Environmental pollutants may exert adverse physiological effects by disrupting normal endocrine function. Chemicals with this capacity, designated endocrine disrupters (EDs), are defined as exogenous substances that alter the function(s) of the endocrine system, thereby producing adverse health effects in an intact organism or its progeny or (sub)populations.

The endocrine disruption hypothesis was originally developed for chemicals that affected the oestrogen-signalling pathway. Thus, most research on endocrine disruption to date has been focused on oestrogenic effects. However, it is now becoming generally accepted that several types of compounds can interact with components of cell-regulatory systems, including steroid and thyroid hormone-receptor families. Endocrine disruption via nuclear receptors in cells of many organs of the body could affect the development and functioning of brain, cardiovascular, skeletal and urogenital systems.

Considerable progress has been made in the identification and quantification of a wide array of chemicals with endocrine disrupting properties. Research efforts have been centred on compounds that persist and bioaccumulate in organisms and their environment. Exposure to less persistent compounds has only recently been addressed. The existing safety assessment framework for chemicals is, unfortunately, poorly equipped to deal with EDs; tests and bioassays used take no account of the effects of simultaneous exposure to multiple chemicals, and may lead to a serious underestimation of the risks.

The vulnerability of a given species to EDs is determined by numerous factors: the intrinsic properties of the chemical; the magnitude, duration, frequency …