- EDC exposure during vulnerable life stages with high sensitivity may derail future development. During pregnancy, the exposure of the unborn child is a big concern because it is unable to protect itself as normal compensatory mechanisms and detoxification mechanisms that operate in the adult are not yet in operation. Exposure in the womb can therefore lead to serious and permanent effects through changes to the genetic programming of a child’s normal development (perturbations of developmental programming). These effects resulting from exposure in early life will only become apparent later on in life [i]. Puberty may also be a sensitive life stage for impacts from EDCs.
- New animal research has found that effects may even be carried over to subsequent generations that were not originally exposed [ii]. These insights come from the new scientific field of epigenetics, which deals with the study of heritable changes that are not caused by changes in the DNA sequence. It illustrates that the damage might not be restricted to the individual exposed but may have more far-reaching consequences.
- The extrapolation from effects at high dose levels to low dose effects which is usually applied to derive so-called “No observed adverse effect levels” (NOAELs) has higher uncertainties for EDCs as compared to many other chemicals. For some EDCs non-monotonic dose responses (NMDRs) and low dose adverse effects have been demonstrated [iii], [iv]. Different effects can sometimes be seen at high doses as compared to low dose effects.
All of the arguments above cast doubt about whether the current approach of setting safe levels of exposure is appropriate (see also this question). At the same time we know that the general population is already exposed, including unborn babies and children.
It is likely that the usual risk assessment approach, which only looks at the risks of each substance in isolation, leaves wildlife and people at risk. Therefore special regulatory attention is needed which requires exposure reduction and replacement by safer substances or technologies.
This page is part of CHEM Trust’s Hormone Disrupting Chemicals FAQ – Full list of questions here.
[i]. Zoeller et al.: Endocrine-disrupting chemicals and public health protection: a statement of principles from The Endocrine Society, Endocrinology, 153, 9, 2012, 4097-4110. doi:10.1210/en.2012-1422; also Barouki et al.: Developmental origins of non-communicable disease: Implications for research and public health, Environmental Health 2012, 11:42. http://www.ehjournal.net/content/11/1/42
[ii]. D.M. Walker, A. Gore: Transgenerational neuroendocrine disruption of reproduction, Nature Reviews Endocrinology 7, 197-207 (April 2011)
[iii]. Vandenberg et al: Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses, Endocrine Reviews, 2012,33(3), 378-455
[iv]. Ulla Hass et al, Centre on Endocrine Disruptors, DTU, National Food Institute: Input for the REACH-review in 2013 on endocrine disruptors, 2013. http://www.mst.dk/NR/rdonlyres/54DB4583-B01D-45D6-AA99-28ED75A5C0E4/154979/ReachreviewrapportFINAL21March.pdf