Toxics Program, World Wildlife Fund
A remarkable change has occurred in the last fifteen years in scientific knowledge about development, molecular biology, and toxicology. This burgeoning information raises serious questions about the adequacy of existing methods for assessing risks from man-made and naturally occurring chemicals. Hormone disrupting
15Richard A Liroff, a political scientist, is Senior Fellow in the Toxics Program at World Wildlife Fund in Washington, DC. The opinions expressed here are his own and not necessarily those of World Wildlife Fund.
chemicals illustrate this new challenge. ("Hormone disrupting chemicals" frequently are referred to as "endocrine disruptors," substances that affect hormones produced by the endocrine glands. This essay deliberately opts for the broader term, which is more readily understood by nonscientists).
Hormone disruption refers to a chemical's ability to mimic or block the action of the body's own hormones, or its ability to interfere with normal hormone production or breakdown in some way. Chemicals that are able to disrupt sex and thyroid hormones have been particularly under the spotlight, but other hormones, such as those of the adrenal gland, may also be subject to disruption. The overall result appears to be damage to reproductive, immune, and nervous systems, and increases in birth defects, selected cancers, and learning disabilities. For the last three decades, there has been a disconcerting increase in the incidence of such human health disorders as breast cancer, testicular cancer, hypospadias (a birth defect where the urethra does not open at the end of the penis) and learning disabilities.
For some disorders registering increases, such as prostate cancer and autism, at least part of the rise is a consequence of clearly identifiable changes in diagnostic methods and definitions. Nevertheless, scientists suspect that some of these adverse trends in public health may be associated with exposures to chemicals in daily life. Much more is known about effects in wildlife and laboratory animals than about effects on human health, but knowledge about human health effects is growing. The accumulating evidence prompted the International Programme on Chemical Safety, a consortium of the World Health Organization and other United Nations agencies, to convene an expert panel to produce a "state-of-the-science" review of hormone disruptors. In 2002, the panel urged that research on human health effects be given a high priority, because there is strong "biological plausibility," based on evidence from laboratory animals and wildlife, that hormone disrupting chemicals are damaging human development and reproduction (Damstra et al., 2002).
The history of DDT provides useful insight into how scientific understanding of hazards from toxic chemicals has shifted at the close of the 20th century and the dawn of the 21st. DDT has a prominent public profile. It represents the double-edged character of chemical technology; it was welcomed enthusiastically on account of its perceived benefits, but it ultimately was viewed more negatively as its adverse effects surfaced. While mostly used to protect crops from agricultural pests, DDT once was considered a miracle chemical for preventing illness and death from malaria. After its pesticidal properties were recognized in the late 1930s, it was deployed to protect military personnel during World War II. It was then the basis for an ambitious malaria eradication campaign in the 1950s and 1960s. The campaign fell short of its eradication goal in many places, but it nevertheless is credited with saving millions of lives.
Rachel Carson highlighted DDT's adverse environmental effects in her 1962 book, Silent Spring. Ten years later, in 1972, U.S. EPA banned DDT for agricultural use in the United States. U.S. EPA's decision was based on DDT's suspected carcinogenicity and evidence that it was thinning eggshells and contributing to population declines in bald eagles and other birds. As of 2004, DDT is used legally in about two dozen countries, where it is sprayed inside homes to control malaria. For such use, DDT historically has been regarded as relatively safe, in the sense that it is not acutely toxic to humans except in very large doses.
In 2002, the U.S. Department of Health and Human Services published an updated toxicological profile of DDT and its breakdown products (ATSDR, 2002). The profile underscores how much has been learned about DDT in the years since U.S. EPA's ban, particularly with respect to DDT's hormone-disrupting characteristics. For example, in two studies published in 1987 and 1995, the length of a mother's ability to breastfeed her children was found to be inversely related to the concentration of p,p-DDE ("para-para-DDE") in her breast milk (ATSDR, 2002). Research published in 2001, based on studies of American women in the 1960s, found increased odds of having pre-term and low birthweight ("small-for-gestational-age") infants among those women having elevated blood concentrations of DDE (ATSDR, 2002). Since it is generally accepted that pre-term birth and low birthweight can contribute to infant mortality, U.S. EPA's decision to ban the use of DDT in 1972 might have increased the survival odds of American infants, even if the agency did not realize it at the time. Conversely, since blood concentrations of DDE have been found to be high in countries that use DDT for malaria control, the toxicological profile reports that "adverse reproductive outcomes may be a concern for women in countries where these chemicals are still used" (ATSDR, 2002).
The remarkable recovery of bald eagle, peregrine falcon, and brown pelican populations in the last 30 years provides strong evidence that U.S. EPA did the right thing in outlawing DDT in 1972. Yet the DDT tale also raises the important public policy question about how much should be known or suspected about a chemical before steps are taken to remove it from the marketplace. While this topic is the subject of more detailed discussion in Section 3.3.2 of this book, it is worth noting that scientists frequently find only associations between exposures and effects. They do not always know exactly how a chemical works, that is, its "mechanism of action." For example, the WHO expert panel determined that "there is strong evidence that eggshell thinning results from exposure to DDE," but added "there is continued uncertainty with respect to the precise mechanism of action of DDE" (Damstra et al., 2002). This begs the question of what might have been the fate of America's bald eagle population if regulation had been contingent upon more precise scientific knowledge about how DDE works.
The DDT story is instructive in other ways as well. For example, scientists historically have stressed that "the dose makes the poison." A corollary of this belief is that while high doses of a chemical may be toxic, lower doses are less likely to be. But scientific evidence gathered in the last 10-20 years indicates that this dogma requires modification - that it is not only the dose that makes the poison, but the timing. For example, in reporting on DDT and its breakdown products, the toxicological profile indicated that adverse developmental effects depended on the dose administered, the timing of exposure during or after gestation (the period in the womb), and the specific chemical administered (ATSDR, 2002). Some of the DDT-related chemicals were associated with female hormonal effects in the reproductive system. One was associated with anti-androgenic (compromising of male hormone) effects.
The importance of timing in making judgments about potential hazards from chemicals was underscored by publication in 1993 of the landmark National Academy of Sciences (NAS) report, Pesticides in the Diets of Infants and Children (NAS, 1993). The NAS report found both quantitative and qualitative differences in the toxicity of pesticides between children and adults. The report noted "special windows of vulnerability - brief periods early in development when exposure to a toxicant can permanently alter the structure or function of an organ system" (NAS, 1993).
A principal public policy consequence of the NAS report was the enactment of the Food Quality Protection Act of 1996. This law, amending the Federal Food Drug and Cosmetic Act and the Safe Drinking Water Act, not only called upon U.S. EPA to take special measures to protect children from pesticides, but also required U.S. EPA to establish a screening and testing program for hormone-disrupting chemicals. As of 2004, no such screening and testing requirements had been promulgated. Public and private sector laboratories around the world have been collaborating in designing and validating suitable screens and tests. Progress has been slow in part because so much of what is known and is being learned about hormone disruption is at the frontier of developmental biology and toxicology.
Although a formal screening and testing program is still several years in the future, industry will still face substantial pressure from a concerned public, particularly as biomonitoring programs - measurements of chemicals in human blood, fat, and urine - proliferate. Monitoring contaminants in breast milk provides not only a measure of a newborn infant's exposure, but also an indication of the chemicals that babies have been exposed to in the womb as their brains, testicles, uteruses, and other vital organs have developed. As more and more chemicals are found in mothers' milk, parents will ask with increasing urgency whether the health of their children has been compromised by the chemical industry's products.
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