#HealthyLifeMatters: Reproductive Effects Of Pollution | A Must-Read!

In recent decades, there has been a great deal of interest within the scientific community and popular media concerning endocrine disrupting chemicals (EDCs)—environmental agents that interfere with our natural hormones and may disrupt reproduction, development, and homeostasis.
Proven or suspected EDCs occur in industrial solvents and lubricants, pesticides, plastics (including the plastic lining of food cans), prescription drugs and medical devices, and even infant soy milk formulas. We’re exposed to EDCs through food, drinking water, contaminated air and soil, and household chemicals, and in certain occupations such as farming and manufacturing that use such chemicals. Some EDCs may affect not only the exposed person, but also that person’s descendants through the DNA methylation and epigenetic effects. Your grandchildren could be genetically affected by your chemical exposures today.

EDCs act by several mechanisms. They or their metabolites can mimic the effects of estrogen by activating its receptors; antagonize the effects of androgens; alter gene expression; or disrupt positive and negative feedback loops that regulate the body’s secretion of its own estrogens and androgens. EDCs are suspected or implicated, at least tentatively, in a broad spectrum of reproductive abnormalities—in males, cryptorchidism, hypospadias (a urethra opening ventrally on the penis instead of at the tip), low sperm count and reduced motility, and testicular cancer; in females, premature breast development, premature menopause, breast cancer, uterine fibroids, endometriosis, and disrupted ovulation and lactation.

Some authorities hypothesize that EDCs may underlie historical trends in declining sperm count and increasing breast cancer over the last 50 to 70 years. But in many such cases, the data are contradictory, weak, or in dispute. The evidence, however disturbing, is often vague and indirect. It is enormously difficult to prove a link between a particular reproductive disorder and a suspected EDC. For one thing, we cannot experiment on this with humans, and the results of animal experiments often don’t translate to humans.
For another, the effects may be delayed by years, decades, or perhaps even generations; and there are so many variables in human life that they cover up the trail of causation—prenatal or infant exposure with no effects visible until adulthood; changes in occupation, residence, and environmental exposure; migration and international adoption; and exposure to complex mixtures of environmental chemicals—making it impossible to single out any one cause or to know how they interact to produce effects that no one of them would produce alone. Despite such difficulties, EDCs pose a compelling problem under continuing investigation.

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