A current public health issue concerns the fact that endocrine-disrupting chemicals (EDCs) may adversely affect human health in both children and adults (Colborn et al. 1993; Kavlock 1999; Landrigan et al. 2003; Longnecker et al. 2003; Rice et al. 2003). Recent experimental data suggest that EDCs affect not only the reproductive system but also the immune system, thereby raising additional concerns (Barnett and Rodgers 1994; Blake et al. 1997; Ahmed 2000). Fetal exposure to EDCs is of particular concern, since these chemicals could potentially alter critical immune developmental pathways, which may have long-lasting consequences. The development of the fetal immune system is tightly regulated to favor the selection of competent immune cells and to eliminate dangerous autoreactive lymphocytes. Any alterations in the normal fetal immune development (e.g., exposure to EDCs) may have permanent or long-lasting adverse consequences.
The synthetic estrogen DES can cross placenta, is considered a model EDC, and serves as an excellent prototype to study the immunological consequences of prenatal exposure to EDC since both clinical and experimental data are available. It is estimated that 3 to 5 million Americans have been exposed to DES during fetal life (Giusti et al. 1995). As indicated in the preceding section, this cohort, after sexual maturity, may be at increased risk for developing a number of maladies, including immune abnormalities. Ahmed et al. (1999, 2000) have recently proposed that individuals prenatally exposed to EDCs, including DES, may have a deviant immunological response when exposed to estrogenic compounds during adult life. In support of this hypothesis, these authors found that activated splenocytes from prenatal DES-exposed mice secrete augmented levels of IFNg when exposed to a second dose of DES during adult life (as late as 1 to 1.5 years of age). This suggests that prenatal DES exposure may preprogram the highly sensitive fetal immune system for augmented IFNg secretion when exposed to a second dose of EDC later in life. This is termed "EDC-induced immunological imprinting" (Karpuzoglu-Sahin et al. 2001). Understanding this alteration of IFNg secretion by splenocytes from mice that received both prenatal and adult-life DES exposure (DES/DES mice) is crucial, since IFNg is a key T helper-1 (Th-1) cytokine that regulates the functions of all cells of the immune system, and plays a major role in autoimmune diseases and in infection and tumor immunity. These results imply that fetal exposure to other immunomodulatory compounds may preprogram these individuals to respond abnormally to subsequent immunomodulatory endocrine disruptors during adult life. These studies are therefore likely to be applicable to other EDCs and other immune-altering chemicals and thus have broad health implications.
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