• the natural environment (water, soil and air)
• household products
• pesticides
• processed foods
• plants (fruits, vegetables, beans, grasses and more contain natural compounds known as phytoestrogens)
• pharmaceutical products
• plastics
• industrial chemicals

Concerns stem from wildlife and laboratory studies associating reproductive and developmental problems in animals (such as feminization of males, lower fertility and higher infant mortality) with exposure to "high" concentrations of synthetic environmental estrogens. Many animals living in or near contaminated areas have these kinds of health problems: fish; frogs, salamanders and other amphibians; alligators, turtles and other reptiles; birds (especially fish-eating species like gulls, terns, ospreys, eagles, pelicans); and marine mammals (whales, sea otters).

Laboratory experiments (using animals and cells) also point to an association between certain kinds of contaminants and endocrine disruption. Many studies using molecular biology are showing how the foreign substances interact with the endocrine system's hormones, target cells and receptor sites.

Probably the most convincing evidence that synthetic chemicals can act like hormones comes from the DES experience. DES, a strong synthetic estrogen banned since the 1970s, serves as a model. The drug, which is far more potent than other environmental estrogens, was given to pregnant women during critical fetal development to prevent misarriages and was used in cattle feed. Daughters and sons of women who took the drug have higher reproductive problems and cancer rates than those not exposed to DES in the womb. Laboratory studies confirmed that DES causes reproductive problems and cancer (including the rare rete-testicular cancer in males) in male and female mice.

In general, no one really knows whether long-term exposure to low levels of environmental estrogens and other hormones causes health problems in adult wildlife and humans. It may be that developing fetuses and embryos, whose growth and development is highly controlled by the endocrine system, may be the most vulnerable to and may have the most lasting effects from environmental estrogens.

To confuse matters more, scientists themselves disagree about research conclusions. And, as the issue leaves the realm of science and moves into public policy arenas, the debates will become even more heated and polarized. Right now, it seems, opinions fall into one of three camps:

1. Some strongly believe that wildlife and laboratory evidence show that synthetic chemicals that act like estrogens have the potential to cause - and may already have caused - severe health problems. To them, the only questions that remain are:
   • How many health problems are related to environmental estrogens?
   • How severe will those problems be?
   • What will the consequences be for future generations?
   • What should be done to reduce public and wildlife exposure?

2. Many believe there may be reason for concern but call for more research to clarify murky areas. They believe a better understanding of how environmental estrogens may impact the endocrine system will help identify the most harmful substances and lead to less human and wildlife exposure to these compounds.

3. Others remain skeptical, believing that scientific data are inconclusive. Pointing to the lack of strong cause and effect evidence, they advocate more research and believe policy decisions should be put off until more is known about the subject.

How can such different opinions be represented when science is involved? To better understand, think of the 30-year controversy surrounding cigarette smoking and human health or the disagreement about whether or not the ozone hole exists.

Sound scientific data from both issues does not show absolute cause and effect: that one thing -like smoking - causes the other - lung cancer. Or that environmental hormones cause diverse health effects.

In cases like environmental estrogens, which involve complex biological systems and diverse health responses, cause and effect data are impossible to find. But, even without certain scientific evidence, the potential health, social and economic risks are forcing government, organizations and the general public to take notice.

In these cases, we rely on scientific, political and public debate to weigh the evidence and decide how to deal with the potential health problems. Governments around the world are taking action by gathering information, funding more research initiatives, developing screening and testing programs for synthetic chemicals and setting up new policies.

Individuals are becoming informed through media articles, books, world wide web sites and grassroots organizations. Several actions, including banning chemicals and reducing pesticide use, have been recommended by advocacy groups. Staying informed and becoming involved in the debate can help you discern the issues and form an opinion on the best course of action. On a day-to-day level, reduce contact and risk by following the ten tips outlined in The World Wildlife Fund's online pamphlet, Reducing your risk: A guide to avoiding hormone-disrupting chemicals.

Many questions, such as the following, remain unanswered and await further research.

1. Does exposure to minimal amounts (background levels that an average person would be exposed to on a daily basis) of synthetic chemicals that are known to act like estrogens cause reproductive, health and behavioral problems in wildlife and humans?

2. Does exposure to environmental estrogens pose a greater threat to developing embryos than to adults, thus impacting fertility and health of the future generation?

3. How do variables such as profession, age, dose of exposure, diet, genetics and other factors influence susceptibility to these foreign substances?

And what about toxicity? Up until now, health risk has been defined as cancer. Government health agencies use cancer risk as a guide to decide safe doses and exposure. Now, we may need to look further and redefine toxicity to include long-term reproductive and developmental problems caused by endocrine modulating chemicals. And, if these substances do pose health threats, how do we accurately measure toxicity and evaluate the risk not only to adult human health but to our developing and growing offspring?

The author's of Our Stolen Future describe it this way (1).

Hormone-disrupting chemicals are not classical poisons or typical carcinogens. They play by different rules. They defy the linear logic of current testing protocols built on the assumption that higher doses do more damage. For this reason, contrary to our long-held assumptions, screening chemicals for cancer risk has not always protected us from other kinds of harm. Some hormonally active chemicals appear to pose little if any risk of cancer . . . such chemicals are typically not poisons in the normal sense. Until we recognize this, we will be looking in the wrong places, asking the wrong questions, and talking at cross purposes.

To further understand how environmental estrogens work and if they threaten wildlife and human health, several questions focusing on research and toxicity need to be asked and answered.

• Can wildlife and animal data be applied to humans, when it is clear that some of these compounds have different effects in different kinds of animals?

• Can laboratory tests on cell cultures explain and predict how environmental estrogens interact with the endocrine system in living organisms especially since these chemicals can affect more than one endocrine organ in an animal? So, does the study of a single cell type provide a good, accurate picture of how hormone-like substances interact with a living organism?

• How do mixtures of compounds (like the way they are found in the environment) react and interact with each other, the endocrine system and natural hormones?

• How do such things as length of exposure, dose, route of exposure (ingested, inhaled), age and gender influence toxicity?

• Which animals will the most vulnerable: insects, fish, amphibians, reptiles, mammals (including humans)? Which age will be the most vulnerable to potential effects: fetuses, newborns, children, adolescents or adults?

1. Colborn, T., D. Dumanoski and J.P. Myers. 1996. Our Stolen Future: Are we threatening our fertility, intelligence, and survival?: A scientific detective story. New York: Penguin Books (http://www.ourstolenfuture.org/).

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