As expected, there are three major sources of evidence supporting the existence of endocrine disruption by environmental pollutants. The first source of evidence is the typical laboratory studies that confirm a chemical’s disruption mechanism at the in vivo or in vitro level. The second source is the observations gathered on wildlife animals, primarily on the effects on their population growth and reproductive activities. The third source is the data from epidemiology studies or from well-designed exposure trials in humans (or even in wildlife).

Many in vitro assays are currently being used in U. S. EPA’s mandated Endocrine Disruptor Screening Program (EDSP). These assays are used as the first tiered test to confirm the potential of hundreds to thousands of chemicals as endocrine disruptors, while currently EDSP’s main focus is on those disruptors that are estrogenic or antiandrogenic.

Some of the more recent in vivo examples include the study by Markowski et al. (2001), in which rats were shown to reduce motivation in standard behavioral tests following perinatal exposure to extraordinarily low doses (parts per trillion) of TCDD (dioxin). The doses tested were comparable to the background levels in people living in many places. Another study by Rice (2000) showed that infant monkeys developed a syndrome analogous to attention deficit hyperactivity disorder when these primates were exposed to very low levels of PCBs from birth. Still another study (Gray et al., 1999) demonstrated that low doses (parts per million) of the fungicide vinclozolin given to pregnant rats were capable of altering the sexual development in the male offspring, including reduction of sperm counts, retention of nipples, shortening of anal-genital distance, and some other reproductive malformations.