Endocrine Disrupting Chemicals

What are endocrine disrupting chemicals (EDCs)?

An Endocrine Disrupting Chemical (EDC) or Endocrine Disruptor (ED) is any chemical that can interfere with normal hormone functions in humans and/or animals (1).   The human endocrine system is a collection of glands which secrete different types of hormones, (including oestrogen) that regulate the body’s growth and metabolism, sexual development, and behaviour. Naturally occuring hormones are usually active at very low doses.  A healthy endocrine system is essential to the normal functioning of the human body.

Where are EDCs found?

Some EDCs are present in our natural environment including phytoestrogens (found in plants), however, most EDCs are synthetic compounds (2).  Almost 1000 compounds are known or suspected to be EDCs (3). Only a small fraction of these has been investigated in tests capable of identifying endocrine effects in intact organisms.

EDCs are present in a wide variety of products including plastics, pesticides, cosmetics, fragrances, food, kitchen cleaners, adhesives, paints, clothing, medical equipment, and toys. 

EDCs are widespread in the environment, in rivers, estuaries, soil, sewage treatment systems, drinking water and in polluted air (4).  Mostly they originate from human activity such as wastewater effluent, agricultural runoff; leaching from landfill and industrial pollution.

EDCs are commonly detected in wild-life and human body fluids and tissues (5).  EDCs enter the human body principally through ingestion of contaminated food and water, or through skin from personal care products and exposure to soil or dust particles.

Why should we be concerned?

There is now a large amount of scientific data that strongly suggests that exposure to EDCs could be causing long term, and in some cases, irreversible damage to wildlife, our environment and human health.  Many synthetic EDCs are persistent organic pollutants, such as polychlorinated biphenyls (PCBs), and decompose very slowly. Their concentrations increase constantly up the food chain and will be highest amongst those at the top (including humans).

The detrimental effects of EDCs amongst wildlife are well documented. They include reproductive disorders including “testicular feminisation” in fish (6,7), cancers, adrenal and bone disorders (8), reduced biodiversity, population decline (9,10,11), greater susceptibility to infection (12,13), neurotoxicity and thyroid  problems (14,15). The demonstrable effects of EDCs in wildlife could be indicative of long term effects in the human population.   Whilst it is more difficult to demonstrate their effects, there is now strong scientific evidence that EDCs could be linked to a range of adverse health problems amongst humans. This is also the view of the UN environment agency, the World Health Organisation (16), the European Environment Agency (17) and many research scientists worldwide (18). 

Some EDCs have been reported to cause adverse effects at very low dose levels. There is also concern that exposure to multiple EDCs can cause ‘combination effects’. Therefore, even when each individual chemical is present at a level below the threshold considered to cause harm, in combination with others they could form a hazardous cocktail in the human body (19,20).

Links to Breast Cancer

High levels of natural oestrogens, which stimulate growth and differentiation of mammalian epithelial tissue, are an important factor in breast cancer risk (21). Synthetic oestrogens are known to be associated with increased breast cancer risk (22). Hormone replacement therapy (oestrogen plus progesterone or oestrogen alone) used by postmenopausal women increases breast cancer risk significantly, as does the birth control pill (although to a much lesser degree).

Diethylstilbestrol (DES) a synthetic oestrogen used by pregnant women to prevent miscarriage, was the first synthetic EDC  shown to affect human health. After several decades of use it was found that it enhanced breast cancer rates significantly in both exposed woman and their children (23). DES was withdrawn from use in the UK in 1974. 

We remain exposed to many other EDCs which have been linked to breast cancer. For example, Bisphenol A (24) Phthalates  (25,26,27,28,29), Monoethyl phthalate (30),  Parabens (31), a number of metals, known as “metalloestrogens”, (32),  cadmium (33) and aluminium salts (34) have all been linked to adverse effects on the mammary gland.

There is also considerable evidence that exposure to EDCs during critical moments of development, for example in the womb, during early infancy, childhood or during puberty, could also increase the risk of developing breast cancers later in life (See full Background Breifing for references or seperate webpage on In-utero exposures).

Whilst,  it should be noted that not all scientists believe EDCs contribute to breast cancer incidence (35) , the evidence that they play some part in increasing our vulnerability to the disease is starting to mount up.   

Breast Cancer UK position

  • Breast Cancer UK is calling for the regulation of chemicals to be strengthened and improved, based on the precautionary principle, to pro-actively protect public health; 
  • Hazardous chemicals, including EDCs,  to be recognised as preventable risk factors for breast cancer in all UK National Cancer Plans;
  • The extension of EU Article 60 (3) of the REACH Regulation, to ensure EDCs are, by default, classed as Substances of Very High Concern (SVHC), for which no safe thresholds can be determined;
  • An increase in the proportion of cancer research funding for prevention and the   investigation of the environmental and chemical causes of breast cancer.

