The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform

Hugh A. Tilson - One of the best experts on this subject based on the ideXlab platform.

  • Neurotoxicology risk assessment guidelines Developmental Neurotoxicology
    Neurotoxicology, 2000
    Co-Authors: Hugh A. Tilson
    Abstract:

    EPA's Neurotoxicity Risk Assessment Guidelines were recently published in final form in the Federal Register (1998). This document was developed over a period of nearly ten years and is intended to establish operating principles used in the evaluation of data for neurotoxicity risk assessment. The guidelines contain a number of assumptions and definitions of key concepts, as well as guidance as to the evaluation of various behavioral and structural changes produced by chemical exposure in humans and animals. With regard to Developmental neurotoxicity, risk assessors should be aware that chemical-induced neurotoxicity in adults may not always be a good predictor of Developmental neurotoxicity. Adverse effects on the developing nervous system can occur prior to conception up to the time of sexual maturity, depend on the time of exposure relative to a critical state of nervous system development, can be seen at any time during the lifespan of the organism, may lead to delayed onset or latent effects, and may elicit compensatory mechanisms that obscure underlying neurotoxicity. Adverse effects include persistent alterations in function or structure of the nervous system or a change in the time or appearance of any endpoint. Relative to neurotoxicity in adult animals, there are several special concerns in hazard characterization of Developmental studies, including maternal toxicity, the use of the litter as the statistical unit, and time of exposure relative to the ontogeny of various structural or functional endpoints. Dose-response evaluation of data from Developmental studies is similar to that for adults, although a safety factor of 10 may be applied to protect children's health. The guidelines also note that exposure patterns of children differ from those of adults resulting in a greater intake of chemicals on a per body weight basis. The guidelines note several research needs, including more information on mechanisms of Developmental neurotoxicity, mechanistically based dose-response models, impact of early exposure to chemicals on late-onset disease, studies on threshold, and experiments on potential interactions between chemicals in mixtures.

  • the role of Developmental Neurotoxicology studies in risk assessment
    Toxicologic Pathology, 2000
    Co-Authors: Hugh A. Tilson
    Abstract:

    A number of questions have been raised about the use of the US Environmental Protection Agency's Developmental Neurotoxicity Testing Guideline (DNTG) in the hazard identification of chemicals. The applicability and sensitivity of animal tests in the DNTG relative to human Developmental neurotoxicity have recently been questioned. In a workshop held in 1989, participants compared the effects of several known Developmental neurotoxicants in humans and animal models and concluded that the DNTG would have detected known human Developmental neurotoxicants. They also concluded that although procedural differences may differ in the testing of humans and animals, the neurobiologic functions (ie, autonomic, sensory, motor, and cognitive) affected by chemical exposure were similar. In cases where the DNTG has been compared with other measures of reproductive and Developmental toxicity, the DNTG has been relatively sensitive and specific. To date, DNTGs have been required 12 times, for 9 pesticides and 3 solvents. T...

  • Developmental Neurotoxicology of endocrine disruptors and pesticides identification of information gaps and research needs
    Environmental Health Perspectives, 1998
    Co-Authors: Hugh A. Tilson
    Abstract:

    There is increasing evidence that some environmental chemicals can interrupt neuroDevelopmental processes during critical periods of development, resulting in effects on sensory, motor, and cogniti...

  • the concern for Developmental Neurotoxicology is it justified and what is being done about it
    Environmental Health Perspectives, 1995
    Co-Authors: Hugh A. Tilson
    Abstract:

