BLOG: What if BPA was only the tip of the iceberg?
Published 31 Mar 2017
Bisphenol A alternatives contained in “BPA-free” products could be more dangerous than BPA.
Last year, Breast Cancer UK awarded a research grant to Dr Michael Antoniou, along with his research associate Dr Robin Mesnage, at King’s College London, to evaluate the endocrine disrupting properties of herbicides and compounds used to make plastics. In this science blog, Dr Mesnage explains the background to their most recent findings which have just been published as a preprint.
More than 80 years ago, bisphenol A (BPA) was discovered to have oestrogen hormone mimicking effects. Discarded by the pharmaceutical industry, it was nonetheless used as a plasticizer and added to polycarbonate plastic or epoxy resins for decades, before some researchers rediscovered its ability to disturb the hormonal system. Thousands of studies are now reporting adverse health effects of BPA in humans, including reproductive and neurobehavioural disorders. Due to mounting evidence of harm and public pressure, BPA is being phased out by plastics’ manufacturers and “BPA-free” products are now found in supermarkets. What if BPA was only the tip of the iceberg?
The way plastic is manufactured has not changed significantly and new bisphenols have been introduced to replace BPA. We are getting exposed to BPS, BPAP, BPAF, BPB, BPZ... the list is growing with the imagination of industry chemists. These compounds are already widely found in human urine, raising questions about their safety. BPA alternatives are structurally related to BPA and we, at King’s college London, wondered if they could have comparable endocrine disrupting effects. In order to test our hypothesis, we have compared the endocrine disrupting effects of the most common BPA alternatives on breast cancer cells.
We used a wide range of technologies to monitor the function of breast cancer cells exposed to BPA alternatives. We investigated if the BPA alternatives were able to increase the proliferation of the breast cancer cells. This is a hallmark of two thirds of breast cancers which have their proliferation driven by oestrogen receptor alpha activation. Our findings revealed that all BPA alternatives were able to substitute for oestradiol in promoting cell growth through oestrogen receptors in human breast cancer cells. The activities of all the genes were monitored using a technique known as transcriptional profiling, which measures the activity of thousands of genes simultaneously. The breast cancer cells exposed to BPA alternatives displayed the hallmarks (or signature) of endocrine disrupting effects through oestrogen receptors. Surprisingly, BPAF, BPB and BPZ, contained in “BPA-free” plastics, were more oestrogenic than BPA.
Our discovery has critical value for society. This is why we decided to publish the study prior to peer-review (1). We believe that public health data should be made public as soon as possible. We encourage all scientists to do the same. Sharing scientific discoveries before they get published in peer-reviewed scientific journals, where it is not possible to amend them, also improves the quality of the studies because it allows a critical input from the scientific community.
The research carried out by our team at King’s College London, reveal that BPA-free products are not necessarily safer. BPA is the tip of the iceberg. Our discovery has profound consequences, both at the scientific and societal level. The clinical relevance in hormone-dependent breast cancer progression should be investigated. A global push to remove all bisphenols from consumer products would be necessary to protect the health of the population.
Dr. Robin Mesnage
Research Associate | Cellular and Molecular Toxicology
King’s College London
Department of Medical and Molecular Genetics
1. Robin Mesnage, Alexia Phedonos, Matthew Arno, Sucharitha Balu, J. Christopher Corton, and Michael N Antoniou (2017). Transcriptome profiling reveals bisphenol A alternatives activate estrogen receptor alpha in human breast cancer cells. BioRxiv preprint posted March 2, 2017. http://biorxiv.org/content/early/2017/03/02/112862