World Wildlife Fund, September 1998
Half a century ago, scientists made the unsettling discovery that man-made compounds, such as the pesticide DDT, accumulate in the bodies of people and wildlife. Today synthetic chemical contamination is pervasive and global. There is no clean, uncontaminated place and no person untouched by this chemical legacy. Each of us now carries several hundred synthetic
chemicals that were not present in the bodies of our great grand-parents at the turn of the century.
The question of how contaminants affect health has become all the more urgent since scientists recently recognized a new kind of hazard known as "endocrine disruption." Through a series of accidental discoveries, researchers stumbled on the fact that some widespread, man-made chemicals, called "endocrine disruptors," can interfere with the body’s own hormones and
jeopardize health.
In the past five years, the scientific investigation of this problem has intensified and provided steadily growing evidence linking these synthetic endocrine-disrupting compounds to impaired health in wildlife and people. This exploration is ongoing and far from complete.
Although uncertainties remain about the impact of these compounds on human health, the emerging science has heightened concerns and provided sufficient evidence of damage to wildlife to justify immediate protective measures. The time has already come for precautionary action to reduce our reliance on suspect chemicals and to establish screening and testing programs to assess chemicals for hormone-disrupting hazards.
A conversation disrupted
Hormones, which are produced in a variety of organs known as endocrine glands, travel in the bloodstream carrying messages from one part of the body to another. In adults, these hormone messages govern sex and reproduction and also coordinate organs and tissues that work in concert to keep the body functioning properly.
Before birth, hormone signals play an even more vital role: They orchestrate critical events in early development, such as sexual differentiation and the proper construction of the brain. Because hormones are so key in early development, synthetic chemicals that disrupt such internal messages pose a particular hazard to the unborn. Studies also have found that contaminant exposure levels that cause no apparent damage to adults can have devastating effects on those exposed in the womb. In one study, a fetus proved 100 times more sensitive to a hormone-disrupting contaminant than an adult.
Normal development depends on getting the right amount of the right chemical messenger to the right place at the right time. If these messengers don’t arrive or arrive in the wrong amounts, the offspring’s development is irreparably altered. Disruption at this stage of life can cause permanent damage with consequences that last a lifetime.
A New Kind Of Hazard
Until recently, the research and regulation of synthetic chemicals focused primarily on the dangers of genetic mutation, cancer, and gross birth defects. In probing endocrine disruptors, scientists are investigating entirely new mechanisms and novel avenues through which synthetic chemicals can upset normal biological processes and undermine health and well-being. Evidence is
mounting that endocrine disruptors can do damage at extraordinarily low doses—measured in parts per trillion—and that they are already compromising the health and intelligence of the next generation.
The problem of endocrine disruption centers on synthetic chemicals that sabotage the body’s internal communication system. In the body’s constant conversation with itself, a large part of the communication takes place through hormones and other chemical messengers (see "A Conversation Disrupted," above).
Endocrine disruptors can upset the body’s internal communication in several different ways. Many man-made chemicals mimic natural hormones and send false messages. Other synthetic compounds block hormone receptors that receive the messages traveling in the bloodstream and prevent true messages from getting through. Some cause disruption by preventing the synthesis
of the body’s own hormones or by accelerating their breakdown and excretion. Whatever the mechanism, the bottom line is the same: Any chemical that interferes with hormones can scramble vital messages, derail development, and undermine health.
The 1996 book Our Stolen Future, by WWF senior scientist Dr. Theo Colborn with coauthors Dianne Dumanoski and Dr. John Peterson Myers, documents the emerging scientific case on these hormonally active chemicals and the hazard they pose to wildlife and people. Wildlife studies and laboratory experiments provide solid evidence that synthetic chemicals have
contributed to dwindling wildlife populations by disrupting hormones, altering sexual development, impairing reproduction, and undermining the immune system. Taken as a whole, the broad body of evidence also shows that people are not only at risk, but already affected. Studies have documented health effects in people at exposures only slightly higher than "background levels" considered typical in the human population.
Although the investigation of human health effects has hardly begun, researchers have already found immune system changes, neurological and motor delays, and learning problems in children exposed in the womb to background levels of PCBs, a family of hormone-disrupting, persistent contaminants. (See "Scientific Assessment Work Sessions," below). Epidemio-logical studies
are also documenting disturbing trends showing that people are increasingly suffering from health problems seen in wildlife and laboratory animals that have been exposed to synthetic endocrine disruptors. This growing human evidence includes reports of declining sperm counts in some parts of the world, rising rates of benign prostatic enlargement and testicular cancer, and an increasing incidence of other genital defects in males.