    In general, it is believed that the possibility of an adverse Developmental outcome following conception is relatively high. In most cases, the cause of the defect is not clear, although exposure to chemical agents at a critical period during development has been proposed to play a significant role. Consequently, regulatory agencies such as the U.S. Environmental Protection Agency (U.S. EPA) have promulgated testing guidelines for assessing Developmental neurotoxicity of chemicals in animal testing protocols. Concerns have been expressed about the use of behavioral tests to evaluate chemicals for Developmental neurotoxicity, since some investigators believe that they lack predictive validity for human Developmental neurotoxicity. Other investigators have indicated that results from such studies are difficult to interpret because of a lack of standardization and sensitivity of the tests. Furthermore, it has been argued that the developing organism is not especially sensitive to chemicals or, if effects are observed, the developing organism is capable of compensating for the deficit. Recent research, however, has adequately demonstrated that developing organisms are especially vulnerable to chemical agents if the exposure occurs at a critical period during development, while other studies have supported the assumption that functional or behavioral effects observed in animal models can be extrapolated to humans. These findings support the routine assessment of chemicals for Developmental neurotoxicity using functional end points and suggest that currently available methods could be used to determine more precisely the mechanism of chemical-induced Developmental defects.

  • Developmental Neurotoxicology Risk Assessment
    Neurotoxicology, 1995
    Co-Authors: Hugh A. Tilson
    Abstract:

    Publisher Summary This chapter provides an overview of the Developmental Neurotoxicology risk assessment. The area of Developmental Neurotoxicology has evolved rapidly over the last several years. From initial experiments in animal models showing that Developmental exposure can result in long-lasting behavioral changes, a number of studies performed in different laboratories have demonstrated that exposure to a wide range of chemicals during development can have adverse effects on the structure and/or function of the nervous system. A number of generally recognized human Developmental neurotoxicants now exist, including ethanol, methyl mercury, lead, heroin, methadone, cocaine, diphenylhydantoin, and polychlorinated biphenyls. Because of the potential human hazard, several countries require chemicals to be tested for potential Developmental neurotoxicity for premarket approval. In the United States, Developmental toxicity is often considered to be a component of reproductive toxicity and typically involves exposure during major organogenesis, assessment of maternal toxicity during pregnancy, and evaluation of mother and offspring prior to term. This chapter discusses in detail regulation of Developmental neurotoxicants and study design issues for Developmental Neurotoxicology. The chapter also describes the quantitative aspects of Developmental Neurotoxicology risk assessment.

Evamaria S Collins - One of the best experts on this subject based on the ideXlab platform.

  • multi behavioral endpoint testing of an 87 chemical compound library in freshwater planarians
    Toxicological Sciences, 2019
    Co-Authors: Siqi Zhang, Danielle Hagstrom, Patrick Hayes, Aaron Graham, Evamaria S Collins
    Abstract:

    : There is an increased recognition in the field of toxicology of the value of medium-to-high-throughput screening methods using in vitro and alternative animal models. We have previously introduced the asexual freshwater planarian Dugesia japonica as a new alternative animal model and proposed that it is particularly well-suited for the study of Developmental Neurotoxicology. In this article, we discuss how we have expanded and automated our screening methodology to allow for fast screening of multiple behavioral endpoints, Developmental toxicity, and mortality. Using an 87-compound library provided by the National Toxicology Program, consisting of known and suspected neurotoxicants, including drugs, flame retardants, industrial chemicals, polycyclic aromatic hydrocarbons (PAHs), pesticides, and presumptive negative controls, we further evaluate the benefits and limitations of the system for medium-throughput screening, focusing on the technical aspects of the system. We show that, in the context of this library, planarians are the most sensitive to pesticides with 16/16 compounds causing toxicity and the least sensitive to PAHs, with only 5/17 causing toxicity. Furthermore, while none of the presumptive negative controls were bioactive in adult planarians, 2/5, acetaminophen and acetylsalicylic acid, were bioactive in regenerating worms. Notably, these compounds were previously reported as Developmentally toxic in mammalian studies. Through parallel screening of adults and developing animals, planarians are thus a useful model to detect such Developmental-specific effects, which was observed for 13 chemicals in this library. We use the data and experience gained from this screen to propose guidelines for best practices when using planarians for toxicology screens.

