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Open AccessJournal ArticleDOI

The developmental neurotoxicity of arsenic: cognitive and behavioral consequences of early life exposure.

TLDR
The published literature indicates that arsenic is a human developmental neurotoxicant, and 15 epidemiological studies indicate that early life exposure is associated with deficits in intelligence and memory.
Abstract
Background More than 200 million people worldwide are chronically exposed to arsenic. Arsenic is a known human carcinogen, and its carcinogenic and systemic toxicity have been extensively studied. By contrast, the developmental neurotoxicity of arsenic has been less well described. The aim of this review was to provide a comprehensive review of the developmental neurotoxicity of arsenic. Methods We reviewed the published epidemiological and toxicological literature on the developmental neurotoxicity of arsenic. Results Arsenic is able to gain access to the developing brain and cause neurotoxic effects. Animal models link prenatal and early postnatal exposure to reduction in brain weight, reductions in numbers of glia and neurons, and alterations in neurotransmitter systems. Animal and in vitro studies both suggest that oxidative stress may be a mechanism of arsenic neurotoxicity. Fifteen epidemiological studies indicate that early life exposure is associated with deficits in intelligence and memory. These effects may occur at levels of exposure below current safety guidelines, and some neurocognitive consequences may become manifest only later in life. Sex, concomitant exposures, and timing of exposure appear to modify the developmental neurotoxicity of arsenic. Four epidemiological studies failed to show behavioral outcomes of arsenic exposure. Conclusions The published literature indicates that arsenic is a human developmental neurotoxicant. Ongoing and future prospective birth cohort studies will allow more precise definition of the developmental consequences of arsenic exposure in early life.

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Citations
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Journal ArticleDOI

Heavy metals (Pb, Cd, As and MeHg) as risk factors for cognitive dysfunction: A general review of metal mixture mechanism in brain.

TL;DR: An account of the current knowledge about the individual metal induced cognitive dysfunction mechanisms and common Mode of Actions (MOAs) of quaternary metal mixture (Pb, Cd, As, MeHg) are illustrated to help advancement in mixture toxicology and development of next generation predictive model (such as PBPK/PD) combining both kinetic and dynamic interactions of metals.
Journal ArticleDOI

Perinatal and Childhood Exposure to Cadmium, Manganese, and Metal Mixtures and Effects on Cognition and Behavior: A Review of Recent Literature

TL;DR: There is suggestive evidence that prenatal/childhood Cd exposure may be associated with poorer cognition, but additional research is clearly needed, and no studies found a significant relationship with attention deficit hyperactivity disorder.
Journal ArticleDOI

Metals and Neurodegeneration.

TL;DR: The literature relating to the role of metals in neurodegeneration is surveyed, showing a strong correlation between aberrant metal exposure and a number of neurological diseases.
Journal ArticleDOI

Environmental arsenic exposure: From genetic susceptibility to pathogenesis.

TL;DR: Understanding the molecular mechanisms of arsenic exposure and its subsequent health effects will support efforts to reduce the worldwide health burden and encourage the development of strategies for managing arsenic-related diseases in the era of personalized medicine.
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TL;DR: In soil, fertilizers containing inorganic nitrogen and wastes containing organic nitrogen are first decomposed to give ammonia, which is then oxidized to nitrite and nitrate, which are taken up by plants and used in the synthesis of organic nitrogenous compounds.
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Arsenic in Drinking Water

TL;DR: Arsenic in drinking water: not just a problem for Bangladesh D. van Halem, S. A. Bakker, G. L. Amy, and J. C. van Dijk Delft University of Technology.
Journal ArticleDOI

Developmental neurotoxicity of industrial chemicals

TL;DR: Two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation.
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