Prenatal Exposures to Environmental Chemicals and Children's Neurodevelopment: An Update

This review surveys the recent literature on the neurodevelopmental impacts of chemical exposures during pregnancy. The review focuses primarily on chemicals of recent concern, including phthalates, bisphenol-A, polybrominated diphenyl ethers, and perfluorinated compounds, but also addresses chemicals with longer histories of investigation, including air pollutants, lead, methylmercury, manganese, arsenic, and organophosphate pesticides. For some chemicals of more recent concern, the available literature does not yet afford strong conclusions about neurodevelopment toxicity. In such cases, points of disagreement among studies are identified and suggestions provided for approaches to resolution of the inconsistencies, including greater standardization of methods for expressing exposure and assessing outcomes

A Strategy for Comparing the Contributions of Environmental Chemicals and Other Risk Factors to Neurodevelopment of Children

Background: The impact of environmental chemicals on children’s neurodevelopment is sometimes dismissed as unimportant because the magnitude of the impairments are considered to be clinically insignificant. Such a judgment reflects a failure to distinguish between individual and population risk. The population impact of a risk factor depends on both its effect size and its distribution (or incidence/prevalence)

Social Ecology of Children’s Vulnerability to Environmental Pollutants

BACKGROUND: The outcomes of exposure to neurotoxic chemicals early in life depend on the properties of both the chemical and the host’s environment. When our questions focus on the toxicant, the environmental properties tend to be regarded as marginal and designated as covariates or confounders. Such approaches blur the reality of how the early environment establishes enduring biologic substrates. OBJECTIVES: In this commentary, we describe another perspective, based on decades of biopsychological research on animals, that shows how the early, even prenatal, environment creates permanent changes in brain structure and chemistry and behavior. Aspects of the early environment—encompassing enrichment, deprivation, and maternal and neonatal stress—all help determine the functional responses later in life that derive from the biologic substrate imparted by that environment. Their effects then become biologically embedded. Human data, particularly those connected to economically disadvantaged populations, yield equivalent conclusions. DISCUSSION: In this commentary, we argue that treating such environmental conditions as confounders is equivalent to defining genetic differences as confounders, a tactic that laboratory research, such as that based on transgenic manipulations, clearly rejects. The implications extend from laboratory experiments that, implicitly, assume that the early environment can be standardized to risk assessments based on epidemiologic investigations. CONCLUSIONS: The biologic properties implanted by the early social environment should be regarded as crucial elements of the translation from laboratory research to human health and, in fact, should be incorporated into human health research. The methods for doing so are not clearly defined and present many challenges to investigators

A Child with Chronic Manganese Exposure from Drinking Water

The patient's family bought a home in a suburb, but the proximity of the house to wetlands and its distance from the town water main prohibited connecting the house to town water. The family had a well drilled and they drank the well water for 5 years, despite the fact that the water was turbid, had a metallic taste, and left an orange-brown residue on clothes, dishes, and appliances. When the water was tested after 5 years of residential use, the manganese concentration was elevated (1.21 ppm; U.S. Environmental Protection Agency reference, < 0.05 ppm). The family's 10-year-old son had elevated manganese concentrations in whole blood, urine, and hair. The blood manganese level of his brother was normal, but his hair manganese level was elevated. The patient, the 10-year-old, was in the fifth grade and had no history of learning problems; however, teachers had noticed his inattentiveness and lack of focus in the classroom. Our results of cognitive testing were normal, but tests of memory revealed a markedly below-average performance: the patient's general memory index was at the 13th percentile, his verbal memory at the 19th percentile, his visual memory at the 14th percentile, and his learning index at the 19th percentile. The patient's free recall and cued recall tests were all 0.5-1.5 standard deviations (1 SD = 16th percentile) below normal. Psychometric testing scores showed normal IQ but unexpectedly poor verbal and visual memory. These findings are consistent with the known toxic effects of manganese, although a causal relationship cannot necessarily be inferred

Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood

Background: Animal studies suggest that early-life lead exposure influences gene expression and production of proteins associated with Alzheimer’s disease (AD)

Dental Amalgam Restorations and Children’s Neuropsychological Function: The New England Children’s Amalgam Trial

BACKGROUND: A concern persists that children’s exposure to mercury vapor from dental amalgams produces neurotoxicity. OBJECTIVE: Our goal was to compare the neuropsychological function of children, without prior exposure to dental amalgam, whose caries were repaired using either dental amalgam or mercury-free composite materials. METHODS: We conducted a randomized controlled trial involving 534 6- to 10-year-old urban and rural children who were assessed yearly for 5 years using a battery of tests of intelligence, achievement, language, memory, learning, visual–spatial skills, verbal fluency, fine motor function, problem solving, attention, and executive function. RESULTS: Although the mean urinary mercury concentration was greater among children in the amalgam group than the composite group (0.9 vs. 0.6 μg/g creatinine), few significant differences were found between the test scores of children in the two groups. The differences found were inconsistent in direction. Analyses using two cumulative exposure indices—surface years of amalgam and urinary mercury concentration—produced similar results. CONCLUSIONS: Exposure to elemental mercury in amalgam at the levels experienced by the children who participated in the trial did not result in significant effects on neuropsychological function within the 5-year follow-up period