  • Planarian cholinesterase: in vitro characterization of an evolutionarily ancient enzyme to study organophosphorus pesticide toxicity and reactivation
    Archives of Toxicology, 2017
    Co-Authors: Danielle Hagstrom, Hideto Hirokawa, Limin Zhang, Zoran Radic, Palmer Taylor, Evamaria S Collins
    Abstract:

    The freshwater planarian Dugesia japonica has recently emerged as an animal model for Developmental Neurotoxicology and found to be sensitive to organophosphorus (OP) pesticides. While previous activity staining of D. japonica , which possess a discrete cholinergic nervous system, has shown acylthiocholine catalysis, it is unknown whether this is accomplished through an acetylcholinesterase (AChE), butyrylcholinesterase (BChE), or a hybrid esterase and how OP exposure affects esterase activity. Here, we show that the majority of D. japonica cholinesterase (DjChE) activity departs from conventional AChE and BChE classifications. Inhibition by classic protonable amine and quaternary reversible inhibitors (ethopropazine, donepezil, tacrine, edrophonium, BW284c51, propidium) shows that DjChE is far less sensitive to these inhibitors than human AChE, suggesting discrete differences in active center and peripheral site recognition and structures. Additionally, we find that different OPs (chlorpyrifos oxon, paraoxon, dichlorvos, diazinon oxon, malaoxon) and carbamylating agents (carbaryl, neostigmine, physostigmine, pyridostigmine) differentially inhibit DjChE activity in vitro. DjChE was most sensitive to diazinon oxon and neostigmine and least sensitive to malaoxon and carbaryl. Diazinon oxon-inhibited DjChE could be reactivated by the quaternary oxime, pralidoxime (2-PAM), and the zwitterionic oxime, RS194B, with RS194B being significantly more potent. Sodium fluoride (NaF) reactivates OP-DjChE faster than 2-PAM. As one of the most ancient true cholinesterases, DjChE provides insight into the evolution of a hybrid enzyme before the separation into distinct AChE and BChE enzymes found in higher vertebrates. The sensitivity of DjChE to OPs and capacity for reactivation validate the use of planarians for OP toxicology studies.

  • Planarian brain regeneration as a model system for Developmental Neurotoxicology
    Regeneration (Oxford England), 2016
    Co-Authors: Danielle Hagstrom, Olivier Cochet-escartin, Evamaria S Collins
    Abstract:

    Freshwater planarians, famous for their regenerative prowess, have long been recognized as a valuable in vivo animal model to study the effects of chemical exposure. In this review, we summarize the current techniques and tools used in the literature to assess toxicity in the planarian system. We focus on the planarian's particular amenability for Neurotoxicology and neuroregeneration studies, owing to the planarian's unique ability to regenerate a centralized nervous system. Zooming in from the organismal to the molecular level, we show that planarians offer a repertoire of morphological and behavioral readouts while also being amenable to mechanistic studies of compound toxicity. Finally, we discuss the open challenges and opportunities for planarian brain regeneration to become an important model system for modern toxicology.

Cheng Wang - One of the best experts on this subject based on the ideXlab platform.

  • inhalation anesthetic induced neuronal damage in the developing rhesus monkey
    Neurotoxicology and Teratology, 2011
    Co-Authors: Xiaoju Zou, Fang Liu, Xuan Zhang, Tucker A Patterson, Ralph Callicott, Shuliang Liu, Joseph P Hanig, Merle G Paule, William Slikker, Cheng Wang
    Abstract:

