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Exposure to environmental chemicals during development can result in fetal death in the most severe cases, or structural malformations and/or functional alterations in the embryo or fetus. The realization that developmental exposure to drugs and chemicals like diethylstilbestrol (DES) can cause permanent functional changes that are not overtly toxic like ionizing radiation or teratogenic like thalidomide, yet result in increased susceptibility to disease/dysfunction later in life, has led to a new field of toxicology called the developmental origins of disease. The DES episode is a salient reminder of the potential toxicity and carcinogenicity that may be caused by hormonally active chemicals if exposure occurs during critical windows of susceptibility. There is general agreement that the age of puberty is getting earlier for both boys and girls, and this has been attributed to exposure to environmental chemicals especially endocrine-disrupting chemicals (EDCs) during prenatal and/or early childhood life.
Between two and five per cent of all live-born infants have a major developmental defect. Up to 40 per cent of these defects have been estimated to result from maternal exposure(s) to harmful environmental agents that directly or indirectly create an unfavourable intrauterine environment. A spectrum of adverse effects can occur, including death, structural malformation, and/or functional alteration of the fetus/embryo. The traditional focus of the science of developmental toxicology has been on the role of agents (environmental or drugs) that cause either premature death of the fetus or birth defects. In recent years, attention has turned to examining the effects of in-utero or neonatal exposure to environmental agents on functional changes in tissues, e.g. permanent changes in tissue function that are not the result of overtly or grossly teratogenic effects but that result in increased susceptibility to disease/dysfunction later in life.
The epidemiology data that support the concept of the fetal basis of adult disease, together with the preliminary data showing alterations in gene expression and tissue imprinting due to in-utero exposures to some environmental agents, provide an attractive framework for understanding delayed functional effects of toxicant exposures. We propose that exposure to certain environmental chemicals, alone or in combination with altered nutrition, leads to aberrant developmental programming that permanently alters gland, organ or system potential.
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