[Selected aspects of xenoestrogens'mode of action taken from a group of persistent organochlorine compounds]

Abstract

The presence of many chemical pollutants in the environment and their potential impact to human health creates rather justified anxiety. Many of these pollutants feature such unwelcome characteristics as: persistence in different environmental media, ability to bioaccumulate and biomagnify in individual food chains, as well as ability to undergo long-range atmospheric transport. Compounds meeting these criteria include above all a large group of persistent organochlorine compounds. Recently, debate has increased concerning endocrine disrupting activity of these compounds and especially their ability to produce biologic responses comparable to those of endogenous estrogens (e.g., 17 beta-estradiol). It has been hypothesized that these compounds, among others, may be associated with increased incidence of breast cancer and other estrogen-related cancers in women due to increased proliferation of breast epithelial cells. The organochlorine xenoestrogens may produce this effect following binding to a hormone receptor (with or without metabolic activation) or by affecting the 17 beta-estradiol pathways leading to increased formation of more potent estrogenic metabolites. Numerous studies performed since early 1990s have examined the relationship between organochlorines levels in serum or adipose tissue and breast cancer, but the results are not consistent. This may be caused by various criteria of selecting the case and control groups, different compounds analyzed or different statistical approaches. None of these studies included endocrine disruptors' exposure in early and critical stages of development--from conception up to puberty age--the results of which would manifest in far future. Nevertheless the results of measurements, especially in adipose tissue are more reliable for this purpose because they reflect the whole life exposure and may be recognized as one of many environmental risk factors of cancer development.