Abstract
Experimental studies suggest a myriad of mechanisms by which inorganic arsenic can interfere with central nervous system development, and, indeed, epidemiological studies published in the last dozen years suggest that exposure to arsenic impairs children’s cognitive development. Most of the studies have been conducted in developing countries (e.g., Bangladesh, India, Mexico), where exposure to arsenic is thought to be considerably higher than it is in developed countries. This review summarizes the results of these studies, focusing in particular on issues pertinent to risk assessment, including the existence of critical windows of vulnerability, characteristics of the dose-effect relationships (e.g., the lowest adverse effect level, the functional form), the most sensitive neurodevelopmental endpoints, and potential effect modifiers such as host characteristics (e.g., methylation efficiency, sex) and co-exposures to other neurotoxicants (e.g., lead, manganese). At present, the epidemiological data do not permit firm conclusions to be drawn regarding these issues. Several factors that complicate an effort to compare the results of studies are identified, including use of a variety of indices of external and internal exposure, and inconsistency in the measurement of important potential confounders for neurodevelopmental outcomes.
Highlights
The adverse effects of inorganic arsenic on health are well-known and include cancer, skin lesions, lung disease, and cardiovascular disease [1,2,3]
This review focuses on studies that investigated whether arsenic exposures lower than those responsible for the milk powder poisoning episode, and, below those those associated with changes in skin pigmentation, produce milder forms of neurodevelopmental dysfunction, as measured by endpoints such as neonatal behavior, intelligence, neuropsychological function, and behavior
Other data consistent with this hypothesis is the finding from the Bangladeshi prospective study that it was only neurodevelopment at 5 years, and not at 7 and 18 months (Bayley Scales of Infant Development, Problem-Solving Test), that was associated with arsenic exposure [37,38]. This finding might have a methodological explanation, as children’s urinary arsenic level at 5 years was approximately 50% higher than it was at 18 months of age, and neurodevelopmental testing at 5 years of age is generally more reliable than is testing at 7 or 18 months of age
Summary
The adverse effects of inorganic arsenic on health are well-known and include cancer (lung, urinary bladder, skin, and possibly liver, kidney, and prostate), skin lesions (hyperkeratosis, pigmentation changes), lung disease (pulmonary interstitial fibrosis), and cardiovascular disease [1,2,3]. This review focuses on studies that investigated whether arsenic exposures lower than those responsible for the milk powder poisoning episode, and, below those those associated with changes in skin pigmentation, produce milder forms of neurodevelopmental dysfunction, as measured by endpoints such as neonatal behavior, intelligence, neuropsychological function, and behavior This is a relatively new field of research, as the first epidemiological studies of low-level arsenic exposure were published only at the turn of the 21st century. Children with low micronutrient status and protein intake might show greater adverse effects because these deficiencies reduce the efficiency of arsenic methylation Unless such factors are addressed in analytic models, the dose-effect relationships might not be comparable across studies. Tests developed and normed on children in the United States were adapted and, as a result, analyzed as raw rather than standardized scores due to uncertainty about the validity of the US norms
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