resins.
In comparing unhatched baby herons from contaminated areas with cleaner eggs over a five-year period, scientists found that body weight and brain weight decreased with increasing levels of dioxin. Other brain abnormalities (some even visible without magnification) also were detected in the birds with higher dioxin exposure from the mill effluent. Later studies, completed after dioxin discharges were cut by 90%, measured an immediate improvement in great blue heron reproduction.
The nervous system interacts with the endocrine system to control reproduction, growth and behavior. Although the effects on the dioxin-exposed great blue herons was significant, no one knows for sure what effect lesser exposures to environmental pollutants may be having on great blue herons and related water birds across the globe.
Similar to great blue herons, wood ducks can have their reproduction disrupted by exposure to dioxins and furans. Nesting by wood ducks in a dioxin- and furan-contaminated wetland system in central Arkansas was affected, and birth defects were correlated with the contamination.[55] Hatching success was lowered in nests as much as 36 miles downstream from the contamination site.
Reduced productivity was associated with concentrations as low as 20-50 ppt in eggs (as measured by "toxic equivalency factors," or TEFs, of all dioxins and furans present). As noted elsewhere in this report, that is about the same range of TEFs to which humans now are exposed.
A massive and little-publicized crash of Alaskan sea duck populations is underway. Here are the sorry statistics: [56]
Scoters (three species) have declined 33% during the period 1957-1992
Oldsquaws have declined 67% during the period 1977-1992
Spectacled eider (a threatened species) have declined 94-98% during the period 1957-1991
Steller's eider (a candidate endangered species) have declined recently.
The causes are unknown. No diseases have been found. However, scientists have noted unusually high cadmium levels in scoters wintering in Oregon and Washington. The higher the cadmium levels, the less the ducks weighed. The source of the cadmium is unknown.
As noted earlier regarding the decline of western amphibians during the same time period, cadmium can damage immune systems and also interfere with endocrine systems of animals.
"Rats with wings!" That's what many people think about gulls. Every city with a waterfront has hordes of gulls scavaging food on beaches, parks, streets and anywhere else there may be an edible tidbit. But Dr. Michael Fry, a University of California ecotoxicologist who studies gulls' most intimate habits, has a different perspective: "We think of gulls as garbage birds. The gulls look at it as eating our leftovers. It's the same stuff we eat."
Gulls are trying to tell us that their diet contains something bad, says Fry. "What we've got here is a second generation [pollution problem]. It's in the eggs of these birds."
Some toxic chemicals common in the environment, such as PCBs, can bioconcentrate in gull eggs by as much as 25 million times the concentration in water.[57] Not surprisingly, gull reproduction, health and behavior has been affected. For example, during the 1970s, herring gull reproduction on eastern Lake Ontario dropped to 10% of normal levels.[58] Amounts of DDE, mirex and dioxin in gull eggs appeared to peak around 1972. When gulls born in those years of peak pollution started breeding, biologists noted that odd sexual behavior was suddenly commonplace. Pairs of females, or polygynous trios of two females and one male, would use the same nest (7% of nests).
Feminized populations of water birds are generally associated with organochlorine contamination of the aquatic food chain. Embryonic exposure to DDT and other hormone copycats increases the number of females in the population, increases female-female pairings when the birds become adults and causes embryonic abnormalities in males that makes them unable to breed as adults. In effect, the estrogenic DDT "chemically castrates" male gulls.
Populations of western gulls in southern California, glaucous-winged gulls in Puget Sound, ring-billed gulls and California gulls in Washington and Idaho, and herring gulls and ring-billed gulls in the Great Lakes are also being feminized.[59]
The causes have not been determined in all cases, but DDT likely has been a factor due to its powerful estrogen-like characteristics. For example, in the 1970s the breeding population of western gulls on Santa Barbara Island near Los Angeles, an area heavily polluted by DDT/DDE, crashed from 3,000 birds to 850. As many as 14% of the nests were attended by two females.
Herring gulls throughout the Great Lakes have also suffered from enlarged thyroids, similar to effects in Great Lakes salmon described earlier. Goiter was especially pronounced prior to 1985. The condition is believed to be caused by various toxic pollutants affecting gull embryos and contaminating the diet of adult gulls.[60] By 1991, goiter in gulls was improving but is still present today.[61,62] Herring gulls nesting on islands in western Lake Erie and in Saginaw Bay on Lake Huron remain the most seriously affected. Gulls in western Lake Erie and upstream in the Detroit River also suffer "alarmingly low" Vitamin A deficiency, a condition that can be caused by toxic pollutants. This likely is impairing reproduction and immune functions. Immune systems have been disrupted in herring gulls living at other polluted sites throughout the Great Lakes, including near a Canadian pulp and paper mill on Lake Superior.[63]
Endocrine disruptions in tern populations are at least as severe as those of gulls described above. Some of the smaller terns, because of their high metabolic rates, are at especially high risk when their nesting sites are in polluted ecosystems.
Endangered roseate terns and common terns nesting on Bird Island in Buzzards Bay near New Bedford, Massachusetts, exhibit feminized sexual characteristics; 4% of nests contain eggs from two or more females.[64] Only one in four of male common tern embryos appears normal; the rest are becoming hermaphrodites with both male and female gonads. Researchers have been unable to obtain funding to analyze the livers of the tern chicks to determine chemical exposure, according to Dr. Theo Colborn.
Forster's terns nesting on Green Bay, one of the most polluted estuaries in the Great Lakes, have been studied since 1983. In that year, egg hatching success was only 26% (compared to 88% in an inland colony).[65] None of the hatched young survived. Many of the dead embryos and chicks had various defects. Adult abandonment of nests and poor parental care also was prevalent. Nearly all (>90%) the severe bioeffects were attributed by researchers to two dioxin-like congeners of PCBs. Nevertheless, the complex mixture of pollutants is one reason why precise cause-and-effect linkages are nearly impossible to prove.
