King's College London | Breast Cancer UK

King’s College London

Breast Cancer UK is pleased to announce that Dr Michael Antoniou, from King’s College London, has been awarded a research grant to investigate the endocrine disrupting effects of low dose EDC mixtures of herbicides and plasticisers (bisphenol compounds). This work is an extension of Dr Antoniou’s current investigation, also funded by Breast Cancer UK, which evaluates the endocrine disrupting properties of the herbicide glyphosate (see below).

Evaluating the Endocrine Disrupting Properties of Mixtures of Herbicides and Plasticisers

Endocrine disrupting chemicals that will be tested include the herbicides glyphosate, 2,4-D and dicamba, and the plasticisers bisphenol A (BPA), and BPA variants (e.g. bisphenol F, bisphenol Z, bisphenol B) which are increasingly being used as BPA substitutes.

Bisphenol A is oestrogenic and may cause adverse health effects, including breast cancer. For these reasons, BPA is being phased out by plastics manufacturers and replaced with BPA variants. Identifying whether or not potential replacements for BPA are oestrogenic is important, and such data may be used to justify a ban on the use of all bisphenols as plasticisers.

Glyphosate is under consideration for reauthorization in the EU and its use is likely to be restricted. If glyphosate is restricted, it seems likely use of dicamba and 2,4-D will increase. 2,4-D is oestrogenic and has been linked to breast cancer and dicamba is a potential EDC with possible cancer links. Hence, the oestrogenic effect of these herbicide combinations is highly relevant.

Evaluating the Endocrine Disrupting Properties of Glyphosate

Breast Cancer UK is funding research, being carried out at King’s College London, into the potential endocrine (hormone) disrupting effects of glyphosate and commercial glyphosate formulations.

Glyphosate-based herbicides (weedkillers) are the world’s most abundantly used pesticides both in agriculture and domestically. Recently, WHO listed glyphosate as a probable cause of cancer in humans [1]. Glyphosate is not currently listed as an endocrine disrupting chemical (EDC), despite evidence [2], [3] which suggests it may interfere with oestrogen signaling that could lead to breast tumour formation and/or progression.  

Human breast cancer cells, whose growth under laboratory conditions is either dependent or independent on the presence of oestrogen, will be exposed to environmentally relevant (real world exposure) concentrations of glyphosate and commercial glyphosate formulations. Commercial glyphosate formulations are a mixture of glyphosate and a complex array of additional chemicals collectively labeled as “inert adjuvants” but which are proving to be toxic in their own right.  Hence the need to test commercial glyphosate formulations alongside glyphosate alone. Cells will also be exposed to selective inhibitors of oestrogen receptors (e.g., tamoxifen) to determine their role in any toxic, endocrine disruptive effects observed. EDC effects will be determined by measuring cell survival, cell growth rates, and gene expression profiling (transcriptomic analysis), which provides insight into which biochemical pathways are affected.

This research will help advance our understanding of the potential dangers of glyphosate arising from EDC effects and how it interacts with oestrogen receptors to create a potentially carcinogenic environment, which may contribute to either the formation of breast cancer or stimulate its progression.

[1] Guyton, K. Z. et al., (2015). Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate. Lancet Oncology, published online March 20, 2015. doi: 10.1016/S1470-2045(15)70134-8.

[2] Hokanson et al., (2007). Alteration of estrogen-regulated gene expression in human cells induced by the agricultural and horticultural herbicide glyphosateHuman and Experimental Toxicology 26(9):747-745.  

[3] Thongprakaisang et al., (2013). Glyphosate induces human breast cancer cells growth via estrogen receptors. Food and Chemical Toxicology 59:129-136.

Last updated July 04, 2016

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