    The combination of nitrous oxide gas (N(2)O) and isoflurane (ISO) vapor is commonly used in pediatric surgical procedures for human infants and children to produce unconsciousness and analgesia. Because of obvious limitations it is difficult to thoroughly explore the effects of pediatric anesthetic agents on neurons in human infants or children. Due to the complexity of the primate brain, the monkey is often the animal model of choice for Developmental Neurotoxicology experiments, and it is in the rhesus monkey that the phenomenon of interest (anesthetic-induced neuronal cell death in the brain) has been previously reported. Recent reports indicate that exposure of the developing brain to general anesthetics that block N-methyl-D-aspartate (NMDA)-type glutamate receptors or potentiate gamma-aminobutyric acid (GABA) receptors can trigger widespread apoptotic cell death in rodents. The present study was performed to determine whether prolonged exposure of developing nonhuman primates to a clinically relevant combination of nitrous oxide and isoflurane produces neuronal damage. Postnatal day (PND) 5-6 rhesus monkeys were exposed to N(2)O (70%) or ISO (1.0%) alone, or N(2)O plus ISO for 8 h. Inhalation of the combination of 70% N(2)O+1% ISO produces a surgical plane of anesthesia. Six hours after completion of anesthetic administration the monkeys were examined for neurotoxic effects. No significant neurotoxic effects were observed for the monkeys exposed to N(2)O or ISO alone. However, neuronal damage was apparent when N(2)O was combined with ISO as indicated by increased numbers of caspase-3-, Silver staining- and Fluoro-Jade C-positive cells in the frontal cortex, temporal gyrus and hippocampus. Electron micrographs indicated typical swelling of the cytoplasm and nuclear condensation in the frontal cortex. These data suggest that prolonged exposure to inhaled anesthetics (a combination of N(2)O and ISO) in the developing rhesus monkey results in neuronal damage, and that the cell death observed is apoptotic and necrotic in nature.

  • Developmental Neurotoxicology research principles models techniques strategies and mechanisms
    2011
    Co-Authors: William Slikkerjr, Cheng Wang
    Abstract:

    Developmental Neurotoxicology Research. Principles, Models, Techniques, Strategies, And Mechanisms - Libros de Medicina - Toxicologia - 129,60

  • comprar Developmental Neurotoxicology research principles models techniques strategies and mechanisms william slikkerjr 9780470426722 wiley
    2011
    Co-Authors: William Slikkerjr, Cheng Wang
    Abstract:

    Tienda online donde Comprar Developmental Neurotoxicology Research. Principles, Models, Techniques, Strategies, And Mechanisms al precio 136,08 € de William SlikkerJr | Cheng Wang, tienda de Libros de Medicina, Libros de Toxicologia - Toxicologia

  • application of a systems biology approach to Developmental Neurotoxicology
    Reproductive Toxicology, 2005
    Co-Authors: William Slikker, Cheng Wang
    Abstract:

    Systems biology can be applied to enhance the understanding of complex biological processes such as apoptosis in the developing brain. Systems biology, as applied to toxicology, provides a structure to arrange information in the form of a biological model. The approach allows for the subsequent and iterative perturbation of the initial model with the use of toxicants, and the comparison of the resulting data against the proposed biological model. It is postulated that the exposure of the developing rat to NMDA antagonists, e.g., ketamine or phencyclidine (PCP), causes a compensatory up-regulation of NMDA receptors, thereby making cells bearing these receptors more vulnerable to excitotoxic effects of endogenous glutamate. Although comprehensive gene expression/proteomic studies and mathematical modeling remain to be accomplished, a biological model has been established and perturbed in an iterative manner to allow confirmation of the biological pathway for NMDA antagonist-induced brain cell death in the developing rat.

Danielle Hagstrom - One of the best experts on this subject based on the ideXlab platform.

  • multi behavioral endpoint testing of an 87 chemical compound library in freshwater planarians
    Toxicological Sciences, 2019
    Co-Authors: Siqi Zhang, Danielle Hagstrom, Patrick Hayes, Aaron Graham, Evamaria S Collins
    Abstract:

    : There is an increased recognition in the field of toxicology of the value of medium-to-high-throughput screening methods using in vitro and alternative animal models. We have previously introduced the asexual freshwater planarian Dugesia japonica as a new alternative animal model and proposed that it is particularly well-suited for the study of Developmental Neurotoxicology. In this article, we discuss how we have expanded and automated our screening methodology to allow for fast screening of multiple behavioral endpoints, Developmental toxicity, and mortality. Using an 87-compound library provided by the National Toxicology Program, consisting of known and suspected neurotoxicants, including drugs, flame retardants, industrial chemicals, polycyclic aromatic hydrocarbons (PAHs), pesticides, and presumptive negative controls, we further evaluate the benefits and limitations of the system for medium-throughput screening, focusing on the technical aspects of the system. We show that, in the context of this library, planarians are the most sensitive to pesticides with 16/16 compounds causing toxicity and the least sensitive to PAHs, with only 5/17 causing toxicity. Furthermore, while none of the presumptive negative controls were bioactive in adult planarians, 2/5, acetaminophen and acetylsalicylic acid, were bioactive in regenerating worms. Notably, these compounds were previously reported as Developmentally toxic in mammalian studies. Through parallel screening of adults and developing animals, planarians are thus a useful model to detect such Developmental-specific effects, which was observed for 13 chemicals in this library. We use the data and experience gained from this screen to propose guidelines for best practices when using planarians for toxicology screens.

