Are synthetic organic chemicals used in pesticides, industrial production, and consumer products putting people and wildlife at risk by interfering with their endocrine systems? This hypothesis has been debated within the scientific community for about 10 years, and many areas of scientific uncertainty still exist. In particular, scientists and policymakers want to know more about human risks from exposure to ambient levels of chemicals found to be hormonally active in laboratory studies.
Undoubtedly, debates over the human effects of endocrine-disrupting chemicals will keep scientists occupied for years. So far, however, discoveries that have helped build the environmental endocrine hypothesis have already sparked a quiet revolution in science and policy by influencing the way we think about chemical risks. In fact, some nations are beginning to take precautionary measures based on the weight of evidence that is mounting from diverse sources.
New Framework Emerges
Scientists widely agree that chemical endocrine disruptors affect some wildlife, including birds, alligators, and fish. Strong but sparser evidence also indicates that endocrine-disrupting chemicals adversely affect humans who are exposed to them.
There are a number of serious human diseases whose causes are not well understood. Among them are breast cancer and diseases of the reproductive system, immune system, and thyroid gland. The knowledge that chemicals can mimic or block the body's own endogenous hormones provides a new conceptual and theoretical approach to investigating the causes of these diseases.
Some of the new hypotheses that implicate endocrine-disrupting chemicals point to fetal exposure to synthetic chemicals as the initiating cause of a disease. The growth of interest in this hypothesis may be traced to the 1991 Wingspread Workshop, organized by Theo Colborn, chief scientist at the World Wildlife Fund and the first person to recognize and publicize the broad implications of endocrine-disrupting chemicals. At that workshop, participants presented laboratory and field data that provided compelling evidence connecting persistent organic chemicals in the environment to abnormal reproductive and developmental effects associated with endocrine disfunction in wildlife.
Historically, the assessment of chemical risk to humans has centered on two types of effects: acute toxicity and carcinogenicity. Recent discoveries that wildlife populations have been adversely affected by synthetic chemicals that mimic or block natural hormones in animals have provided researchers the impetus to look more systematically at other, less straightforward effects of contamination. These include reproductive and developmental abnormalities that may be triggered by exposure of the fetus to chemicals at levels that do not affect the adult animal, and multigenerational effects that may appear in the offspring of adults initially exposed at a prenatal or neonatal stage in their development.
In addition, a significant time gap may separate exposure and observed effects on mature organisms. Abnormal cells produced during early gestation have been implicated in adult-onset diseases. Among the diseases being investigated for connections to endocrine-disrupting chemicals are prostate, testicular, and breast cancers.
Two new laws passed by Congress in 1996 - the Food Quality Protection Act and the amendments to the Safe Drinking Water Act - require the U.S. Environmental Protection Agency to develop a screening and testing program for endocrine-disrupting chemicals. The timetable established by Congress stipulates that the screening and testing program should be ready for implementation by August 1998, a schedule that was unduly optimistic. These new laws state that criteria should be developed for assessing the risks of a class of chemicals - such as atrazines and endosulfans used in pesticides and phenols used in plastics - whose endocrine effects are new to the scientific community. …