Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) / Chapter Skim
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Executive Summary
Executive Summary
Pages 1-9
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The most frequently recognized class of developmental defects are the structural abnormalities (e.g., neural tube and heart defects) , which represent the majority of the developmental defects identified at birth.
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In this report, the committee documents many recent advances in research in the areas of developmental biology and genomics. These extraordinary advances are significant for developmental toxicology and risk assessment because they present opportunities to improve substantially the detection of developmental toxicants and to elucidate the mechanisms by which toxicants induce developmental defects.
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Reasons for this incomplete understanding include the lack of knowledge about normal developmental processes, the complexity of developmental toxicity, the broad spectrum of agents and chemical mixtures present in the environment, and the variety of potential mechanisms by which they might cause toxicity. Ideally, a full description of the mechanism of action by which a chemical causes developmental toxicity includes the following types of mechanistic information: (1)
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Molecular components of these processes are substantially conserved (i.e., the structure and function of the components have not changed throughout evolution) among animal phyla, including mammals; they regulate development by signaling specific cells to activate proteins called transcription regulators, which turn specific genes on and off.
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Charge 3: Evaluate How Recent Advances in Developmental Biology and Genomics Can Be Used to Improve Qualitative and Quantitative Risk Assessment for Developmental Effects. The committee concludes that the major recent advances in developmental biology and genomics can be used to improve qualitative and quantitative risk assessments by integrating toxicological and mechanistic data on a variety of model test animals with data on human variability in genes encoding components of developmental processes, genes encoding enzymes involved in the metabolism of chemicals, and genes encoding receptors and transporter proteins that move these chemicals and their metabolites in and out of the cell.
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. Greater use of model systems for developmental toxicity and risk assessment.
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For example, early fetal loss in human development occurs in 20-30% of initial pregnancies and, although many of these losses are due to chromosomal aberrations, exposure to a toxicant during early times in development can lead to loss of the embryo or fetus as well as specific structural defects and functional deficits. Use of genetically modified model systems could provide mechanistic information to improve the understanding of early fetal loss as well as morphological alterations and later functional deficits by providing sensitized systems for evaluating developmental defects.
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To support the growth of knowledge in developmental toxicology and to organize information in a way that is useful for risk assessment, an inclusive national developmental toxicant database should be established, with entries from industry, academia, and government. The developmental toxicant database should include chemical toxicant information as well as information on known molecular targets and associations with developmental defects, both from animal tests and from humans.
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Programs, such as workshops and professional meetings, should be organized so that researchers of developmental toxicology, developmental biology, genomics, medical genetics, epidemiology, and biostatistics can come together to exchange new insights, approaches, and techniques related to the analysis of developmental defects and to risk assessment. By accelerating the necessary research, cooperative research projects would move forward the recommendations of this report.
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