Endocrine Disrupting Chemicals 2012 - World Health Organization

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10. The tip of the iceberg Because only a small fraction of the hundreds of thousands of synthetic chemicals in existence have been assessed for endocrine disrupting activity, and because many chemicals in consumer products are not identified by the manufacturer, we have only looked at the “tip of the iceberg”. How many EDCs are there? Where do they come from? What are the human and wildlife exposures? What are their effects individually and in mixtures during development and adulthood and even across generations? What are their mechanisms of action? How can testing for EDCs be improved? All of these questions need answers. 18 State of the Science of Endocrine Disrupting Chemicals – 2012
11. Testing for EDCs Since there are data from epidemiological studies showing associations between human disease end-points and EDC exposures, it is likely that endocrine diseases and disorders are occurring at current exposure levels. Put another way, this means that there are situations in which individually safe exposures of EDCs have reached a collectively harmful level or in which levels thought to be safe are not so. When chemicals are tested for endocrine disrupting activity under specific validated guideline studies, it is customary to examine three doses to determine a level not apparently associated with observable effects. This level, termed the no-observed-adverse-effect level, is then divided by a so-called safety or uncertainty factor (of 100, for example) to extrapolate to levels expected to be safe for humans or wildlife. The doses declared safe are not actually tested, nor are the mixtures. These studies also assume that there is a threshold for EDC effects, that there will be no effects at low doses and that the dose–response curve rises with increasing dose. As noted above, there is no threshold for EDC effects due to the presence of active hormone pathways, and EDCs are likely to have effects at low doses. Consequently, their dose–response curves will not necessarily rise in proportion to dose. Regulatory guideline studies also focus on histopathology and organ and body weights as the end-points. As noted above, EDCs can cause many diseases and affect many disease end-points that are not currently assessed in regulatory studies. Also, risk assessment approaches do not always assess toxicity during development, which is the most sensitive window for EDC action, and also do not follow the animals for their lifetime, which is needed to assess resulting diseases. Testing for EDCs 19
Page 1 and 2: State of the Science of Endocrine D
Page 3: State of the Science of Endocrine D
Page 7 and 8: Preface This Summary for Decision-M
Page 9 and 10: 1. Introduction This document prese
Page 11 and 12: ◦ Developmental neurotoxicity wit
Page 13 and 14: Early prenatal Mid- Late prenatal P
Page 15 and 16: 4. Endocrine disruptors and human h
Page 17 and 18: There are other trends of concern i
Page 19 and 20: 7. Why should we be concerned?—Po
Page 21 and 22: Presentation of Disease over the Li
Page 23 and 24: Wildlife and humans are exposed to
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Page 29 and 30: POPs such as PCBs and DDT were bann
Page 31 and 32: suggests links between maternal pht
Page 33 and 34: Hormone-related cancers: Despite a
Page 35 and 36: 14. Concluding remarks EDCs have th
Page 37 and 38: 15. References Chen D, Hale RC (201

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