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Environmental Oestrogens and Breast Cancer: Evidence for Combined Involvement of Dietary, Household and Cosmetic Xenoestrogens

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Environmental Oestrogens and Breast Cancer: Evidence for Combined Involvement of Dietary, Household and Cosmetic Xenoestrogens ANTICANCER RESEARCH 30: 815-828 (2010) Review Environmental Oestrogens and Breast Cancer: Evidence for Combined Involvement of Dietary, Household and Cosmetic Xenoestrogens PHILIPPA D. DARBRE and AMELIA K. CHARLES Biomedical Sciences Section, School of Biological Sciences, University of Reading, Reading, RG6 6UB, U.K. Abstract. Many environmental compounds with oestrogenic in incidence over the past 50 years has turned this disease activity are measurable in the human breast and oestrogen into the most common cancer of women in much of the is a known factor in breast cancer development. Exposure to Western world (2, 3). In England and Wales alone, breast environmental oestrogens occurs through diet, household cancer incidence has nearly doubled over the past 30 years products and cosmetics, but concentrations of single from 21,446 new cases recorded in 1979 (84.5 per 100,000 compounds in breast tissue are generally lower than needed population) to 40,452 new cases recorded in 2006 (145.6 per for assayable oestrogenic responses. Results presented here 100,000 population) (4). and elsewhere demonstrate that in combination, chemicals Along with the rising incidence, it seems that the biology can give oestrogenic responses at lower concentrations, of breast cancer may also be altering. In the UK in the early which suggests that in the breast, low doses of many 1970s, fewer than 10% of breast tumours were ductal, compounds could sum to give a significant oestrogenic lobular or medullary tumours but by the end of the 1990s, stimulus. Updated incidence figures show a continued this percentage had risen to 75%, with ductal carcinomas disproportionate incidence of breast cancer in Britain in the alone comprising 60% of all breast cancer cases (5). In upper outer quadrant of the breast which is also the region addition, the relative proportion of breast tumours which to which multiple cosmetic chemicals are applied. contain oestrogen receptors (ER) and are hormone Conclusion: If exposure to complex mixtures of oestrogenic responsive has also been reported to be rising, not only in chemicals in consumer products is a factor in breast cancer the UK (6, 7) but also in France (8) and the USA (9, 10). development, then a strategy for breast cancer prevention Another notable change has been in the relative rise of breast could become possible. cancer in the UK amongst affluent women which cannot be attributed solely to higher compliance with screening and Breast cancer is not a new condition but has formed a which is in striking contrast to other types of cancer where component of mankind’s struggle against disease since the deprivation gap continues to widen (5). ancient times. Egyptian papyrus scrolls dating from 3000 BC Although many risk factors have been identified for describe tumours of the breast, and cases of breast cancer breast cancer, the underlying causes of the rising incidence were recorded in ancient Greece by Hippocrates (460- remain to be identified. Loss of function of breast cancer 375BC) (1). However, the unprecedented worldwide increase susceptibility genes such as BRCA1 and BRCA2 which function in DNA repair processes can predispose to breast cancer development in about 5% of cases (11). Lifestyle factors such as smoking, alcohol, radiation exposure and Correspondence to: Dr. Philippa D. Darbre, Biomedical Sciences diet have also been identified as components of risk (2, 3). Section, School of Biological Sciences, The Hopkins Building, The However, the main influence in development of breast University of Reading, Whiteknights, Reading RG6 6UB, U.K. Tel: cancer remains hormonal and, in particular, related to +44 01183787035, Fax: +44 01183786642, e-mail: p.d.darbre@ lifetime exposure to oestrogen (2, 3). Epidemiological reading.ac.uk evidence has established links between breast cancer Key Words: Environmental oestrogens, breast cancer, cosmetics, development and exposure to physiological oestrogens antiperspirant, deodorant, paraben, aluminium, organochlorine, through early onset of menarche, late menopause, phytoestrogen, breast cysts, review. nulliparity, late age of first pregnancy, practices of breast 0250-7005/2010 $2.00+.40 815 ANTICANCER RESEARCH 30: 815-828 (2010) feeding (2, 3), and exposure to pharmacological oestrogens Mechanisms of Action of Environmental Oestrogens through use of the contraceptive pill (12) and hormone replacement therapy (13, 14). In addition to the Within the cell, oestrogens act by binding to intracellular epidemiological evidence, the ability of oestrogen to drive oestrogen receptors (ERα and ERβ) which function as the growth