The improvements in Forster's tern hatching rates between 1983 and 1988 were due to lower exposure of the tern adults and embryos to Green Bay pollutants, especially PCBs. But it was not necessarily due to less overall pollution. It has important lessons for other regions of the country.
By 1988 the Green Bay hatching rate appeared to improve, and egg contamination by PCBs was lower. Yet nearly half of the tern chicks died from a condition aptly named "wasting syndrome." The chicks appear to grow normally for the first several weeks of life, but then for the next few weeks lose weight and simply waste away and die. The syndrome, now known as "Great Lakes embryo mortality, edema and deformities syndrome" (GLEMEDS), is associated with exposure to dioxin-like pollutants, including some PCBs.
In the two years prior to the low tern reproduction on Green Bay in 1983, spring floods of the heavily-polluted Fox River that discharges to Green Bay were 2´ times higher than in years of better tern reproduction. It is likely that heavy loads of PCBs and other pollutants from pulp mills and farms poisons that were buried in Fox River mud were flushed into the bay and the terns' habitat.
The re-suspended toxic pollutants could have been immediately absorbed by algae, which were eaten by zooplankton, which were eaten by minnows. The terns, arriving after the peak of the floods for spring breeding and egg laying, dined on the minnows and other aquatic life laced with hormone copycat pollutants. No wonder their chicks all died.
Caspian tern reproduction on Lake Huron's Saginaw Bay, which is badly polluted like Green Bay, also collapsed following record floods in September 1986.[67] Toxic muds in the industrialized Saginaw River were flushed into the bay. During the two years following the flood, tern hatching success fell to as low as zero. Birth deformities in hatched chicks were 163 times greater than normal. Fewer than expected adult Caspian terns returned to nest on Saginaw Bay, suggesting abnormally high adult mortality, as well.
As with the Forster's terns on Green Bay, nearly all (>98%) of the severe bioeffects in the immature Caspian terns were attributed by researchers to two dioxin-like congeners of PCBs. Actual dioxins (2,3,7,8-TCDD) contributed only 1% of the toxicity.
Common terns, Forster's terns and black terns on Saginaw Bay also appear to have declined precipitously in years after the flood. Terns have suffered from poor reproductive success and developmental toxicity since the 1980s in other areas as well.[20,68]
Bald eagles in the contiguous U.S. are back from the brink of extinction. Today, their population exceeds 11,000 birds. Yet estrogenic chemicals in the environment continue to retard their recovery. Due to widespread exposure to DDT/DDE since the 1940s, bald eagles nearly vanished from the contiguous 48 states. With uses of DDT severely restricted in 1972, eggshell thinning problems decreased as the levels of this estrogenic pesticide declined in the food chain.
The Great Lakes region graphically demonstrates, however, that critical problems persist. DDE and PCBs in the environment continue to impair productivity, affect egg hatchability (including eggshell thinning) and cause birth defects.[69-71]
As with other creatures, the effects on eagles from endocrine disrupting chemicals depend upon the timing of exposure, dose and persistence of the contaminant in the young or adult eagle. Nevertheless, the level of environmental contaminants in the food chain clearly is controlling the productivity of eagles along the Great Lakes, in Voyageurs National Park in northern Minnesota and likely in other areas with similar food chain contamination, such as the lower Columbia River, Maine and the Channel Islands off southern California.
The primary cause appears to be certain types of PCBs that have dioxin-like qualities that can impair avian endocrine systems. Fish in the Great Lakes and tributary rivers have higher levels of PCBs than fish from inland lakes and in rivers where dams block fish from swimming up from the Great Lakes.
Not surprisingly, then, eagles eating the "cleaner" fish in inland waters are reproducing much better than eagles eating the more PCB-laden fish from the Great Lakes. Inland nesting eagles in the Great Lakes region increased from 162 breeding pairs in 1977 to 418 breeding pairs in 1993. Eagles along the Great Lakes also increased from 26 pairs to 134 pairs during this period. However, the coastal populations were able to increase only because of the influx of young eagles from the healthy inland populations. Great Lakes coastal reproduction remains barely self-sustaining, due to the developmental effects of contaminants.
Birth defects in baby eaglets illustrate the problem. In 1993, biologists found four female bald eaglets with bill and feet deformities at nest sites near the Great Lakes in Michigan.[72] The cross-billed eaglets, deformed progeny of the U.S. national symbol, are graphic evidence of the risks from continued exposure by wildlife and people to hormone copycats in the environment. Biologists cannot conclude unequivocally that the Great Lakes' toxic-contaminated food chain caused the deformities, but the evidence suggests this is exactly what happened.
Prior to 1993, such birth defects rarely had been seen in bald eagles. Between 1966 and 1992, only 11 bald eagles in North America were documented with deformed bills.69 The sudden increase in observed deformities is disturbing, and highlights concern over continuing levels of hormone copycat pollutants in the environment.
Deformed avian beaks have been found in a variety of fish-eating birds in the Great Lakes region, including herring gulls, ring-billed gulls, common terms, Caspian terns, Forster's terns, black-crowned night herons, great blue herons, double-crested cormorants and Virginia rails. Also, bill defects and deformed toes have been found in 2 of 115 white-tailed eagle nestlings in Sweden; the deformities have been linked to PCB contamination in the Baltic Sea food chain.
Songbirds throughout North America are declining. Causes include destruction of habitat in breeding areas and on southern wintering ranges and chemical exposures. The potential killing effects of pesticides on songbirds have been understood at least since the 1960s, when ornithologists at Michigan State University determined that DDT sprayed on elm trees was killing campus robins.
Yet, the current-day impact on songbirds of agricultural and forest pesticides, through direct spraying and accumulation through food, is poorly understood. The effects of exposure of songbirds to potential endocrine disruptors has largely been ignored.
