A large number of chemical pollutants including phthalates, alkylphenolic compounds, polychlorinated biphenyls and polychlorinated dibenzodioxins, organochlorine pesticides, bisphenol A, and metals including lead, mercury, and cadmium have the ability to disrupt endocrine function in animals. Some of these same chemicals have been shown to alter cognitive function in animals and humans. Because hormonally mediated events play a central role in central nervous system development and function, a number of researchers have speculated that the changes in cognitive function are mediated by the endocrine-like actions of these chemicals. In this paper we review the evidence that cognitive effects of chemicals classified as environmental endocrine disruptors are mediated by changes in hormonal function. We begin by briefly reviewing the role of gonadal steroids, thyroid hormones, and glucocorticoids in brain development and brain function. We then review the endocrine changes and cognitive effects that have been reported for selected endocrine-disrupting chemicals, discuss the evidence for causal relationships between endocrine disruption and cognitive effects, and suggest directions for future research.

Cognitive effects of endocrine-disrupting chemicals in animals.

Publisher Summary This chapter focuses on the origin and development of hormone receptors. Studies of evolution show that there are no unique signal molecules, only those which are selected to be hormones and which are more suitable than others to perform the hormone function. It is also probable that there are no unique hormone receptors, only those structures which are able to recognize the environment. These structures develop into receptors following an encounter with a molecule suitable for signal transmission. Hormonal imprinting occurs at the first encounter of the prospective hormone and the prospective receptor. This results in more specific receptors and more numerous receptors being produced by the cell. The receptors are transmitted to the offspring generations. The hormonal imprinting that occurs at the beginning of the evolutionary sequence retains its role in the higher organisms and influences the maturation of receptors around the period of birth. Imprinting is necessary to complete the program of receptor formation. Imprinting is not age-dependent but depends on the stage of development; it can be developed also in immature, differentiating cells in adults. The recognition system of cells is universal but there are several ways it can be expressed. In each method there are receptors and ligands.

Phylogeny and Ontogeny of Chemical Signaling: Origin and Development of Hormone Receptors

Effects of gestational and lactational exposure to TCDD or coplanar PCBs on spatial learning

Hormonal imprinting: its role during the evolution and development of hormones and receptors.

Learning and memory in rats gestationally and lactationally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Neonatal treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) accounted for a considerable decrease in the number of thymic glucocorticoid receptors in both male and female rats, as assessed at 6 weeks of age. TCDD also gave rise to a marked and prolonged increase in microsomal enzyme activity in the female rats but had practically no such effect on the males. These experimental observations attract attention on to the lasting microsomal inducer effect of the herbicide contaminant dioxin which damages foreign receptors and substantiate the chemical imprinting potential of aromatic hydrocarbons.

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Papers

Persistent influence of neonatal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment on glucocorticoid receptors and on the microsomal enzyme system.