  • Planarian cholinesterase: in vitro characterization of an evolutionarily ancient enzyme to study organophosphorus pesticide toxicity and reactivation
    Archives of Toxicology, 2017
    Co-Authors: Danielle Hagstrom, Hideto Hirokawa, Limin Zhang, Zoran Radic, Palmer Taylor, Evamaria S Collins
    Abstract:

    The freshwater planarian Dugesia japonica has recently emerged as an animal model for Developmental Neurotoxicology and found to be sensitive to organophosphorus (OP) pesticides. While previous activity staining of D. japonica , which possess a discrete cholinergic nervous system, has shown acylthiocholine catalysis, it is unknown whether this is accomplished through an acetylcholinesterase (AChE), butyrylcholinesterase (BChE), or a hybrid esterase and how OP exposure affects esterase activity. Here, we show that the majority of D. japonica cholinesterase (DjChE) activity departs from conventional AChE and BChE classifications. Inhibition by classic protonable amine and quaternary reversible inhibitors (ethopropazine, donepezil, tacrine, edrophonium, BW284c51, propidium) shows that DjChE is far less sensitive to these inhibitors than human AChE, suggesting discrete differences in active center and peripheral site recognition and structures. Additionally, we find that different OPs (chlorpyrifos oxon, paraoxon, dichlorvos, diazinon oxon, malaoxon) and carbamylating agents (carbaryl, neostigmine, physostigmine, pyridostigmine) differentially inhibit DjChE activity in vitro. DjChE was most sensitive to diazinon oxon and neostigmine and least sensitive to malaoxon and carbaryl. Diazinon oxon-inhibited DjChE could be reactivated by the quaternary oxime, pralidoxime (2-PAM), and the zwitterionic oxime, RS194B, with RS194B being significantly more potent. Sodium fluoride (NaF) reactivates OP-DjChE faster than 2-PAM. As one of the most ancient true cholinesterases, DjChE provides insight into the evolution of a hybrid enzyme before the separation into distinct AChE and BChE enzymes found in higher vertebrates. The sensitivity of DjChE to OPs and capacity for reactivation validate the use of planarians for OP toxicology studies.

  • Planarian brain regeneration as a model system for Developmental Neurotoxicology
    Regeneration (Oxford England), 2016
    Co-Authors: Danielle Hagstrom, Olivier Cochet-escartin, Evamaria S Collins
    Abstract:

    Freshwater planarians, famous for their regenerative prowess, have long been recognized as a valuable in vivo animal model to study the effects of chemical exposure. In this review, we summarize the current techniques and tools used in the literature to assess toxicity in the planarian system. We focus on the planarian's particular amenability for Neurotoxicology and neuroregeneration studies, owing to the planarian's unique ability to regenerate a centralized nervous system. Zooming in from the organismal to the molecular level, we show that planarians offer a repertoire of morphological and behavioral readouts while also being amenable to mechanistic studies of compound toxicity. Finally, we discuss the open challenges and opportunities for planarian brain regeneration to become an important model system for modern toxicology.

William Slikker - One of the best experts on this subject based on the ideXlab platform.