Scientists have discovered troubling hints about the damaging effects of the cumulative effects of repeated pesticide exposures to adult songbirds and nestlings throughout the nesting season and over several years. The chronic dose, averaged over a lifetime of exposure, is usually what scientists measure and what regulators use to set so-called "safe" limits of exposure. That is of little use in the real world of birds and animals, however. More important is the cumulative and sublethal dose that a bird receives from repeated exposures to multiple applications of combinations of insecticides, herbicides and fungicides, particularly in the presence of other stresses, such as viruses, parasites and bad weather.
On a Georgia pecan and peanut farm, researchers studied effects of multiple pesticide applications on cardinals, mockingbirds and brown thrashers.[73] The repetitive chemical exposures appeared to cause significant decreases in egg hatchability and, possibly, complete reproductive failure.
During their nesting season, the birds were exposed to many pesticides, including phosalone, endosulfan, monocrotophos, dimethoate, fonofos and methomyl, plus the fungicide triphenyltin hydroxide. Researchers did not investigate the potential impairment of the birds' endocrine systems in their study.
Dolphins have been dying in mass numbers since 1987 all along the Atlantic Coast of North America, in the Gulf of Mexico and in the Mediterranean Sea.[74,75] , Half of all the bottlenose dolphins along the Atlantic Coast died in 1987-88. Recovery of this population, even if the cause of the deaths is eliminated, could take 35 to 100 years.
The dolphins are dying from infections; the reason for the infections is dysfunctional immune systems. The cause of the damaged immune systems has not been proven, but appears to be correlated with DDE and PCB concentrations in the dolphins. In another example, Dall's porpoises in the North Pacific show decreasing testosterone levels with increasing levels of PCBs and DDE.[76]
A direct cause-and-effect link between contaminated fish and declining seal populations in Europe has been firmly established. Between 1950 and 1975, the population of common seals near the Netherlands collapsed from more than 3,000 to less than 500 animals.[77] This was the same time period that the Rhine River, which flows into the seals' home of the Dutch Wadden Sea, was becoming industrialized and highly polluted.
Patterns of hormone levels in the pregnant seals suggested that estrogen-mimicking traits of pollutants, most likely PCBs, could have caused the reproductive failure, but the precise mechanism of damage was not determined. The developmental damage occurred early in pregnancy before implantation of embryos in the seals' uteri.
Viruses and infections also have attacked seals, due to depressed immune systems. In other areas, hormone production was disrupted in adrenal gland and testicular tissue from grey seals and harp seals exposed to cadmium, methylmercury and PCBs.[78]
An endangered population of fewer than 500 beluga whales lives where the St. Lawrence River, carrying the outflow of all the Great Lakes, meets the Atlantic Ocean. These ghostly white mammals are the sickest whales in the world due to the toxic poisons they carry and pass on to their offspring.
Pollutants from industries, cities and farms surrounding North America's inland seas contaminate the whales and their food. Eels, which migrate to the ocean from Lake Ontario carrying high levels of toxic chemicals, are a favorite food of the whales. Major contaminants include DDT, PCBs, the insecticide Mirex, lead and mercury. Says Qué bec scientist Dr. Pierre Bé land regarding the whales' contamination, "There's nothing you can think of that's not there."
Despite years of study, scientists still do not know exactly what is ailing the whales, although effects from estrogenic chemicals is likely a factor. Forty percent of the whales that have been studied have tumors a condition normally rare among whales of the world.[79,80] Direct effects from cancer-causing pollutants and indirect effects from damaged immune systems are thought to cause the tumors. Effects on the whales' endocrine systems also are likely; ovaries of females are not as active as those of belugas from the Arctic region. One hermaphroditic whale has been discovered.[81] Few young are being produced and few survive.
Bé land and his Qué bec colleagues have dedicated their lives to saving the belugas, which are an integral part of the history and culture of the St. Lawrence region. Nevertheless, Bé land confesses his sometimes discouragement at trying to stop the pollution: "I don't know if really we have made a difference. We have not seen any change as far as the whales are concerned."
Recently, a pregnant beluga that died of unknown causes was autopsied by scientists at the University of Montré al. Her lactational glands were dried up. "The baby obviously wouldn't have survived," says researcher Sté phane Lair.
PCBs are deadly to mink and river otter reproduction, so it is not surprising that these creatures have disappeared from many Great Lakes coastal areas and other places where the fish and other aquatic life that they eat is con taminated with toxic chemicals.
Known for their playful antics on rivers and mud slides, the dark brown otters are amphibious weasel-like creatures that weigh from 10 to 30 pounds and eat about three pounds of food a day, especially bottom-feeding suckers and clams that tend to build up high levels of toxic chemicals in the ir tissues.
In Michigan, otter once were common throughout the state's waterways. But based on otter trapping records kept by the state, virtually no otters were trapped within five miles of Lake Michigan during a recent six-year period, except along the extreme northern coast where the lake is least polluted.[82] Furthermore, the majority of the few otters taken with ten miles of the lake were trapped on inland waters above dams that block runs of contaminated Lake Michigan fish. Human disturbance and development have contributed to the otters' demise, but the evidence suggests that food chain contamination with toxic chemicals is an over-riding cause. Near Lake Superior and northern Lake Huron, where fish are less contaminated, otters commonly were trapped. But none were taken near Saginaw Bay on Lake Huron, one of the Great Lakes' most polluted areas. These tre nds are comparable to the inland versus coastal reproductive rates of bald eagles in the Great Lakes region.
Otters also are rare in other areas of their historic range that have suitable habitat but have contaminated food, including near Green Bay on Lake Michigan and within five miles of Lake Ontario in New York. Links between trace levels of toxic chemicals in rivers and declines in the populations of otters have been discovered in Oregon, Great Britain and Sweden.
Experiments at Michigan State University show that most mink, a close relative of otters, die within three months when fed a diet containing 30% Lake Michigan salmon. Those that survive suffer nearly complete reproductive failure. In a related study, [83] all the offspring (kits) of mink that were fed a diet of 40% Saginaw Bay carp died within 24 hours of birth. A diet of as little as 10% of the carp reduced kit sur vival and average kit body weight. The group of researchers concluded that their study supported suspicions that PCBs are responsible for the marked decline in mink populations in certain areas adjacent to the Great Lakes.