No one knows how many of the tens of thousands of synthetic chemicals in general commerce in the United States pose such a hazard, because none have been screened specifically for hormonal or message-disrupting activity. To date, scientists have identified more than 70 individual chemicals or chemical families that disrupt hormones or undermine development. About half
of these are persistent compounds that resist degradation, accumulate in fat, and become concentrated in the food web. Over decades, such persistent contaminants can accumulate in a woman’s body fat and provide a source of exposure for an unborn child or nursing infant. These hormone-disrupting chemicals are found literally everywhere—in household products beneath the kitchen sink and in the fat of polar bears in the remote Arctic. In daily life, one encounters hormonally active compounds in pesticides, detergents, cosmetics, plastic toys, and food containers. These compounds are pervasive contaminants in our food
and in every ecosystem on Earth.
The Growing Proof
Evidence from Wildlife
Wildlife studies have been an important part of the case against endocrine disrupting chemicals since the problem first emerged. This body of scientific evidence is already substantial and has continued to grow. In recently published studies, scientists have reported some striking new findings:
Florida alligators. The alligators in Florida’s Lake Apopka have been a regular feature in news coverage of the endocrine disruption issue because of their dramatic symptoms: stunted penises that are sometimes only one-third normal size. But skeptics had doubted the broader significance of the Lake Apopka studies by researcher Lou Guillette and his colleagues, because it was assumed that the reproductive problems stemmed from a chemical accident that dumped a pesticide into the lake. A new study highlights the hazards of chronic contamination and shows that the problem of hormone disruption and reproductive problems in alligators extends beyond Lake Apopka. The discovery of alligator hormone abnormalities and reproductive failure in other Florida lakes that have not had chemical accidents makes it clear that chronic contamination may be as hazardous to wildlife as acute incidents.
Great Lakes fish. New studies have made a persuasive case that contaminants were in part or wholly responsible for the loss of the lake trout in the 1950s. Fishery officials had blamed the crash of the native lake trout on habitat destruction, overfishing, and predation by an introduced parasite, the sea lamprey. However, University of Wisconsin researchers implicated dioxin contamination in the extinction when they showed that the developing trout in the egg die with a concentration of as little as 5 parts per trillion of toxicity equivalents of dioxin and dioxin-like PCBs. Using core samples from lake sediment and computer models, U.S. Environmental Protection Agency (EPA) scientists have concluded that dioxin contamination reached a level high enough to begin killing trout developing in eggs and undermining trout reproduction in the 1940s.
Albatross in the North Pacific. An investigation of albatross nesting in a "pristine" environment on remote Midway Island has underscored the global nature of the chemical contamination problem. In a recent study, researchers reported the startling news that these long-lived seabirds in the middle of the North Pacific carry combinations of persistent contaminants such as PCBs, furans, and dioxins that are known to cause reproductive and health effects in Great Lakes fish-eating birds.
Whales in the North Pacific. A study of contamination in North Pacific minke whales found an upward trend in contaminants such as PCBs and the pesticide chlordane between 1987 and 1994. This contradicts the widespread impression that PCBs and chlordane are old problems that already have been addressed. The research team concluded that increasing levels indicate a "continuous fresh input of PCBs and [chlordane] in the North Pacific marine environment."
Otters in the Columbia River. Recent work on free-living otters has shown that mammals are also at risk from chemical contamination. Researchers from the National Biological Service found delayed or inadequate development of the reproductive tract in male otters as well as a significant dose-response relationship between these problems and synthetic contaminants such as certain PCBs, dioxins, and pesticides. The more heavily contaminated young males had smaller bones (baculums) within their penises and lighter testicles than others who were less contami-nated. In this study, the animal with the highest levels of synthetic contaminants had no testicles at all.
Evidence from Laboratory Experiments
Although wildlife studies have been invaluable, they have inherent limitations. They document associations or correlations between health problems and particular man-made contaminants without being able to establish for certain whether a particular chemical is, indeed, responsible for the observed effect. Laboratory studies have, therefore, played an important role in the
development of the endocrine-disruption issue by confirming the links between contaminants and health problems seen in the field and by providing insight into how synthetic contaminants cause this damage. Controlled laboratory studies have also helped answer whether the contaminant levels encountered in the environment are high enough to warrant concern. The recent laboratory work on endocrine disruption has opened two important new lines of investigation:
Contamination from plastic. Recent studies have heightened concerns about hormone-disrupting compounds that leach from plastics and have demonstrated that some chemicals widely encountered in plastics pose a hazard even at very low doses. In ongoing mouse studies, researchers found that doses of bisphenol A (an ingredient in the lining of metal food cans, polycarbonate water jugs, and dental sealants applied to children’s teeth) comparable to the amounts currently ingested by people can alter the development of the male reproductive organs. Male mice whose mothers were exposed to bisphenol A at levels as low as 2 parts per billion showed changes that would cause them to have permanently enlarged prostate glands. At doses of 20 parts per billion, they showed a permanent 20 percent decrease in daily sperm production.