of breast tumours in vivo is well established in ligand-activated transcription factors (82). Binding of an both clinical studies and animal models, and oestrogen oestrogenic compound results in release of associated heat- action on growth of breast cancer cells in cell culture shock proteins, dimerisation of receptor ligand complexes, systems in vitro has been extensively documented (15, 16). binding of the dimers to oestrogen response elements in the This involvement of oestrogen in the progression of breast DNA and transactivation of gene expression. Global gene cancer is the basis for the successful use of endocrine expression analysis using microarrays has shown that therapy as a targeted treatment for breast cancer (17). oestradiol regulates the expression of hundreds of genes (83, 84), and whilst environmental oestrogens can regulate the The case for a Contributory Role of expression of some genes in a similar manner, the global Environmental Oestrogens in Breast Cancer patterns of gene expression with different environmental oestrogens can vary (84). The realisation that so many environmental compounds can interact with specific Since epidemiological, experimental and clinical studies leave biological receptors has challenged concepts of classical no doubt that oestrogen is involved in the development and toxicology because this mode of action allows for progression of breast cancer, the ability of environmental compounds to act at lower concentrations and for effects to chemicals with oestrogenic properties to drive the be targeted via the genome to influence patterns of gene development and growth of breast tumours is also worthy of expression. Although this has been the most studied mode of serious consideration. Over the past 15 years, it has become action, environmental oestrogens may also influence non- evident that pollutant chemicals with oestrogenic properties, genomic pathways of oestrogen action (85) and synthesis or which are present in the environment, can impact on endocrine bioavailability of physiological oestrogens (86). health of wildlife, influencing reproduction, particularly in Many studies have now reported on the ability of a range aquatic populations (18-21). However, it remains to be of environmental compounds to competitively bind to determined as to whether the oestrogenic properties of these oestrogen receptors, to transactivate gene expression and to same chemicals can impact on human health and specifically influence the growth of cells dependent on oestrogen for their on breast cancer (18, 22). Many of these environmental growth (87). Animal models have shown that oestrogenic oestrogenic chemicals can be measured in the human breast, actions can also be found in vivo, most noteably in increasing and although their presence does not of itself imply any uterine weight in the immature rodent (88). One universal causality, it does confirm that many such chemicals are now observation has been that such compounds bind more weakly ubiquitously present in human breast tissue (22). to oestrogen receptors than do physiological oestrogens and Environmental oestrogens may enter the human breast in competitive binding assays, higher concentrations of the from dietary consumption of residues of organochlorine environmental compounds are invariably needed compared pesticides or polychlorinated biphenyls (PCBs) (18, 23-25) with 17β-oestradiol (89). This weaker binding affinity has and of phytoestrogens (26), or from exposure in the domestic resulted in such compounds being labelled and even environment to bisphenol A (27) and phthalates (28, 29) of dismissed as ‘weak’ oestrogens. However, when ligand plastics, alkyl phenols (30) of detergents, or polybrominated efficacy is considered as well as ligand binding affinity (90), diphenylethers (PBDEs) (31-33) in soft furnishings. Topical the efficacy of many of these compounds is not application of cosmetic chemicals with oestrogenic correspondingly low and they can give the same magnitude properties provides another exposure route (22, 34-36) and of response as 17β-oestradiol when sufficient concentration evidence for the presence of cosmetic chemicals with is present (41). Figure 1 shows the growth of MCF7 human oestrogenic activity in the human breast is summarised in breast cancer cells in culture with five different alkyl esters Table I (37-78). Studies over the past 10-15 years have fallen of p-hydroxybenzoic acid (parabens) compared to 17β- short of linking any one chemical to causation of breast oestradiol (91, 92). The lower ER-binding affinity of parabens cancer but the environmental reality is that the human breast compared with 17β-oestradiol (91, 92) necessitates higher is exposed not to one but to a multitude of oestrogenic concentrations of the parabens to be added to the growth chemicals (79, 80), that variations in lifestyle will result in assay but when sufficient concentrations
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