The panthers of Florida's wilds are almost gone. As if dodging traffic and losing their homes to land development wasn't enough, the last 30 to 50 Florida panthers possibly are being exterminated by invisible estrogenic contaminants.
Lately, two-thirds of their male cubs have been born with one or more undescended testes, a condition known as "cryptorchidism." [84] Other apparently normal males are sterile or produce deformed sperm. Some males are highly feminized and have abnormally high levels of estrogen; females may have abnormally high levels of testosterone. Exposure of developing embryos to contaminants, possibly mercury, consumed by the mothers in their food is the most likely cause of the problems.
The precise sources of the estrogenic mayhem, however, have not been discovered. In a last ditch effort to limit the damage, the U.S. Fish & Wildlife Service has banned the use of pesticides with estrogenic properties in federal wildlife refuges in the southeastern U.S. Still, the action may be too little, too late to save the Florida panther.
Like the tiny female mosquitofish in Florida, female black bears and grizzly bears in Alberta, Canada, have been found with male sex organs.[85] In this "pseudohermaphroditism," the upper part of the bear's reproductive tract is female and the lower part male. Reproduction by these animals apparently is functionally normal, although difficult to picture.
The condition was found in 4 of 15 female black bears and 1 of 4 female grizzly bears studied between 1984 and 1986. The most severe case observed was a 7-year-old female black bear accompanied by two 7-month-old cubs at the time of death. The bear's vagina developed internally into a urethra, and emerged externally as a penis-like structure some five-inches in length (somewhat shorter than the penis of an average adult male black bear).
As described in the report by University of Alberta biologist Marc Cattet: "If the two cubs were conceived by the 7-year-old female, an adult male black bear would have had to insert its penis into the urethra of the penis-like structure of the female during mating, and the neonates would have had to emerge from the opening of the structure during parturition." He concluded this was, indeed, possible.
Given the high rate of the genital abnormalities among the Alberta bears, Cattet concluded that exposure of the developing fetuses to some androgen-like chemical eaten by the mothers, which could include herbicides or natural substances in plants, was the most likely cause. Similar male hormone-mimicking pollutants in some pulp and paper mill effluents also are suspected of causing reproductive and developmental effects in exposed fish.
Sitting on top of the world and on top of the food chain are 20,000 to 40,000 polar bears. They eat fish-eating seals almost exclusively and may have the highest dietary intake of fat of any animal in the world. This makes them highly vulnerable to effects of global pollution, despite polar bears' seemingly-pristine Arctic home.
Pollution rides into the Arctic on the winds. When winter's bone-chilling polar air masses reach south into the U.S., Europe and Asia, they do more than close schools and strand motorists. These weather fronts also collect toxic air pollution from industrial and urban centers and then transport these poisons north to the land of the great white bears. For example, the amount of PCBs falling from the Arctic sky in snow, rain and dust are comparable to amounts falling on the Great Lakes. The amount of the chlorinated pesticide lindane dumped from the Arctic sky, however, is about 100 times higher than in the Great Lakes region.[86] Reasons for this surprising finding are unclear.
Pollutants also reach the Arctic from northern-flowing tributary rivers, carrying pesticides and industrial compounds from human activities to the south, especially in Russia. In addition, unknown quantities of toxic chemicals drift north with the oceans' currents. Toxic chemicals are even imported to the Arctic in the bodies of migratory fish, marine mammals and birds.
Polar bears fast and live off their accumulated fat during much of the year, including the months before and after birth of their cubs. So, nutrients supplied to the cubs in the uterus and during nursing come from stored fats. Therefore, cubs are particularly hard hit by any fat-stored environmental contaminants. To make matters worse, a polar bear embryo lives for many months after fertilization before being implanted in the mother's uterine wall (compared to 8-10 days in human embryos); this appears to make them particularly susceptible to interference from organochlorines.[87] During this period, the embryo develops slowly and is nourished by its limited supply of yolk and by materials secreted by glands in the mother's genital tract.
Chemical contaminants identified in polar bear tissues include numerous congeners of PCBs; a variety of compounds related to the pesticide chlordane, including heptachlor epoxide; DDT and related compounds; several isomers of hexachlorocyclohexane; dieldrin; and heavy metals.[88]
Scientists believe that the slow decline in reproductive performance of some polar bear populations may be due, at least in part, to exposure to such estrogenic compounds in the Arctic food chain. For example, in Norway's icy wilderness, polar bears have up to 90 ppm PCBs in their fat, and they average 30 ppm in their fat.[89] In 1992, reproduction appeared far below normal among 14 females studied by polar bear expert Oystein Wiig, at the Norwegian Polar Institute.
Based on the available data, all trophic levels in all the major
ecosystem types of North America and elsewhere have species that
apparently are undergoing traumatic population decreases. Almost
all of these identified population declines and reproductive effects
have the possibility, if not the proof, of being associated with
hormone copycat pollutants of human origin. The levels of some
of these contaminants in wildlife tissues that have been associated
with these effects is close to levels identified in some humans.
Sperm production by the average man in western countries, including the U.S., today is half what it was in 1940. Average sperm count has declined 42% and average volume of semen diminished by 20%. [90] No one is certain at what point such decreasing sperm counts lead to widespread infertility among men.
Recent surveys in Great Britain and the United States do show an increase in infertility in the last twenty years. One in twenty men are either subfertile or infertile, and usually doctors have no idea why.[91] It is impossible to predict how many of these men's reduced fertility is due to chemical exposure, but it is not unreasonable to conclude that environmental contaminants are contributing.[92,93]
The most likely effect of endocrine disruption in men is a reduction in sperm production and also in the sperm's ability to fertilize an egg. The reproductive system of male rats is exceptionally sensitive to dioxin, leading researchers to believe that human males may be susceptible as well. In normal human males, the number of sperm produced per ejaculate is normally close to the level required for fertility. Thus, even a small reduction in daily sperm production can lead to infertility.
