The endocrine system is comprised of a series of ductless glands that produce hormones that are released into the blood stream. The major hormone-producing glands of the endocrine system include the pituitary, thyroid and parathyroids, hypothalamus, adrenals, pancreas, ovary, and testes. These systems are necessary for normal bodily functions and are instrumental in regulating growth and development, mood, metabolism, sexual function, and reproductive processes. The brain, heart, lungs, kidneys, liver, thymus, skin, and placenta also produce hormones. In order for the hormones to carry out their functions, there must be receptors in the body that respond to the hormones. When a hormone comes in contact with its receptor, it fits together like a key in a lock and the hormone sends a signal to the cell to carry out some function. Hormonal signals may also cascade through complex pathways to an ultimate site of action, with interference at any point having the potential of blocking or changing the intended result.
There are chemicals in the environment that mimic or modify the behavior of hormones. Some of these chemicals act like a hormone and fit the receptor for that hormone stimulating the body to perform some function. Other chemicals can block the receptor so that the hormone cannot reach its target, while others interact with the hormone itself or the gland producing the hormone making it either ineffective in performing its normal function or interfering with the timing of critical events during development. Endocrine disruptors are a diverse group of chemicals including some pesticides, flame retardants, chemicals used in plastics production, cosmetic ingredients, pharmaceuticals, natural products such as plant-derived estrogens and many more. The Prague Declaration on Endocrine Disruption during May 2005 concluded that the existing safety assessment framework for chemicals is ill-equipped to deal with endocrine disruptors. Testing does not account for the effects of simultaneous exposure to many chemicals and may lead to serious underestimations of risk.
An example of the kind of response that researchers have found in studies of endocrine disruption includes those of male fish exposed to wastewater from sewage treatment plants. In this example male fish were found to produce elevated concentrations of the egg yolk precursor vitello-genin. This is of interest because while male fish can produce vitellogenin, they normally do not because as males they never receive the signal from their endocrine system to produce eggs. Since the male fish normally never receive the signal to produce vitellogenin, the signal must be coming from some exogenous source. It has been known for sometime that pharmaceuticals and personal care products (PPCPs) that are excreted from our bodies through urine and feces contain traces of the drugs and personal care products we are exposed to. One of those products routinely found in wastewater is ethynylestradiol, a synthetic estrogen found in birth control pills and other estrogen therapies. Laboratory studies of male fish exposed to environmentally relevant levels of ethynylestradiol have shown elevated levels of vitellogenin. While this does not point directly to ethynylestradiol in the effluent as the causative endocrine disruptor, it does show that it is one possible chemical causing the observed elevation of vitellogenin. Therefore, the production ofvitellogenin in male fish is a biomarker for exposure to some chemical that is stimulating the production of vitellogenin. The real question then becomes, does the elevated concentration of vitellogenin in the male fish have any negative implications for the populations of fish. Studies of a dosed lake in the experimental lakes area (see the section 'Experimental lakes') that contained well-defined populations of lake trout, white sucker, fathead minnow, and pearl dace showed that males and female fathead minnow and pearl dace showed elevated whole body concentrations of vitellogenin within 7 weeks of the addition of environmentally relevant concentrations of ethynylestra-diol to the lake. Egg development was delayed in the fathead minnow and the pearl dace, testes development was severely impaired and testes-ova (testes containing ovarian tissue) were observed in males of these species. Reproductive failure was observed in both ofthese minnow species during the second year of ethynylestradiol addition, answering, in this example, that population effects were indeed observed.
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