Developmental damage from PCB exposure. Laboratory experiments with rats have identified the ear as a particularly sensitive target for prenatal disruption from the persistent contaminants PCBs and have added weight to the theory that PCBs do their damage by disrupting thyroid hormones, which are vital to proper development of the brain and nervous system. The studies done by the EPA lab in Research Triangle Park, North Carolina, found that PCB exposure during early development caused permanent auditory deficits, particularly in the ability to hear the lowest frequencies. The researchers suggest that this loss may reflect the effects of thyroid disruption on the development of the cochlea in the inner ear. Because this research confirms that PCBs interfere with thyroid hormones, it would also explain why other studies have implicated these persistent contaminants in behavioral disorders such as attention deficit and hyperactivity and in learning problems.
Evidence from Human Studies
The greatest uncertainties about endocrine disruptors concern people and the question of how great a toll hormone-disrupting synthetic chemicals are taking on human health. In most cases, there is no way to answer these questions definitively because there is no unexposed population to study as a control group and because scientists do not for ethical reasons conduct experiments on people. Nevertheless, compelling new findings are emerging in this research arena:
Contaminated fish and learning problems.
An ongoing study by researchers at Wayne State University has documented significant deficits in intelligence and learning in children exposed to PCBs and other contaminants in the womb. Drs. Joseph and Sandra Jacobson found significant learning and attention problems in children of women who had eaten contaminated fish from Lake Michigan in the six years prior to pregnancy. In their most recent examination of these children at 11 years of age, they found the most highly exposed have difficulty paying attention, suffer from poorer short- and long-term memory, were twice as likely to be at least two years behind in reading comprehension, and were three times as likely to have low IQ scores. This work is striking not only because of the lasting impact seen in children, but also because the fish-eating mothers were not highly contaminated. The levels measured in their bodies fall on the high end of what is considered the "normal" background range for PCBs in the human population. In a similar study at the State University of New York (Oswego), researchers found measurable neurobehavioral deficits in the newborn children of women who had eaten the equivalent of 40 pounds of Lake Ontario salmon in a lifetime, thereby replicating the Lake Michigan study. In additional tests, these children showed abnormal reflexes, a shorter attention span, and an intolerance to stress. The Oswego study has been the first to document a wide range of effects on temperament stemming from prenatal exposure to contaminants.
The role of PCBs and dioxin in learning and behavior problems. In a review of the scientific evidence on contaminants and human health, a branch of the U.S. Public Health Service recently concluded that PCBs and dioxins are responsible at least in part for the neurological and behavioral deficits reported in children exposed in the womb. This assessment by the Agency for Toxic Substances and Disease Registry based this judgment on "remarkable parallels" in the human epidemiological evidence and corroboration from wildlife and laboratory evidence: "[T]he collective weight of the evidence indicates that certain PCB/dioxin-like compounds found in fish...can cause neurobehavioral deficits. Further, the evidence indicates that these compounds have produced some effects in some Great Lakes fish consumers."
Genital defects. A recent medical study reports rising rates of genital defects in male infants in the United States, which—together with similar reports of increasing incidence from five European countries—indicates a disturbing health trend. The study, which used data from two surveillance systems tracking birth defects, found that the rate of hypospadias, a defect involving misplacement of the urethra, doubled between 1970 and 1990. This defect arises from incomplete masculinization of the male genitals and has been replicated in the laboratory with anti-androgens such as DDE and vinclozolin (a commonly used fungicide on fruits and vegetables).
Testicular cancer in young men. In recent decades, the incidence of cancer of the testicles in men under age 34 has been increasing rapidly in many countries and poses a challenge to epidemiologists trying to determine the cause. According to recent studies, this cancer in young men almost certainly arises from events early in life or even in the womb—a hypothesis supported by the higher rate of testicular cancer among men with developmental defects such as hypospadias and undescended testicles. Researchers also note that striking geographical variations in the pattern of this disease point to the importance of environmental influences. Another clue has come from animal studies, which support the theory that estrogens may play a key role in promoting testicular cancer and raise the question of whether synthetic chemicals that mimic estrogen are contributing to soaring testicular cancer rates.