Dichlorodiphenyldichloroethylene is a chemical compound formed by the loss of hydrogen chloride from DDT, of which it is one of the more common breakdown products. Due to DDT’s massive prevalence in society and agriculture during the mid 20th century, DDT and DDE are still widely seen in animal tissue samples. DDE is particularly dangerous because it is fat-soluble like other organochlorines; thus, it is rarely excreted from the body, and concentrations tend to increase throughout life. The major exception is the excretion of DDE in breast milk, which transfers a substantial portion of the mother's DDE burden to the young animal or child. Along with accumulation over an organism's lifetime, this stability leads to bioaccumulation in the environment, which amplifies DDE’s negative effects.
DDE has been shown to be toxic to rats at 79.6 mg/kg. DDE and its parent, DDT, are reproductive toxicants for certain birds species, and major reasons for the decline of the bald eagle, brown pelicanperegrine falcon, and osprey. These compounds cause egg shell thinning in susceptible species, which leads to the birds’ crushing their eggs instead of incubating them, due to the latter’s lack of resistance. Birds of prey, waterfowl, and song birds are more susceptible to eggshell thinning than chickens and related species, and DDE appears to be more potent than DDT. A research shows that an elevated blood levels of DDEs have been tied to an increased risk for celiac disease in young people. An elevated blood levels of DDEs have been tied to an increased risk for celiac disease in young people.
Mechanism
The biological mechanism for the thinning is not entirely known, but it is believed that p,p'-DDE impairs the shell gland's ability to excrete calcium carbonate onto the developing egg. Multiple mechanisms may be at work, or different mechanisms may operate in different species. Some studies have shown that although DDE levels have fallen dramatically, eggshell thickness remains 10-12 percent thinner than before DDT was first used. Some studies have indicated that DDE is an endocrine disruptor and contributes to breast cancer, but more recent studies provide strong evidence that there is no relationship between DDE exposure and breast cancer. What is more clear is that DDE is a weak androgen receptor antagonist and can produce male genital tract abnormalities.
