1

BCUK Fact Sheet | Endocrine Disrupting Chemicals

The human endocrine system is a collection of

glands which secrete different types of hormones

that regulate the body’s growth and metabolism,

sexual development, and behaviour (Fig 1).

Hormones are released into the bloodstream and

transported to tissues and organs. They bind to

specific target cells and initiate biological

processes that ultimately lead to changes in cell

function. Oestrogens are responsible for female

sexual development and reproduction.

Androgens are responsible for the development

and maintenance of male sexual characteristics.

Hormones are active at very low doses and their

regulation is tightly controlled by the endocrine

and central nervous systems. Hormone related

diseases that result in hormone imbalance are

common and may be caused by over or

underproduction of specific hormones, or

insensitivity of target cells. A healthy endocrine

system is essential to the normal functioning of

the human body

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 animals1. Although details of how

EDCs exert their effects are not fully understood

some general mechanisms have been described2,3.

Some EDCs are “agonists” or “mimics” . These are

structurally similar to naturally occurring

hormones. They are able to bind to specific

hormone receptors, which in turn induce the

chemical reactions normally associated with

natural hormones. Some are “antagonists”, so

prevent hormone-receptor binding thus blocking

subsequent actions. Others can alter the

concentration of naturally circulating hormones.

There are also those that cause heritable changes

through “epigenetic” modification, which changes

gene expression without altering the underlying

DNA gene sequence. This mechanism is

particularly relevant in relation to prenatal and

early exposures.

Some EDCs are present in our natural

environment including phytoestrogens (found in

plants), however, most EDCs are synthetic

compounds4. Almost 1000 compounds are

known or suspected to be EDCs5. Only a small

fraction of these has been investigated in tests

capable of identifying endocrine effects in intact

organisms.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

What is the Endocrine System?

Fig 1: Major Endocrine Glands

2

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 air6. 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 tissues7. For example,

Bisphenol A (BPA), used widely in the

manufacture of plastics and epoxy resins is

routinely identified in human urine, blood,

amniotic fluid and breast milk8,9, and has been

detected in fat tissue and the placenta10. 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). For example,

significant levels of PCBs and other contaminants

are found routinely in polar bears11 including

those which live in relatively uncontaminated

arctic regions12. This is a result of consuming

contaminated fish that have bio-accumulated

PCBs in other more polluted locations.

The detrimental effects of EDCs amongst wildlife

are well documented. They include reproductive

disorders including “testicular feminisation” in

fish13,14, cancers, adrenal and bone disorders15,

reduced biodiversity, population decline16,17,18,

greater susceptibility to infection19,20,

neurotoxicity and thyroid problems21,22.

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

Organisation23, the European Environment

Agency24 and many research scientists

worldwide25.

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 body26,27.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

Where are EDCs found?

3

High levels of natural oestrogens, which stimulate

growth and differentiation of mammalian

epithelial tissue, are an important factor in breast

cancer risk28.

Synthetic oestrogens are known to be associated

with increased breast cancer risk29. 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 children30. 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,

several studies have linked prenatal Bisphenol A

exposure in animal models to an increased

incidence of mammary gland tumours31.

Phthalates, used in plastics and fragrances, are

weakly oestrogenic in tissue culture, where they

bind oestrogen receptors and act additively with

the natural oestrogens32,33. They have been linked

to early puberty in girls, a risk factor for later-life

breast cancer34,35. They can also induce

proliferation, malignant invasion and tumour

formation in breast cancer cell lines that lack

oestrogen hormone receptors36. Monoethyl

phthalate, a urinary metabolite of diethyl

phthalate (often used in fragrance), was elevated

in women with breast cancer, especially those

who were pre-menopausal37. Phthalates also bind

weakly to androgen receptors, disrupting cellular

actions initiated by androgens38,39. Parabens, used

as preservatives in many personal care products,

are detected in human breast tissue, stimulate

proliferation of breast cancer cells and have been

linked to breast cancer40. A number of metals,

known as “metalloestrogens”, show oestrogenic

and/or anti-androgenic activity and may also be

associated with increased breast cancer risk41.

Exposure to cadmium has been linked to early

puberty and breast tissue changes42 and

aluminium salts, used in antiperspirants to block

sweat ducts, is applied to areas where breast

cancers often occur and has been detected at high

concentrations in breast tumour biopsies43.

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 44,45,46,47,48,49,50.

