All in all, the lesson learnt thus far is that, even if the levels of the environmental endocrine disruptors (EEDs) are each inconsequentially low, their combined level can be sufficient to cause harm to certain human subpopulations. Again, the public’s exposure to EEDs increases substantially if these substances are persistent and bioaccumulative. That is, exposure to any of these pollutants is primarily a function of its availability, which in turn is a function of its persistence and the potential for its bioaccumulation and long-range transport. On the other hand, time of exposure is an equally important factor in the induction of endocrine disruption.

For example, in humans and rodents, serum levels of estrogen were seen to increase steadily throughout most of the pregnancy period, primarily due to a feed-forward mechanism of regulation (Casey et al., 1985). That is, during pregnancy, estrogen levels normally are not subject to a feedback mechanism, otherwise by which the hormone’s biosynthesis would be self-regulated. Therefore, any dose of a xenoestrogen would be additive with the endogenous level (that produced internally), in that the endogenous production can no longer be reduced by feedback control to compensate for such addition (Kendall et al., 2001).

The above observations reconfirm the argument that time of exposure is a critical factor for induction of certain adverse effects. It is certain that the potential for exposure at the wrong time or in the wrong place increases if the EED is more persistent and more bioaccumulative. The importance of time of exposure is not limited to reproductive or developmental effects. The rather long process of carcinogenesis is widely accepted to be multistage in nature. And the action of some cancer initiators from short-term exposure is considered to be irreversible.