The mechanism by which environmental contaminants could be reducing sperm production is not fully understood. Alterations in hormone activity rates in developing male embryos or infants can affect Sertoli cells, which are the nursery cells to produce sperm. Sertoli cell secretions regulate when testicles descend in baby boys, as well as cell division in the testes and development of the urethra. In addition, the number of Sertoli cells are fixed during gestation; the more Sertoli cells, the greater the sperm production in adult males.
"The Sertoli cell is the most important cell in the male body. It's in the driver's seat"e regulating development of the reproductive tract, cell division and sperm production.
--Dr. Richard M. Sharpe
Medical Research Council, Reproductive Biology Unit
Edinburgh, Scotland, United Kingdom
Researchers believe increasing infertility also may be linked to disturbance of men's normal daily hormone cycle. The levels of hormones are regulated by peptide hormones from the hypothalamus region of the brain. These hormones in turn regulate the production of the sex steroids (estrogens and testosterone) from the gonads. Men's pattern of hormone secretion is relatively constant, with a slight daily cycle. Hormone mimicking contaminants at sufficient levels may be disturbing this cycle and the overall levels, resulting in reduced sperm production.
Studies of men occupationally exposed to dioxin reveal a decreased level of circulating testosterone. This same effect is seen in laboratory rats exposed to dioxin; in addition, the dioxin-exposed male rats find it difficult to successfully copulate, even after mounting the female. Reduced levels of testosterone are caused by two hormonal actions: decreased secretion from testes and increased metabolism due to induction of the MFO. The similar results in rats and occupationally exposed men are consistent with the effects expected from contaminant-caused disruption at the cellular level. Thus, the theory of disrupted hormone levels is supported in men exposed to relatively higher doses; research remains to be done at levels encountered in the environment.
Recent research confounds easy explanations. For example, PCBs (Aroclor 1242), which have well-documented inhibitory effects on adult reproductive organs, can paradoxically increase testis adult weight and sperm production when given to young rats, [94] the opposite effect of prenatal dioxin exposure.
Florida's Lake Apopka alligators with short phalluses are graphic evidence of the risks to males from exposure to hormone copycats. Looked at in isolation, the alligators appear but a scientific curiosity. But viewed in context of the feminization of many wildlife species exposed to pollutants and trends of similar maladies in humans, and the alligators appear as an ominous warning to us.
Something is going wrong in the normal development of baby boys. They are more frequently required to undergo operations to correct undescended testicles ("cryptorchidism"); the rate appears to have increased 2- to 3-fold during the past 30 years. A birth defect called "hypospadias," in which the male urinary canal is open on the underside of the penis, also is increasing. "Inter-sex" features in baby boys, where the penis is covered with a layer of fat and genitals have a cleft resembling female features, appear to be increasing.
In some cases where pregnant mothers were exposed to very high levels of toxic chemicals, the mothers' boys have shorter than normal penises, similar to Lake Apopka's alligators. Boys born to women who were exposed to PCB-poisoned rice bran cooking oil in 1978-79 in central Taiwan, the so-called "Yucheng" boys, were found to have significantly shorter penis lengths at ages 11 to 14.[95]
These effects are similar to what happens to male rat pups when their mother is exposed to minute levels of dioxin (64 ng/kg).[96] When the pups reach puberty, researchers see decreased sperm count, altered sexual behavior and shortened penises. (Females show dramatic malformations of the urogenital organs, including, in some cases, no vaginal openings.)
In addition, the rate of sexual development defects and disease in men is sharply increasing, which also could be linked to effects of environmental hormone exposure.[97,98] Studies in some industrialized western nations show that cancer of the testicles, relatively more common in young men than older men, has increased at least 3-fold in the past 30 years. Another possible effect of exposure to estrogen-like contaminants is prostate enlargement in older men. This condition affects 80% of men who live beyond 70 years. The exact cause of prostate enlargement, however, is often unknown. Prostate cancer in men has increased by 80% in the last 20 years.[99] It remains a deadly disease, despite major efforts at early detection and treatment. It also is one of several types of cancers that are more common among farmers, suggesting the possibility that pesticide exposure might be at least partially to blame.
Until recently, the emphasis in studies on reproductive effects from toxic chemicals has been on the male.[100] Yet, of the nearly 100 chemicals that now have been tested for reproductive toxicity by the U.S. National Toxicity Program, all affect the female reproductive system. Even the effects of estrogen-mimicking contaminants are probably least well understood in adult females.
Women normally are exposed to estrogen, but the effects on females of hormone copycats are more difficult to track due to the estrous cycle and the resulting huge differences in circulating hormone concentrations at different stages of the cycle. Studies that have been done on rodents indicate that estrogenic substances produce accelerated sexual maturation, irregular estrous cycles and prolonged estrous. Some female mice also displayed masculine behavior in conjunction with the other effects.
The presence of estrogen mimicking compounds in adult women can impair reproductive capacity by interfering with natural hormone cycles, potentially rendering women unable to conceive or to maintain pregnancy. There is growing outrage over the lack of understanding about the causes of breast cancer, and increasingly vocal demands for a holistic approach to breast cancer research.[101]
Possibly the most important health issue facing women breast cancer may also have links to the estrogenic contaminants. Today, women in the U.S. and Canada who live to age 85 have a one in nine risk of contracting breast cancer in their lifetime, double the risk in 1940.101 The rate may still be climbing. Moreover, breast cancer mortality since the 1940s has increased by 1% per year.[102]
Researchers are unable to determine the causal factor for breast cancer in more than 60% of the cases. Two leading theories of the primary risk factors for breast cancer are exposure to estrogen and high fat diets. The public increasingly is discussing this issue, and articles in the popular press are common. For example:
"Xenoestrogens raise the creepy possibility that if toxic chemicals are estrogens in disguise, personal-risk factors might actually be the result of environmental exposures," notes a recent popular article in Vogue.[103]
The dramatic difference in rates of breast cancer between westernized countries and non-westernized countries has led researchers to investigate the possible contribution of diet to the incidence of breast cancer. Researchers have not been able to establish a clear link between high fat diet and incidence of cancer. Some studies reveal no association, while others show a positive association.