EDCs associated with an increased breast cancer

risk that are no longer in use but are ubiquitous in

the environment include DDT51; dioxins and

polychlorinated hydrocarbons52.

Whilst, it should be noted that not all scientists

believe EDCs contribute to breast cancer

incidence53 , the evidence that they play some

part in increasing our vulnerability to the disease

is starting to mount up.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

Links to breast cancer

4

In addition to breast cancer, EDC exposure has

been linked to a number of endocrine-related

cancers. For example there is strong evidence

that organochlorine pesticides and PCBs are

associated with increased prostate cancer risk54

and this is likely mediated through their

oestrogenic activity55. Aluminium exposure may

also be a risk factor for prostate cancer56.

Methoxychlor, an organochlorine pesticide, and

triclosan, a preservative used in personal care

products may be linked to ovarian cancer57. Other

hormonal cancers thought to be associated with

EDC exposure include testicular, endometrial and

thyroid cancers, although fewer studies have

been carried out.

EDCs may also be linked to infertility,

reproductive problems and miscarriage58,

metabolic disorders including obesity59 and

diabetes60. EDCs which affect thyroid function

may be linked to neurodevelopmental disabilities,

such as autism and attention-deficit hyperactivity

disorder61,62.

The role of EDCs in human health is controversial.

Not all EDCs will necessarily contribute to illness

or disease. Dosage, including cumulative or

combinational effects63 is crucially important, as

well as the chemical nature of the EDC. For

example, consumption of phytoestrogens (found

in soybean products) during adolescence has

been correlated with a decreased risk of breast

cancer64. Nonetheless, EDCs have been clearly

linked to a number of human diseases as

illustrated above and are likely to contribute to

many more unless action is taken to reduce our

exposure.

What is the current Regulatory

position on EDCs?

Current regulation of EDCs across the European

Union is both complex and inconsistent. The

result is that EDCs continue to be used relatively

widely across Europe in a range of different

products.

Under the chemicals regulation REACH (EC

1907/2006) substances with endocrine disrupting

properties for which there is evidence of probable

serious effects to human health or the

environment require authorisation and/or

replacement65. However, the vast majority of

chemicals have never been tested for their

endocrine disrupting properties and as a result

very few are subject to the REACH authorisation

procedure.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

Links to other human diseases

Many everyday products contain EDCs.

© Ambrophoto /Shutterstock.com

5

Where a chemical has been identified as being an

EDC, authorisation may be given if a

manufacturer can demonstrate adequate control

of the risk or if the socio-economic benefits

outweigh the risk and if there is no available

alternative.

This approach has been criticised as failing to take

into account that for many EDCs there may be no

safe thresholds. In addition, current testing

methods are inconsistent and have been criticised

for being inadequate and failing to cover all

potential effects of EDCs66.

The Plant Protection Product Regulation

((EC)1107/2009), which covers pesticides and the

Biocidal Product Regulations ((EU) 528/2012)

which covers disinfectants, pest control products

and preservatives provide stronger protections

against detrimental health effects of EDCs.

Currently, EDCs that may cause adverse effects in

humans cannot be approved for use under these

regulations (a so-called hazard-based approach).

The Medical Devices Directives, soon to become

the Medical Devices Regulations currently also

require devices containing specific phthalates

(DEHP, DBP, DIBP and BBP) to be labelled, and

their use must be justified by manufacturers if

intended for children and pregnant and nursing

women. However, EDCs are still permitted for

use under the EU Cosmetics Regulation ((EC) No.

1223/2009), although this is due for review by

January 2015.

In an effort to introduce greater consistency in

the treatment and authorisation of EDCs, a draft

roadmap for defining criteria for identifying EDCs

within these Regulations and others was recently

published. Options include adding risk assessment

(allowing approval of substances with low ED

activity) and socio-economic considerations

(including risk benefit analysis) to the EDC

classification criteria. However, if adopted, these

proposed changes could weaken current EDC

regulations. An impact assessment and a public

consultation is currently underway.

Meanwhile, many EU member states are taking

unilateral action because of concerns about the

public health impacts of unnecessary exposures

to EDCs and frustrations that the EU is being slow

to act. In December 2012, France banned the

use of tubes containing DEHP in paediatric,

neonatal and maternity wards, which will come

into effect in July 2015. France has negotiated a

national EDCs Strategy (SNPE), (currently open to

public consultation) as part of its 3rd National

Plan on Health and Environment, which will be

adopted in December, 2014.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

Early exposures to EDCs have been linked to an increased risk of breast cancer later in life.