For more information and a full list of reference download our Background briefing on Endocrine Disrupting Chemicals

Further Resources:


  1. IPCS. (2002). Global assessment of the state-of-the-science of endocrine disruptors. Geneva, Switzerland, World Health Organization, International Programme on Chemical Safety.
  2. UNEP/WHO (2013). State of the science of endocrine disrupting chemicals 2012
  3. TEDX.
  4. UNEP/WHO (2013). Op.cit.,
  5. UNEP/WHO (2013). Ibid.,
  6. Gross-Sorokin MY, et al., (2006). Assessment of feminization of male fish in English rivers by the Environment Agency of England and Wales. Environmental Health Perspectives 114 (1):147-51.
  7. Jobling, S, et al., (2009). Statistical Modelling Suggests that Antiandrogens in Effluents from Wastewater Treatment Works Contribute to Widespread Sexual Disruption in Fish Living in English Rivers Environmental Health Perspectives 117 797–802.
  8. UNEP/WHO (2013). Op.cit.,
  9. Sonne, C. (2010). Health effects from long-range transported contaminants in Arctic top predators: An integrated review based on studies of polar bears and relevant model species. Environment International 36: 461–491.
  10. EEA. (2012). The impacts of endocrine disrupters on wild-life, people and their environments—The Weybridge+15 (1996–2011) report.
  11. Kloas W, et al., (2009) Endocrine disruption in aquatic vertebrates. Annual N Y Academy Sciences. 1163: 187-200.
  12. Schwacke LH, et al., (2011). Anaemia, hypothyroidism and immune suppression associated with polychlorinated biphenyl exposure in bottlenose dolphins (Tursiops truncatus). Proceedings of the Royal Society B: Biological Sciences  279(1726): 48-57
  13. Davison NJ, et al., (2011). Infection with Brucella ceti and high levels of polychlorinated biphenyls in bottlenose dolphins (Tursiops truncatus) stranded in south-west England. Veterinary Record 169 (1):14.
  14. Boas M, et al., (2012). Thyroid effects of endocrine disrupting chemicals. Molecular and Cellular Endocrinology 355 (2) 240-248.
  15. UNEP/WHO (2013). Op.cit.,
  16. UNEP/WHO (2013). Ibid.,
  17. EEA. (2012). Op.cit.,
  18. Berlaymont Declaration, (2013).  accessed sep 28
  19. Kortenkamp, A. (2007). ‘Ten Years of Mixing Cocktails: A Review of Combination Effects of Endocrine-Disrupting Chemicals. Environmental Health Perspectives 115(1): 98–105.
  20. Payne, J., Scholze, M. and Kortenkamp, A. (2001). Mixtures of four organochlorines enhance human breast cancer cell proliferation. Environmental Health Perspectives, 109 (4): 391–397.
  21. Travis, RC. and Key, TJ. (2003). Oestrogen exposure and breast cancer risk. Breast Cancer Research 5: 239-247.
  22. Travis, RC. and Key, TJ. (2003). Ibid.,
  23. Reed, CE and Fenton, SE (2013). Exposure to diethylstilbestrol during sensitive life stages: a legacy of heritable health effects. Birth Defects Research Part C Embryo Reviews Today 99(2): 134-46.
  24. Jenkins S, et al.,  (2012). Endocrine-active chemicals in mammary cancer causation and prevention. Journal of Steroid Biochemistry and Molecular Biology. 129(3-5): 191-200.
  25. Jobling, S, et al., (1995). A variety of environmentally persistent chemicals, including some phthalate plasticizers, are weakly estrogenic. Environmental Health Perspectives 103: 582-587.
  26. Kang, SC and Lee, BM (2005). DNA methylation of estrogen receptor α gene by phthalates. Journal of Toxicology and Environmental Health, 68:1995-2003. 
  27. Aksglaede, L., et al., (2006). The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Human Reproduction Update 12: 341–349.
  28. Dhimolea E, et al. (2014). Prenatal Exposure to BPA Alters the Epigenome of the Rat Mammary Gland and Increases the Propensity to Neoplastic Development. PLoS ONE 9(7): e99800.
  29. Hsieh, T.-H., et al., (2012). Phthalates induce proliferation and invasiveness of estrogen receptor-negative breast cancer through the AhR/HDAC6/c-Myc signaling pathway. FASEB Journal, 26(2): 778–787.
  30. Romero-Franco, M, et al.,  (2010). Personal care product use and urinary levels of phthalate metabolites in Mexican women. Environment International 37(5): 867-71.
  31. Darbre PD and Harvey PW. (2014). Parabens can enable hallmarks and characteristics of cancer in human breast epithelial cells: a review of the literature with reference to new exposure data and regulatory status. Journal Applied Toxicology 34(9):925-38.
  32. Darbre PD. (2006). Metalloestrogens: an emerging class of inorganic xenoestrogens with potential to add to the oestrogenic burden of the human breast. Journal of Applied Toxicology. 26(3): 191-7.
  33. Kortenkamp A, et al.,  (2011). State of the art assessment of endocrine disrupters. Final report. European Commission, Directorate-General for the Environment (Project Contract No. 070307/2009/550687/SER/D3).
  34. Exley C, et al.,  (2007). Aluminium in human breast tissue. Journal of Inorganic Biochemistry 101(9):1344-6.
  35. Ingber SZ, et al.,  (2013). DDT/DDE and breast cancer: a meta-analysis. Regulatory Toxicology and Pharmacology 67(3): 421-33.

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