Diet also affects women's circulating estrogen level, thus indicating a link between these two factors, as well as to the possibility of a link to environmental contaminant factors. Fat and fiber are known to alter the intestinal resorption of estrogen. High fat diets increase circulating estrogen levels while high fiber diets are known to decrease estrogen levels. Furthermore, vegetable consumption is associated with the levels of estrogen-binding proteins. A reduction in vegetable consumption results in a decrease in the proteins, increasing the level of circulating estrogen. When exposure to estrogen-mimicking compounds is thrown in the mix, the potential for appreciably increased estrogen levels is amplified.
A pilot study on the relationship of pesticides and PCBs to breast cancer provides further evidence of this possible connection.[104] In this study, the researchers found that women who had breast cancer had 50-60% higher levels of PCBs in their breast tissues. There was also a statistically significant increase in the level of DDT/DDE in these women. The authors warn that other risk factors were not controlled for in this study, but if it is accurate it indicates that a 10 ppb increase in these chemicals increases breast cancer risk by 1%.
In a more recent study of 15,000 New York City women, the women with the highest DDE levels had a 4-times higher risk of breast cancer, compared to women with the lowest DDE levels. [105] In this study, the scientists did control for other risk factors, such as age at first menstruation, age at first pregnancy and family history of breast cancer, and still found positive relationships between breast cancer and DDE.
Scientists theorize that these chemicals are promoters or inducers, and not direct carcinogens. This theory is supported by the findings that these chemicals have estrogenic properties, and that estrogen is known to promote abnormal cell growth. An extension of this theory is that estrogen exposure after maturation plays a role in the full expression of early developmental changes. This would provide an explanation for both the increased risk of breast cancer to women exposed to estrogens in utero and the rare cancers initiated at maturation in the women whose mothers took DES.
Obviously much more research is needed to positively establish the relationship between breast cancer and environmental chemicals. But some current-use pesticides are suspect. For example, atrazine, one of the most widely used herbicides, induces exceptionally rare breast tumors in male animals and also produced reproductive organ tumors and endocrinological effects.[102,106]
Consider the case of declining breast cancer rates in Israel, despite an overall increase in fat consumption. The declining cancer rate appears to correlate with a 1978 ban of three organochlorine pesticides lindane, DDT and alpha-benzene hexachloride previously found in extremely high levels in Israeli milk and, thus, in human tissues and breast milk.
Recent animal studies strongly suggest that human exposure to dioxin, an endocrine-disrupting chemical, may be linked to endometriosis, a dreadfully painful disease currently affecting 10% of reproductive-age women about 6.6 million women in the U.S. alone. The disease appears to becoming more common and afflicting women at younger ages.
Endometriosis causes bits of uterine lining to migrate generally to other pelvic organs and can cause infertility, internal bleeding and other serious problems. Recently, scientists discovered quite by accident that four out of five rhesus monkeys used for long-term dioxin research developed endometriosis (compared to one out of three "control" monkeys).[107] Researchers blame dioxin for the damaging effects on the monkeys' immune and hormonal systems, which led to the incidence of endometriosis.
Are dioxin levels that apparently cause endometriosis in the laboratory monkeys of concern to humans? At just 5 ppt dioxin in the monkeys' food, 71% of the monkeys developed the disease. These monkeys had dioxin levels in their bodies only ten times more than the average level of dioxins currently found in humans.
Other laboratory animal studies also link PCBs with the disease. A German study has found that women with endometriosis have significantly higher levels of PCBs in their blood.[108] The cause of endometriosis remains a mystery, however, as the rate of affliction climbs.[109]
Everyone knows that when they are stressed and run-down and when their immune system seems "low," they get sick easier. The interactions between the immune system, whereby white blood cells produce hormonal secretions that help ward off diseases, and the endocrine and central nervous systems are complex.
There is no doubt, however, that exposure to common environmental chemicals can interfere with these systems. The associations between endocrine-disrupting pollutants and immune system damages in wildlife are well established.[110] Similar associations are being discovered in humans.
The most dramatic evidence may be from humans living closest to the top of the food chain, and hence, most vulnerable to the bioaccumulation of environmental contaminants. The Inuit from Arctic Qué bec rely heavily on meat and blubber from seal and whale. These marine mammals are highly contaminated with PCBs and other toxic chemicals. As a result, the total PCB concentration in the milk fat of Inuit women is about the same as that found in beluga whale blubber. [111]
The health damages from this pollution are beginning to be assessed, and it appears that the children of the Inuit are bearing the greatest burden of effects. Infants have a very high rate of infectious diseases, including respiratory and ear infections (otitis). Vaccinations are less effective than in the general population, suggesting impaired immune systems.
Another concern from endocrine disruption in both adult males and females is thyroid gland enlargement, more commonly known as goiter. The thyroid gland controls growth hormones and the hormones that regulate metabolism; enlargement of the thyroid gland can disrupt metabolism. The exact effects of environmental contaminants on the thyroid are not well understood, but research suggests thyroid dysfunction as contributing to the "wasting syndrome" seen in wildlife in polluted areas. The substances that have been implicated in this syndrome include PCBs, dioxin, DDT, toxaphene and lead.
