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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Developmental toxicants, insidious in modes of action and effects, strike the very origin of our lives: the developing embryo, fetus, neonate, and child; they cause spontaneous abortions, stillbirths, malformations, early postnatal mortality, reduced birth weight, mental retardation, sensory loss as well as other functional or physical changes, including subclinical effects having far reaching social and economic impacts. The large majority of developmental defects have unknown etiologies. With this uncertainty, EPA and the scientific community world-wide give high priority to finding new approaches for assessing etiology and risks of developmental effects. The United Nations Conference on Environment and Development (UNCED) and Agenda 21 mobilized the international community to focus on risks posed by chemicals in the environment, including developmental risks. The international harmonization of test and risk assessment guidelines for developmental effects are priorities. Lead, persistent organic pollutants (POPs), endocrine disruptors, and the improvement of quantitative risk assessment methodologies, particularly for children, are priorities. EPA reinvented its research agenda of assure wide involvement of the National Science Foundation, other federal agencies, and national experts in research to address the U.S.'s public health and environmental priorities.
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PMID:New approaches for assessing the etiology and risks of developmental abnormalities from chemical exposure. 910 Mar 20

Human brain development is slow and delicate, involving many unique, though interrelated, cellular events. The fetus and child are often more susceptible to chemical toxins that alter the structure and/or function of the brain, although susceptibility varies for individual neurotoxicants. Early exposure to neurotoxins has been implicated in neurological diseases and mental retardation. Pesticide exposures pose a particular concern since many are designed to be neurotoxic to pests and can also affect humans. Acknowledging the potential for vulnerability of the developing brain, EPA recently began to "call in" data on developmental neurotoxicity (DNT) from manufacturers of pesticides already registered and considered to be neurotoxic-around 140 pesticides. Chemicals are to be tested following the DNT testing guideline (OPPTS 870.6300). This paper assesses whether tests performed according to this guideline can effectively identify developmental neurotoxicants. We found the testing guideline deficient in several respects, including: It is not always triggered appropriately within the current tiered system for testing; It does not expose developing animals during all critical periods of vulnerability; It does not assess effects that may become evident later in life; It does not include methodology for consideration of pharmacokinetic variables; Methodology for assessment of neurobehavioral, neuropathological, and morphometry is highly variable; Testing of neurochemical changes is limited and not always required. We propose modifications to the EPA testing guideline that would improve its adequacy for assessing and predicting risks to infants and children. This paper emphasizes that deficiencies in the testing methodology for developmental neurotoxicants represent a significant gap and increase the uncertainty in the establishment of safe levels of exposure to developing individuals.
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PMID:Testing methods for developmental neurotoxicity of environmental chemicals. 1073 39

mental retardation: timing and thresholds; (italic)b(/italic)) endocrine dysfunction and developmental disabilities: dose and target implications; (italic)c(/italic)) attention-deficit disorder-ADHD and learning disabilities; and (italic)d(/italic)) new horizons: extending the boundaries. Support for the Rochester conference came from both public and private sources. The National Institute of Environmental Health Sciences (NIEHS), the National Institute of Child Health and Human Development, and the EPA represented the federal government. The conference also received grants from several foundations: the Jennifer Altman Foundation, the Heinz Family Foundation, the National Alliance for Autism Research, the Violence Research Foundation, the Wacker Foundation, and the Winslow Foundation. The second of these conferences helped launch a new Center for Children's Health and the Environment at the Mount Sinai School of Medicine. It was held in New York City on 24-25 May 1999, and was convened specifically to consider the intersection between neurodevelopmental impairment, environmental chemicals, and prevention. Over 300 health scientists, pediatricians, and public health professionals examined the growing body of evidence linking environmental toxins to neurobehavioral disorders. The conference title was Environmental Influences on Children: Brain, Development, and Behavior. The conference began by reviewing well-known examples of deleterious effects of environmental chemicals, including lead and PCBs, on children's brains. The conferees then considered the potential impact of environmental chemicals on neurological disorders with particular focus on ADHD, autism, and Parkinson's disease. The inclusion of Parkinson's disease was intended to signal the notion that exposures in early life may have an influence on the evolution of neurological disease in later life. Support for the Mount Sinai conference came from the Superfund Basic Research Program (NIEHS); The Pew Charitable Trusts; the Institute for Health and the Environment at the University of Albany School of Public Health; the Agency for Toxic Substances and Disease Research (ATSDR); the Ambulatory Pediatric Association; Myron A. Mehlman, PhD; the National Center for Environmental Assessment (EPA); the National Center for Environmental Health (CDC); the National Institute of Child Health and Human Development; the Office of Children's Health Protection (EPA); Physicians for Social Responsibility; The New York Academy of Medicine; The New York Community Trust; and the Wallace Genetic Foundation. The impact of environmental toxins on children's health has become a topic of major concern in the federal government. Eight new research centers in children's environmental health have been established in the past 2 years with joint funding from EPA and NIEHS. Clinical units that specialize in the treatment of children with environmentally induced illness have been developed across the nation with grant support from ATSDR. The American Academy of Pediatrics has just published its (italic)Handbook of Pediatric Environmental Health (/italic)((italic)17(/italic)), the "Green Book," which is available to pediatricians throughout the Americas. Children's environmental health has climbed to a critical position as we launch the new millennium. This monograph marks a significant milestone in the evolution of this emerging discipline.
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PMID:The developing brain and the environment: an introduction. 1085 30

Significant clusters of developmental delay and mental retardation (DD/MR) were identified in children born in South Carolina. Although it is difficult to identify one factor that causes DD/MR, environmental insult including exposure of pregnant women to heavy metals can induce DD/MR in their children. Because it is expensive to measure the concentrations of individual metals in large numbers of environmental samples, the general Microtox toxicity test was used to identify highly toxic soil samples. Approximately 100 soil samples were collected from residential areas and analyzed to determine an effective concentration (EC(50)) of soil required to inhibit 50% light emission of the luminescent bacterial test organism (Vibrio fischeri). The EC(50) values were then transformed to relative toxicity units (RTU). A subset of 56 high and low toxicity soil samples was then analyzed by inductively coupled plasma-atomic emission spectrometry (EPA method 6010) for arsenic, lead, and chromium, which are known neurotoxins. The highest measured arsenic concentration was 30 times higher than the South Carolina residential soil limit. Significant correlations were found between the RTU and soil arsenic and chromium concentrations. Microtox also identified some low arsenic and chromium samples as toxic, presumably because additional unidentified toxicants were present in the soil. In general, however, the Microtox test was effective in identifying soils with elevated concentrations of arsenic and chromium, even in residential neighborhoods where limited soil toxicity was expected.
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PMID:Use of a general toxicity test to predict heavy metal concentrations in residential soils. 1714 Jun 21