ABSTRACT
INTRODUCTION An endocrine disruptor (ED) is a synthetic chemical that when absorbed into the body either mimics or blocks the actions of endogenous hormones and disrupts the body’s normal functions. Increasing numbers of chemicals with endocrine disrupting effects are being identified in wildlife and experimental laboratory animals while the effects of EDs in humans continue to be debated. The potential for human exposure to these chemicals can be linked to diet, water supply, lifestyle, occupation, and numerous environmental sources. Fetuses and young children are predicted to be especially vulnerable to the effects of these chemicals, as sensitive phases in the development of the reproductive and nervous systems occur during these early stages of life. EDs can also interfere with maturation of the endocrine and reproductive systems during puberty. Epidemiologic and scientific reports have implicated the increased body burden of endocrine disrupting chemicals for the adverse effects observed in wildlife and human populations. Underlying the study of EDs is our limited understanding of the pervasive health risks, in particular the endocrine effects, of chronic, insidious exposure to low levels of environmental chemicals that can presumably be amplified in the context of diverse combinations of chemicals (1). Moreover, exposure to low doses of chemicals during critical developmental periods portends a predisposition to the delayed, late onset of diseases that are triggered by additional insults during aging. The limitations in our current understanding of EDs emphasize an important distinction between the more subtle endocrine disrupting effects of low persistent levels of chemical exposure when contrastedwith the acute pathologies provoked by high, overtly toxic doses of chemicals.