Most cases of goiter are attributed to dietary iodine deficiency, but the addition of iodine to table salt has largely reduced this source of disease. So, in the U.S., cases of goiter cannot be attributed to lack of dietary iodine. Great Lakes salmon all have enlarged thyroids; the problems are not iodine-related. Some environmental factor is affecting the endocrine systems of Great Lakes salmon; this same factor could be affecting the human population living in the region. There are reports of the prevalence of endemic goiter in the U.S., specifically in the state of Michigan, that are not attributable to iodine deficiency.[31]
Developing embryos and fetuses, infants and children are most vulnerable to the effects of hormone copycats. The most poignant example is from the estrogenic-drug DES (diethylstilbestrol). Some 5 million mothers in the U.S., and millions more in other countries, were given DES between 1941 and 1971. Some 5 million daughters and sons in the U.S. born since 1940 were exposed in the womb to DES (estimates from DES Action USA, Oakland, CA). Adverse effects from DES exposure were discussed earlier in this report.
In light of what is known about DES effects on offspring of exposed women, it should not be surprising to find related effects being caused by other hormone-mimicking chemicals present in the environment today. PCBs and dioxins, because of their ubiquitous presence in the global environment at relatively high concentrations, are perhaps best understood.
The accidental poisoning of cooking oil with a mixture of PCBs and dibenzofurans in Japan in 1968 and Taiwan in 1978-79 resulted in a large in utero exposure to the children of affected pregnant women. The Taiwan (Yucheng) children have been extensively studied. At birth the exposed children were shorter and weighed less than comparative children and displayed numerous congenital defects. The exposed children also showed a delay in development, with deficits on formal developmental and behavioral assessments.
To date, mothers of the Yucheng children (compared to mothers of unexposed children) consistently say their children have higher activity levels, irregular rhythms, lower adaptability, negative moods and more intense reactions. Researchers' tests confirm that the exposed children, now 8-13 years old, have more health, habit and behavior problems. [112] Assessments of the children's intelligence in 1992 showed consistently poorer performance by all measures. The average IQ was 4 to 5 points below unexposed children. In verbal IQ, the deficits actually increased with age in the Yucheng children; however, overall the IQ deficits appeared to be declining with age.[113]
In Michigan, Drs. Joseph and Sandra Jacobson from Wayne State University have undertaken a long-range study to discern the effects of PCB exposure in utero and through breast milk on the behavioral development of children.[114,115] These studies found a dose-response relationship between the quantity of contaminated Great Lakes fish consumed by the mother and such measures in newborn infants as abnormally weak reflexes, reduced responsiveness, motor coordination and muscle tone. The researchers did not attempt to explain the biochemical basis of the behavioral effects seen, but the connection between endocrine system disruption and later development has been well established in animals and likely is similar in humans.
These same children were again evaluated at the age of four years.[116] In this study, children were tested using common verbal, quantitative and memory tests. While these tests showed no evidence of mental retardation or gross impairment, some specific developmental deficits did emerge. Skills related to short-term memory and attention control processes, such as information retention, transformation and reorganization, were diminished in a dose-dependent fashion.
Further studies indicated that more highly exposed children had slower reaction times to visual stimuli, made more errors on a memory test and took longer to solve problems. Performance on short-term memory tests also depends on selective and sustained attention suggesting that attentional deficits may be contributing to the children's poor performance.
The Jacobsons noted that 17 of 236 children in their most recent study were so hyperactive that they refused to participate in the tests, so are not included in the research results. These 17 children were from mothers with PCB levels in their breast milk significantly higher than mothers of the other children.
Breast milk in U.S. women has an average of 1 ppm PCBs. A recent study of French women, who have similar PCB levels, identified specific PCB congeners in their breast milk; [117] about one-third of the PCBs are congeners that are known endocrine disruptors (IUPAC #28, #52, #138, #153, #169). Human milk also is known to be an important source of mercury exposure in infants.[118]
In a series of studies observing behavioral effects resulting from consumption of toxic-contaminated fish, Dr. Helen B. Daly, at the State University of New York at Oswego, has noted huge behavioral changes in rats fed Lake Ontario salmon. These studies found the rats to be hyperactive, relative to the control rats, when presented with an unpleasant event (mild electric shocks, reduced rewards, new situations, inconsistent rewards over time) and when later presented with a pleasant event (e.g., re-introduction of rewards). The same abnormal activity was observed by Dr. Daly in offspring that never had eaten Lake Ontario salmon, but were born from the female rats who had fed on the pollutant-laced fish.[119] In other words, rats fed Lake Ontario salmon behave "normally" (i.e., like the control rats) only when everything is "going their way."
Daly says the results of her rat studies can help explain why the 17 children in the Jacobson's tests were so uncooperative: "Since this type of test can be considered mildly frustrating, it is not surprising that these were the children whose mothers had the highest levels of contaminants in their breast milk (PCBs were measured, and are used as an ind icator of levels of other chemicals probably transferred from the mother to the baby)."[119]
"These results...can be viewed as providing the 'missing link' between the results observed in wildlife living in the Great Lakes region and children whose mothers had eaten Lake Michigan fish." [119]
-- Dr. Helen B. Daly
State University of New York at Oswego
Short-term memory and selective attention are important in acquiring basic reading and math skills; thus, reduced abilities in these areas could result in diminished school performance and potential in children exposed prenatally. As an example of the potential impact of reduced potential, Daly has estimated the population-wide effects of a theoretical five-point decline in IQ in the U.S. Her scenario results in 4.15 million people with IQ below 70 compared to the current 2.3 million, and only 990,000 with IQ above 130, down from 2.3 million. This scenario demonstrates the magnitude of the seriousness of diminished potential at the population level.
Developmental delay does not necessarily indicate obvious impairment upon maturity. These studies, however, lend further credence to the theories that in utero exposure to low levels of chemical pollutants levels ordinarily found in the environment may result in subtle deficits that do not manifest themselves immediately.
Causal links between effects seen in the children of toxic chemical-exposed mothers and specific pollutants cannot be proven, any more than the links between lung cancer and exposure to "second-hand" tobacco smoke can be "proven." Nevertheless, there are intriguing similarities between the effects seen in the exposed children and the effects typically caused by altered thyroid hormone systems due to exposure in utero to toxic chemicals. These include delayed maturation of the central nervous system and psychomotor development and permanent neurological deficits.
