SCIENCE NEWS: Chemical mixtures affect breast cells more than the same chemicals individually
Published 13 Jun 2018
A new study has confirmed that when breast cells are exposed to multiple endocrine disrupting chemicals (EDCs) at the same time, the potentially harmful effects increase to a greater degree than the effects of individual exposures. This finding, published in the latest issue of Toxicological Sciences, has implications for safe levels of EDCs used in everyday products, in both their formulation and how we use them.
This is of concern because we are exposed to numerous EDCs on a daily basis, from the beauty products we apply directly onto our skin to the household cleaners we use to clean our homes.The study shows clearly that chemicals which appear to be weakly oestrogenic when tested individually may be more oestrogenic when other EDCs are present. Oestrogen exposure throughout a woman’s life has been identified as a major risk factor for the development of breast cancer.
The results highlight the difficulty of establishing the role of an individual chemical in increasing breast cancer risk. They also demonstrate the importance of testing cellular effects of EDCs not only individually, but as components of mixtures.
Breast Cancer UK supports several research projects that examine the effects of EDC mixtures on breast cancer cells. For more information about this work, see here. To read about a new project we will be supporting that investigates the effect of EDCs on breast density and breast cancer risk, see here.
The research in depth
Dairkee and colleagues (1) examined the effects of exposing three EDCs – BPA, methylparaben and PFOA to human breast cells grown in cell culture. These EDCs are found in certain plastics, processed food, cosmetics and household products and have become widespread in the environment (2). Cells were exposed to concentrations of EDCs that are commonly detected in human body fluids. The observed effects of the mixtures corresponded to three “hallmarks” or common traits of cancer, including increased cell proliferation, evasion of programmed cell death and overriding normal cell control mechanisms (through effects on oestrogen receptors) (3). Cellular effects of the three EDCs combined were more pronounced than the effects of each individual compound. They were similar to the effects of natural oestrogen, which is associated with increased breast cancer risk.
The study used “established” cancerous and non-cancerous breast epithelial cell lines (i.e. cells that had been grown in cell culture for a long period and become “immortalised”) and newly isolated (non-cancerous) breast cells, which originated from breast tissue of volunteers at high risk of breast cancer. These cells behave in ways more similar to those in the body and help establish the general relevance of the experiments. When exposed to the chemical mixtures, all types of breast cells displayed several hallmarks of cancer. Overall, the non-cancerous cells showed the more pronounced effects.
1. Research was carried out at from the California Pacific Medical Center, California. The paper cited is:
Dairkee, S.H., Luciani-Torres, G., Moore, D.H., Jaffee, I.M., Goodson, W.H. 3rd (2018). A ternary mixture of common chemicals perturbs benign human breast epithelial cells more than the same chemicals do individually. Toxicological Sciences 2018 May 28. doi: 10.1093/toxsci/kfy126
2. BPA (bisphenol A) is used to make polycarbonate plastics, in resins and inks, and is an oestrogen mimic; methylparaben is used as a preservative in certain cosmetics and processed food and is an oestrogen mimic, and PFOA (perfluorooctanoic acid) is used in electronics, textiles and non-stick cookware and affects secretion of steroid hormones (oestrogen and progesterone).
3. The study examined the effects of exposure of single and chemical mixtures on test cells and the resultant cellular changes associated with oestrogen signalling, characteristic of clinical breast cancer. Five endpoints relative to breast cancer that were examined included (i) increased cell cycle S-phase (ii) increased expression of oestrogen receptor alpha (ER alpha), (iii) increased ER alpha activation (ER alpha phosphorylation at serine 118), (iv) evasion of apoptosis (programmed cell death) and (v) decreased expression ER beta.