  • inhalation anesthetic induced neuronal damage in the developing rhesus monkey
    Neurotoxicology and Teratology, 2011
    Co-Authors: Xiaoju Zou, Fang Liu, Xuan Zhang, Tucker A Patterson, Ralph Callicott, Shuliang Liu, Joseph P Hanig, Merle G Paule, William Slikker, Cheng Wang
    Abstract:

    The combination of nitrous oxide gas (N(2)O) and isoflurane (ISO) vapor is commonly used in pediatric surgical procedures for human infants and children to produce unconsciousness and analgesia. Because of obvious limitations it is difficult to thoroughly explore the effects of pediatric anesthetic agents on neurons in human infants or children. Due to the complexity of the primate brain, the monkey is often the animal model of choice for Developmental Neurotoxicology experiments, and it is in the rhesus monkey that the phenomenon of interest (anesthetic-induced neuronal cell death in the brain) has been previously reported. Recent reports indicate that exposure of the developing brain to general anesthetics that block N-methyl-D-aspartate (NMDA)-type glutamate receptors or potentiate gamma-aminobutyric acid (GABA) receptors can trigger widespread apoptotic cell death in rodents. The present study was performed to determine whether prolonged exposure of developing nonhuman primates to a clinically relevant combination of nitrous oxide and isoflurane produces neuronal damage. Postnatal day (PND) 5-6 rhesus monkeys were exposed to N(2)O (70%) or ISO (1.0%) alone, or N(2)O plus ISO for 8 h. Inhalation of the combination of 70% N(2)O+1% ISO produces a surgical plane of anesthesia. Six hours after completion of anesthetic administration the monkeys were examined for neurotoxic effects. No significant neurotoxic effects were observed for the monkeys exposed to N(2)O or ISO alone. However, neuronal damage was apparent when N(2)O was combined with ISO as indicated by increased numbers of caspase-3-, Silver staining- and Fluoro-Jade C-positive cells in the frontal cortex, temporal gyrus and hippocampus. Electron micrographs indicated typical swelling of the cytoplasm and nuclear condensation in the frontal cortex. These data suggest that prolonged exposure to inhaled anesthetics (a combination of N(2)O and ISO) in the developing rhesus monkey results in neuronal damage, and that the cell death observed is apoptotic and necrotic in nature.

  • application of a systems biology approach to Developmental Neurotoxicology
    Reproductive Toxicology, 2005
    Co-Authors: William Slikker, Cheng Wang
    Abstract:

    Systems biology can be applied to enhance the understanding of complex biological processes such as apoptosis in the developing brain. Systems biology, as applied to toxicology, provides a structure to arrange information in the form of a biological model. The approach allows for the subsequent and iterative perturbation of the initial model with the use of toxicants, and the comparison of the resulting data against the proposed biological model. It is postulated that the exposure of the developing rat to NMDA antagonists, e.g., ketamine or phencyclidine (PCP), causes a compensatory up-regulation of NMDA receptors, thereby making cells bearing these receptors more vulnerable to excitotoxic effects of endogenous glutamate. Although comprehensive gene expression/proteomic studies and mathematical modeling remain to be accomplished, a biological model has been established and perturbed in an iterative manner to allow confirmation of the biological pathway for NMDA antagonist-induced brain cell death in the developing rat.

  • handbook of Developmental Neurotoxicology
    1998
    Co-Authors: William Slikker, Louis W Chang
    Abstract:

    Cellular and Molecular Morphogenesis: K. Jensen, Brain Morphogenesis and Developmental Neurotoxicology. G.B. Grunwald, Cadherin Cell Adhesion Molecules in Normal and Abnormal Neural Development. G. Audesirk and T. Audesirk, Neurocytoskeleton and Neuritic Development. G.J. Harry and A.D. Toews, Myelination, Dysmyelination, and Demyelination. Developmental Biology/Toxicology: R.M. Greene, W. Weston, P. Nugent, M. Potchinsky, and M.M. Pisano, Signal Transduction Pathways as Targets for Induced Embryotoxicity. M.V. Chao, H. Kong, S.O. Yoon, B. Carter, and P. C.-Bonnefil, Trophic Nerve Growth Factors. J.M. Lauder and J. Liu, Neurotoxic and Neurotrophic Effects of GABAergic Agents on Developing Neurotransmitter Systems. P.E. Mirkes and M.A. Shield, Apoptosis. J.F. Grippo, Receptor Mediated. R.H. Finnell and G.D. Bennett, The Periods of Susceptibility to Induced Malformations of the Developing Mammalian Brain. T.B. Knudsen and J.A. Wubah, Transgenic Animal Models. Synaptogenesis and Neurotransmission: A.G. Hendrickx and P.E. Peterson, Neural Crest Cell Migration. H.W. Broening and W. Slikker, Ontogeny of Neurotransmitters: Monoamines. D.A. Jett, Central Cholinergic Neurobiology. L.G. Costa, Ontogeny of Second Messenger Systems. T.R. Guilarte, The N-Methyl-D-Aspartate Receptor: Physiology and Neurotoxicology in the Developing Brain. Nutrient and Chemical Disposition: R.K. Miller, Placental Transfer. M.R. Juchau and H. Chen, Developmental Enzymology: Xenobiotic Biotransformation. E.J. O'Flaherty, PB/PK Models. M.L. Bogle, Nutrition Postnatal Adult. C.L. Keen, Nutrition, Chemistry and Genetics. M. Aschner, Blood-Brain Barrier: Physiological and Functional Considerations. S.F. Ali and S. Hussain, Antioxidant Enzymes: Developmental Profiles and their Role in Metal-Induced Oxidative Stress. J.E. Polifka, Drug and Chemical Components in Breast Milk: Effects on Neurodevelopment of the Nursing Infant. Behavioral Assessment: J.H. Hannigan, Normal Development and Susceptibility. J.S. Meyer, Behavioral Assessment in Developmental Neurotoxicology: Approaches Involving Unconditioned Behaviors and Pharmacological Challenges in Rodents. M.E. Stanton and D. Frederick, Assessment of Behavior/Rodents/Learning Tasks. M.G. Paule, Assessment of Behavior--Primates. Clinical Assessment and Epidemiology: A. van Baar, Evaluation of the Human Newborn Infant. C. Coles and J.A. Kable, Developmental Evaluation of the Older Infant and Child. P.A. Fried, Behavioral Evaluation of the Older Infant and Child. N.L. Day and G.A. Richardson, Epidemiological Studies of the Effects of Prenatal Cocaine Exposure on Child Development and Behavior. J.M. Friedman, Assessment of Case Reports and Clinical Series. Specific Neurotoxic Syndromes: G. Koren, B. O'Hayon, J. Gladstone, and I. Nulman, Fetal Alcohol Syndrome. L.W. Chang and G.L. Guo, Fetal Minamata Disease. L. Hastings and M.L. Miller, Developmental Neurotoxicology of Cadmium. D.C. Rice, Developmental Lead Exposure: Neurobehavioral Consequences. M.G. Paule, Maternal Drug Abuse. D. Desaiah, Developmental Toxicity of Pesticides. E.D. Levin and T.A. Slotkin, Developmental Neurotoxicity of Nicotine. J. Adams and R.R. Holson, Vitamin A Analogs. D.K. Hansen and R.R. Holson, Developmental Neurotoxicity of Antiepileptic Drugs. P.M. Rodier, Neuroteratology of Autism. Risk Assessment: C.A. Kimmel, Current Approaches. J.L. Schardein, Animal/Human Concordance. M. Anderson and K. Krishnan, PB/PK Models. D. Gaylor and W. Slikker, Jr., Quantitative Models. Subject Index.

  • principles of Developmental Neurotoxicology
    Neurotoxicology, 1994
    Co-Authors: William Slikker
    Abstract:

    With 4-8 percent of U.S. children exhibiting anatomical and/or functional deficits, and the occurence of several tragic clinical syndromes resulting from Developmental exposure to such agents as ethanol, lead and methylmercury, there is good reason to focus attention on the principales of Developmental Neurotoxicology. Various animal models have been used to confirm the Developmental neuritoxicity that results from exposure to these agents, and along with clinical evidence, have implicated several other chemical classes such as antimitotics, insecticides, polyhalogenated hydrocarbons, psychoactive drugs, solvents and vitamins as specific agents with developemntal neurotoxic potential