Among pregnant rats exposed to PCBs, thyroxine (T4) hormone levels in blood are reduced in pups, birth weights and postnatal weight gains are lower, liver weights are increased and brain weights are decreased.[120] Specific PCB congeners (IUPAC #118 & #153) were responsible for much of the hypothyroid effects. In other studies, similar effects were found in rats exposed to dioxins. But thyroid effects remain unpredictable and vary among species. In contrast to rats, for example, hamsters and guinea pigs exposed to dioxins increase their thyroxine levels.[121]
What about human babies exposed in the womb and through nursing to typical levels of toxic chemicals in their mothers? A recent study of 38 healthy babies in the Netherlands compared dioxin concentrations in the mothers' milk and thyroxine (T4) levels in the infants at birth and one week later.[121] The babies showed increasing thyroxine levels with increasing dioxin levels in their mothers. The scientists postulated that the dioxins influence thyroid hormone concentrations in infants by interfering with the babies' thyroid hormone regulatory systems. They conclude: "Whether the neurological disorders found by [Jacobsons and others] are related to dioxin- or PCB-induced changes in thyroid hormone concentrations remains unclear."
Hyperactivity and learning deficits are among the likely effects in children exposed in utero to endocrine-disrupting chemicals, based on many related studies. Because of this, troubling, perhaps unanswerable questions are starting to be asked.
"What if the documented declining learning performance and increasing incidence of problem behavior in school children are not functions of the educational system? What if they are the result of exposure to developmental toxicants that have been and are being released into the children's and parents' environment, or to which they have been exposed in utero?" [122] These questions are appropriate, indeed, demand to be asked in light of the apparent links between exposure to certain toxic chemicals and adverse effects in children and in laboratory animals.
If only a small part of the learning and behavioral problems of our children can be attributed to endocrine, immune or nervous system damages caused by maternal or childhood exposure to hormone copycats, the implications for our culture, society and survival are profound.
"I contend, furthermore, that we have allowed these chemicals to be used with little or no advance investigation of their effect on soil, water, wildlife and man himself. Future generations are unlikely to condone our lack of prudent concern for the integrity of the natural world that supports all life."
-- Rachel Carson in Silent Spring (1962)
What, then, are we to do?
The roots of the crisis of environmental releases of hor mone copycats are buried in our culture and lifestyles. Lon g-term solutions must go to these roots. This includes a rea ssessment of our regulatory laws and our approaches to che mical use and management.
Federal laws, such as the Clean Water Act, Clean Air Act and Federal Insecticide, Fungicide and Rodenticide Act must be revised to contend with sublethal effects of long-term exp osures to combinations of chemicals that can impair end ocrine, immune and nervous systems. Regional programs, suc h as the U.S. Environmental Protection Agency's proposed Gre at Lakes Water Quality Initiative, can help lead the way.
Toxic chemicals in diffuse sources of pollution, inc luding urban and farm runoff, must be better controlled. For example, some 20,000 pesticides are registered for agr icultural use in the U.S.; some 1.1 billion pounds of pesticide active ingredients are used annually, three-fourths by farmers.[123] Slowly farmers are moving to sys tems to reduce their costly addiction to poisons; &qu otwhole farm management" and "integrated pest man agement" are two approaches.
It is beyond the scope of this report to deal with the arr ay of such fundamental long-term changes that are pos sible and are beginning. The immediacy of the risks from end ocrine disruptors, however, warrants doing some things rig ht now.
All of us citizens, chemicals makers and users, regulators, scientists and politicians need to stop denying that there is a problem. These are not someone else's problems. Breast and prostate cancer, infertility and birth defects are as close as each of our own families. No one is making up these stories. Something very wrong is happening in the environment.
Recommendations for action by the International Joint Commission (IJC), the U.S.-Canada organization that oversees trans-boundary pollution issues, make sense everywhere:
Recent human health, wildlife and laboratory studies lend further support to the International Joint Commission's conclusion that exposure to persistent toxic substances is the most significant problem facing the Great Lakes region. Among the more recent concerns is the ability of various persistent toxic substances to disrupt natural hormone systems and interfere with critical stages of fetal development.
The Commission is convinced that the time has arrived for all sectors of society to move beyond the politics of confrontation and denial. The severity of the problem, and potential risk to the reproductive, physiological and intellectual faculties of future generations, all point to the need for consensus building on a comprehensive persistent toxic substances strategy. [124]
The quickest fix to many exposure risks would be simply for chemical makers to stop making and selling chemicals tha t have estrogenic or similar qualities. It would require no new laws, taxes or lawsuits. Imagine what a different wor ld it would have been, for example, if Monsanto Chemical Co. had decided 50 years ago not to make and sell PCBs.
The IJC reached this conclusion in 1994:
"It is important and inevitable that the business sector act increasingly to lead rather than resist a broad movement towards manufacturing processes that eliminate the production and use of persistent toxic substances, and that they embrace a new, ecosystemic approach to business and governmental decision-making." [122]
So how did the chemical industry respond to this clarion call? Here is what the executive director of the Vinyl Institute, Robert Burnett, had to say: "The International Joint Commission has lost touch with reality... Their extreme position threatens hundreds of thousands of jobs in the vinyl industry for no reason at all and would deprive us of an environmentally good product. The IJC position does not deserve to be taken seriously." [125]
Chemical makers insist that today's chemical products bear no resemblance to their mistakes of the past. That is why mandatory programs to sunset dangerous chemicals will likely prove necessary.
But even mandatory programs won't be easy. Take dioxin, for example, that terrible and ubiquitous global poison. The more we learn about this chemical, the worse and more complex its effects appear. No one ever tried to create dioxin; it is formed as a by-product in the making of some pesticides and the incineration of plastics in wastes, for example. But the lands, seas and life itself are poisoned with dioxin.
What should we do about just this one chemical, among the hundreds or thousands that may be damaging us? Certainly we should ban it. For starters, we can stop right now the industrial practices that produc