During recent years, numerous newspaper and magazine articles have suggested that humans may be at risk because small amounts of well known environmental contaminants, such as dioxin, PCBs and DDT, can affect hormone levels. Hormones are produced by the endocrine system as regulators of biological function in target organs. Because hormones play a critical role in early development, toxicological effects on the endocrine system often have an impact on the reproductive system. The term endocrine disruptor is used to describe chemicals that can mimic hormones and may either enhance or counteract their effects. It has been suggested that these hormone changes can, in turn, lead to a variety of health problems including cancer, decreased fertility, and abnormalities in newborns.
Evidence provided to support these claims of human and wildlife harm is largely from laboratory studies in which large doses are fed to test animals, usually rats or mice, and field studies of wildlife species that have been exposed to the chemicals mentioned above. In laboratory studies, high doses are required to give weak hormone activity. These doses are not likely to be encountered in the environment. However the process of bioaccumulation can result in top-level predators such as humans to have contaminants at levels many million times greater than the environmental background levels (Guilette 1994). In field studies, toxicity caused by endocrine disruption has been associated with the presence of certain pollutants. Findings from such studies include: reproductive disruption in starfish due to PCBs, bird eggshell thinning due to DDT, reproductive failure in mink, small penises in alligators due to DDT and dicofol (Guillette 1994, Colburn et al 1996). In addition, a variety of reproductive problems in many other species are claimed to be associated with environmental contamination although the specific causative agents have not been determined. One recent discovery that complicates the situation is that there are many naturally occurring "phytoestrogens", or chemicals of plant origin that exhibit weak estrogenic properties.
Pesticides that behave like the female hormone estrogens can have serious effects on reproductive success and function on animal exposed to them. Reproductive success or fitness is defined by having live reproductively capable offspring that go on to reproduce. Many estrogenic chemicals have been shown to cause the foetuses of exposed animals to be reproductively incapable. Fry and Toone (1986) found when they inject fertilised seabird eggs with DDT and its metabolites. The male chicks produced have varying degrees of intersexuality depending on dosage, reproductive system with both male and female structures. The female chicks had a partial to full developed right oviducts, instead of just left functional structures. In the area where the eggs were collected, there was multiple female-female pairing and low hatchability of eggs. Males exposed as embryos to estrogenic pesticides showed decreased to no sexual behaviour. (Fry and Toone, 1981) Louis Guillette noticed that male alligators from Lake Apopka in Florida have vestigial penis, follicle-like testis and elevated estrogens/testosterone ratios and the female hatching's ovaries were producing multiple egg follicles and eggs with several nuclei (Luoma, 1995, Guillette et al., 1995) The females also had above normal estrogens levels. When he and his colleagues did a similar injection study with DDT and DDE, they produced results similar to those found in the field. The reduction in penis length and the abnormal gonads made the hatchlings reproductively incapable. Both the bird and alligator studies were prompted by the contamination of large water bodies by organochlorins and the low breeding success of the animals living and feeding in these areas. Of particular interest are those chemicals, which mimic the female hormone of estrogen, which is thought to...
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