© Martin Novak /Shutterstock.com

6

In 2012 the Danish government passed a law

banning the use of certain phthalates in indoor

products, due to come into effect in 2015.

However, this law has just been repealed as it

conflicted with EU chemicals legislation.

The United States has an extensive screening

system to test chemicals for potential endocrine

effects, developed by the EPA’s Endocrine

Disruptor Screening Program. Japan’s Ministry of

Environment is also developing programs to test

for chemical health effects. Global EDC test

guidelines and risk assessments are coordinated

by the OECD.

From November 2014 the European

Commission's directorate general for health will

lead development of criteria to identify

endocrine disrupting chemicals, with directorate

general for Environment remaining in charge

overall. It is unclear how this will affect EDC

policy although it seems likely it will result in

significant delays to policy adoption.

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

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.

Further Resources:

European Environment Agency: http://

www.eea.europa.eu/publications/the-

impacts-of-endocrine-disrupters.

Kortenkamp, A. (2008). ‘Breast Cancer and

exposure to hormonally active chemicals:

An appraisal of the scientific evidence

2008.’ CHEM Trust. http://

www.chemtrust.org.uk/breast-cancer/

Report of the Interagency Breast Cancer

and Environmental Research Coordinating

Committee (IBCERCC) (2013). ‘Breast

Cancer and the Environment Prioritising

Prevention Prioritising Breast Cancer’.

http://www.niehs.nih.gov/about/assets/

docs/ibcercc_full_508.pdf

UNEP, 2014. Stockholm Convention on

Persistent Organic Pollutants. http://

www.pops.int

7

1.IPCS. (2002). Global assessment of the state-of-the-science of endocrine disruptors. Geneva, Switzerland, World Health Organization, International Programme on Chemical Safety. http://www.who.int/ipcs/publications/en/ch1.pdf?ua=1 2.Diamanti-Kandarakis E, et al., (2009). Endocrine- disrupting chemicals: an Endocrine Society scientific statement. Endocrine Reviews, 30(4): 293–342. http://www.ncbi.nlm.nih.gov/pubmed/19502515 3.Soto AM, et al., (2013). Does cancer start in the womb? altered mammary gland development and predisposition to breast cancer due to in utero exposure to endocrine disruptors. Journal of Mammary Gland Biology Neoplasia 18(2): 199-208. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933259/ 4.UNEP/WHO (2013). State of the science of endocrine disrupting chemicals 2012 http://www.unep.org/hazardoussubstances/Portals/9/EDC/StateOfEDCScience.pdf 5.TEDX. http://endocrinedisruption.org/endocrine-disruption/tedx-list-of-potential-endocrine-disruptors/overview http://endocrinedisruption.org/endocrine-disruption/tedx- 6.UNEP/WHO (2013). Op.cit., 7.UNEP/WHO (2013). Ibid., 8.Calafat AM, et al., (2008). Exposure of the U.S. population to bisphenol A and 4-tertiary-Octylphenol: 2003–2004. Environmental Health Perspectives 116: 39–44.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2199288/ 9.Ikezuki Y, et al., (2002). Determination of bisphenol A concentrations in human biological fluids reveals significant early prenatal exposure. Human Reproduction 17: 2839–2841.http://www.ncbi.nlm.nih.gov/pubmed/12407035 10.Vandenberg LN, et al., (2010). Urinary, Circulating, and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A. Environmental Health Perspectives 118 (8) 1055-1070. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920080/ 11.Letcher, R.J. et al., (2010). Exposure and effects assessment of persistent organohalogen contaminants in arctic wildlife and fish. Science of the Total Environment 408: 2995–3043 http://www.ncbi.nlm.nih.gov/pubmed/19910021 12.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. http://www.ncbi.nlm.nih.gov/pubmed/20398940 13.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.http://www.unboundmedicine.com/medline/citation/16818261/Assessment_of_feminization_of_male_fish_in_English_rivers_by_the_Environment_Agency_of_England_and_Wales_ 14.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. http://www.ncbi.nlm.nih.gov/pubmed/19479024 15.UNEP/WHO (2013). Op.cit., 16.Sonne, C. (2010). Op.cit., 17.EEA. (2012). The impacts of endocrine disrupters on wild-life, people and their environments—The Weybridge+15 (1996–2011) report. http://www.eea.europa.eu/publications/the-impacts-of-endocrine- disrupters

