These chemicals have been found to act as estrogens, anti-estrogens, androgens, anti-androgens, or to interfere with thyroid hormone, cortisol, insulin, or growth regulators. Moreover, since animals and human foetal development is primarily dependent on hormonal levels at various phases of development, the effects of these endocrine disrupting chemicals on the endocrine, reproductive, neurological, and immune systems have been found to be very serious, if not catastrophic (Windham, 2000).
TCDD dioxin is the most toxic of a class of organochlorine chemicals including chlorinated dibenzo-p-dioxins (CDDs), dibinzofurans (CDFs), polychlorinated biphenals (PCBs), brominated dibenzo-p-dioxins (BDDs), brominated dibenzofurans (BDFs), and polychlorinated pesticides etc. These groups of chemicals have been shown to exert hormonal effects that disrupt the endocrine system of wildlife resulting in adverse effects on reproductive system development and hormones, foetal development, and the immune system at extremely low levels of exposure (Windham, 2000; Are Environmental Hormones Emasculating Wildlife, 1994). Dioxins have been found to have both estrogenic and anti-estrogenic effects depending on the organ or tissue affected. The toxic metals mercury, lead, and cadmium as well as phenols have also been found to have reproductive and endocrine system disrupting effects (Windham, 2000).
Chemicals with estrogenic effects cause cells to produce surplus levels of oestrogen, which has been linked to breast cancer, testicular cancer, lowered sperm counts, and malformation/mutations of male sex organs, and a decreased number of successful male births. Exposure to relatively low levels of these chemicals have been documented to have had catastrophic effects on populations of Beluga whales, alligators, turtles, mink, otters, bald eagles, osprey, cormorants, terns, herring gulls, migratory birds, chickens, lake trout, chinook and coho salmon, etc. For example only 60 parts per billion (ppb) of DDE are required to cause anti-androgenic effects on male test animals (Colborn, 1999; Pritchard, 2004).
These chemicals act in a variety of ways; however, their mechanism of action could be broadly described as mimicking oestrogen thereby increasing oestrogen levels in the blood, anti-estrogenic; binding with oestrogen receptors or anti-androgenic; binding with androgen receptors. Some chemicals known to bind to estrogens receptors include insecticides (dichlorodiphenyl-trichloroethane (o,p'-DDT), methoxychlor, and chlordecone); a monomer used in plastic (bisphenol A); an alkylphenol surfactant used in detergents, cosmetics and toiletries, and other household products (octylphenol); and a plasticizer (butyl benzyl phthalate (BBP). Other compounds known to bind to androgen receptors include the fungicide vinclozolin and 1,1dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p'-DDE) the persistent in vivo metabolite of DDT. Polychlorinated biphenyls (PCBs) and 2,3,7.8-tetrachlorodibenzo-p-dioxin (TCDD) could all disrupt reproduction and development via several mechanisms (CLS, 1999; Developmental Effects, 1993).
Laboratory studies investigating the endocrine disrupting capacity of these chemicals