Definitions

All living organisms depend upon a large and intricate array of chemical signaling systems to guide biological development and regulate cell and organ activity. Over the past two decades, scientific interest in the ability of many environmental contaminants to interfere with these sensitive systems has grown dramatically. A hybrid science, the study of endocrine disruption, has arisen from concerns about the effects of these phenomena on health and the environment. This science incorporates findings and methodologies from multiple disciplines including toxicology, endocrinology, developmental biology, molecular biology, ecology, behavioral biology, genetics, and epidemiology.

The 'Low-Dose' Issue and Inverted-U Dose-Response

Relationships for EDCs Summary Further Reading

EDCs are chemicals that can disrupt any aspect of endocrine processes. Hormonal systems for which there is clear evidence of endocrine disruption include thyroid hormones, androgens, and estrogens. EDCs disrupt development by interfering with the hormonal signals that control normal development of the brain and other organ systems. EDCs can also affect adults by similar mechanisms, because these same hormones also play important regulatory roles in adults. EDCs can act at very low levels of exposure to produce profound effects on the course an organism follows from fertilized oocyte through to maturity, adulthood, and death. The effects of EDCs on developing organisms are of greatest concern, since the disruptive effects of developmental exposure, referred to as organizational effects are permanent and irreversible. EDC exposure also produces measurable, activational effects in adults that may be reversible (they often do not persist when the organism is no longer exposed). A related field of research, 'developmental origins of health and adult disease (DOHAD)', and the new DOHAD society, is converging with research on endocrine disruption. Work in this area shows that exposures during different stages of development, particularly during fetal life, contribute to adult chronic diseases, including obesity, heart disease, diabetes, decreased fertility, impaired immune function, and neurological deficits.

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