18.Kloas W, et al., (2009) Endocrine disruption in aquatic vertebrates. Annual N Y Academy Sciences. 1163: 187-200. http://www.ncbi.nlm.nih.gov/pubmed/19456339 19.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 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3223648/ 20.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. www.unboundmedicine.com/medline/citation/21676987/Infection_with_Brucella_ceti_and_high_levels_of_polychlorinated_biphenyls_in_bottlenose_dolphins__Tursiops_truncatus__stranded_in_south_west_England 21.Boas M, et al., (2012). Thyroid effects of endocrine disrupting chemicals. Molecular and Cellular Endocrinology 355 (2) 240-248.http://www.ncbi.nlm.nih.gov/pubmed/21939731 22.UNEP/WHO (2013). Op.cit., 23.UNEP/WHO (2013). Ibid., 24.EEA. (2012). Op.cit., 25.Berlaymont Declaration, (2013). http://www.brunel.ac.uk/__data/assets/pdf_file/0005/300200/The_Berlaymont_Declaration_on_Endocrine_Disrupters.pdf accessed sep 28 26.Kortenkamp, A. (2007). ‘Ten Years of Mixing Cocktails: A Review of Combination Effects of Endocrine-Disrupting Chemicals. Environmental Health Perspectives 115(1): 98–105. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174407/. 27.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. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240280/. 28.Travis, RC. and Key, TJ. (2003). Oestrogen exposure and breast cancer risk. Breast Cancer Research 5: 239-247. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC314432/ 29.Travis, RC. and Key, TJ. (2003). Ibid., 30.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. http://www.ncbi.nlm.nih.gov/pubmed/23897597 31.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. http://www.ncbi.nlm.nih.gov/pubmed/21729753 32.Jobling, S, et al., (1995). A variety of environmentally persistent chemicals, including some phthalate plasticizers, are weakly estrogenic. Environmental Health Perspectives 103: 582-587. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1519124/ 33.Kang, SC and Lee, BM (2005). DNA methylation of estrogen receptor α gene by phthalates. Journal of Toxicology and Environmental Health, 68:1995-2003. http://www.ncbi.nlm.nih.gov/pubmed/16326419 34.Aksglaede, L., et al., (2006). The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Human Reproduction Update 12: 341–349. http://www.ncbi.nlm.nih.gov/pubmed/16672247

For further information and more web resources please visit our website www.breastcanceruk.org.uk

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals References

8

35.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. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0099800 36. 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. http://www.fasebj.org/content/26/2/778.full.pdf 37.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.http://www.ncbi.nlm.nih.gov/pubmed/21429583 38.Borch, J., et al., (2006). Mechanisms underlying the anti-androgenic effects of diethylhexyl phthalate in fetal rat testis. Toxicology 223: 144–155.http://www.ncbi.nlm.nih.gov/pubmed/16690193 39.Fang, H., et al., (2003). Study of 202 Natural, Synthetic, and Environmental Chemicals for Binding to the Androgen Receptor. Chemical Research Toxicology 16(10): 1338–1358.http://www.ncbi.nlm.nih.gov/pubmed/14565775 40. 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.http://onlinelibrary.wiley.com/doi/10.1002/jat.3027/abstract 41.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. http://www.ncbi.nlm.nih.gov/pubmed/16489580 42.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). http://ec.europa.eu/environment/chemicals/endocrine/pdf/sota_edc_final_report.pdf 43.Exley C, et al., (2007). Aluminium in human breast tissue. Journal of Inorganic Biochemistry 101(9):1344-6.http://www.ncbi.nlm.nih.gov/pubmed/17629949 44.Report of the Interagency Breast Cancer and Environmental Research Coordinating Committee (IBCERCC) (2013). ‘Breast Cancer and the Environment Prioritising Prevention Prioritising Breast Cancer’. http://www.niehs.nih.gov/about/assets/docs/ibcercc_full_508.pdf. 45.Barouki, R, et al., (2012). Developmental origins of non-communicable disease: Implications for research and public health. http://www.toxicology.org/AI/MEET/cct_pptoxiii/pptoxiii_consensus_paper.pdf 46.EEA. (2012). Op.cit., 47.UNEP/WHO (2013). Op.cit., 48. Knower. KC, et al., (2014). Endocrine disruption of the epigenome: a breast cancer link Endocrine Related Cancer 21(2): T33-55.http://www.ncbi.nlm.nih.gov/pubmed/24532474 49.Darbre, PD and Charles, AK (2010). Environmental Oestrogens and Breast Cancer: Evidence for Combined Involvement of Dietary, Household and Cosmetic Xenoestrogens. Anticancer Research 30: 815-828. http://www.ncbi.nlm.nih.gov/pubmed/20393002 50.Soto AM, et al., (2013). Op. cit., 51. Cohn BA, et al., (2007). DDT and breast cancer in young women: new date on the significance of age at exposure. Environmental Health

