Until now, the focal area of endocrine disruption has been on the chemicals that mimic oestrogens (xenoestrogens). But, the recent proof suggests that quite a number of abnormalities in the human breast could be interceded by means of the androgen receptor.
The main identified risk factor remains lifetime exposure to oestrogen. In view of the involvement of oestrogen in the development, progression and treatment of breast cancer, questions have to be asked concerning potential interactions of the many chemicals in the environment which can be stored in breast tissues and which can mimic the action of oestrogen. The source of such compounds can be dietary, from plants (phytoestrogens) or from environmental contaminants of food/water (xenoestrogens) but I have proposed that an alternative route for exposure may be through the long-term regular application to the underarm of a variety of cosmetic ingredients with oestrogenic activity.
The molecular basis of oestrogen action involves the interaction of the oestrogenic ligand with intracellular oestrogen receptors, ER' and ER', which function as ligand-activated transcription factors to alter the expression patterns of hundreds of genes and to regulate growth of human breast cancer cells. This project will compare the ability of different oestrogenic ligands to bind to ER, to regulate gene expression and to increase cell growth. A substantial literature search will be used to identify the oestrogenic potency of the many oestrogenic ligands which can enter the human breast and calculations will be carried out to estimate exposure of the human breast to individual chemicals and to complex mixtures of chemicals.
Much of the existing focal point in the field of endocrine disruption is in the backdrop of the oestrogenic action of a variety of artificial chemicals. The capability of a chemical to unite to the oestrogen receptor, either in vitro or in vivo, has been in use as an explanation of oestrogenicity. The concern is that whether exposure to the chemicals which have steroid-like action can disturb the regular endocrine function, which can lead to distorted reproductive capacity, endometriosis, infertility, and cancers of the uterus, breast, and prostate (Colborn 1995, Jensen et al.1995, Safe 1995). The occurrence of a powerful anti-androgen can actually create an 'oestrogenic environment', thereby producing indications which directs to oestrogen exposure. Vertebrates generate steroids through a system which inhabits the chronological degradation of cholesterol to progestins, hence androgens (e.g. testosterone) and finally oestrogens (e.g. 17'-oestradiol). This pathway is available