Perspectives 115(10):1 406-1414. http://www.ncbi.nlm.nih.gov/pubmed/17938728 52.Brody JG, et al., (2007). Environmental pollutants and breast cancer - Epidemiologic studies. Cancer 109(12): 2667-2711. http://www.ncbi.nlm.nih.gov/pubmed/17503436 53.Ingber SZ, et al., (2013). DDT/DDE and breast cancer: a meta-analysis. Regulatory Toxicology and Pharmacology 67(3): 421-33.http://www.ncbi.nlm.nih.gov/pubmed/24021539 54.Ritchie JM, et al., (2003). Organochlorines and risk of prostate cancer. Journal of occupational and environmental medicine 45(7): 692-702 http://www.ncbi.nlm.nih.gov/pubmed/12855910 55.Soto AM, et al., (1995). The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Environmental Health Perspectives 103 (7): 113-22. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1518887/ 56.McGrath, KG (2009). Apocrine sweat gland obstruction by antiperspirants allowing transdermal absorption of cutaneous generated hormones and pheromones as a link to the observed incidence rates of breast and prostate cancer in the 20th century. Medical Hypotheses 72: 665–674.http://www.ncbi.nlm.nih.gov/pubmed/19307063 57.Kim, JY, et al., (2014). Methoxychlor and triclosan stimulates ovarian cancer growth by regulating cell cycle- and apoptosis-related genes via an estrogen receptor-dependent pathway. Environmental Toxicology and Pharmacology 37(3): 1264-74.http://www.ncbi.nlm.nih.gov/pubmed/24835555 58.Lathi, RB, et al., (2014). Conjugated bisphenol A in maternal serum in relation to miscarriage risk. Fertility and Sterility 102(1): 123-128.http://www.ncbi.nlm.nih.gov/pubmed/24746738 59.Newbold RR, et al., (2007). Developmental exposure to endocrine disruptors and the obesity epidemic. Reproductive Toxicology 23: 290–296.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1931509/ 60.Sargis, R. M. (2014). The Hijacking of Cellular Signaling and the Diabetes Epidemic: Mechanisms of Environmental Disruption of Insulin Action and Glucose Homeostasis. Diabetes Metabolism Journal 38:13-24.http://www.ncbi.nlm.nih.gov/pubmed/24627823 61.Grandjean, P. and Landrigan, P.L. (2014). Neurobehavioural effects of developmental toxicity. The Lancet Neurology 13 (3): 330 – 338.http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(13)70278-3/abstract 62.Boas M, et al., (2012). Op.cit., 63.Travis, RC. and Key, TJ. (2003). Op. cit., 64. Dai, Q, et al., (2001). Population-based case–control study of soyfood intake and breast cancer risk in Shanghai. British Journal of Cancer 85(3), 372–378.http://www.nature.com/bjc/journal/v85/n3/pdf/6691873a.pdf 65.Hecker, M. and Hollert, H. (2011). Endocrine disruptor screening: regulatory perspectives and needs Environmental Sciences Europe 23: 1-15.http://download.springer.com/static/pdf/747/art%253A10.1186%252F2190-4715-23-15.pdf?auth66=1412352066_f348dfa99c13e2b1dc65394e6e4b7f87&ext=.pdf 66.Kortenkamp, A. et al., State of the Art Assessment of Endocrine Disrupters, Final report, Annex 1 – Summary of the State of the Science, 2012. http://ec.europa.eu/environment/endocrine/documents/4_SOTA%20EDC%20Final%20Report%20V3%206%20Feb%2012.pdf

For further information and more web resources please visit our website www.breastcanceruk.org.uk

Breast Cancer UK Ltd, BM Box 7767, London, WC1N 3XX | www.breastcanceruk.org.uk | 0845 680 1322

Charity no: 1138866 | Company Number : 7348408

Registered Address: BCUK Ltd, Solva, Southwick Road, Denmead, Waterlooville, Hants, PO7 6LA

BCUK Fact Sheet | Endocrine Disrupting Chemicals

References continued