Developmental neurotoxicity children

Few nonpathogenic, chemical contaminants simultaneously or sequentially induce in young children developmental neurotoxicity, impaired growth and development, hematotoxicity, early nephrotoxicity, or immuno-toxicity in concert with elevated Pb exposme biomarkers. Similarly, few such contaminants induce simultaneously or sequentially in men or women peripheral neurotoxicity, cardiovascular toxicity, hematotoxicity, various stages of nephrotoxicity, various stages of immunotoxicity, and miscellaneous endpoints such as GI effects in concert with elevated Pb exposure biomarkers. 

Neurotoxic chemical exposure to the fetus and young child may cause adverse developmental neurotoxic effects. These effects are the subject of the next chapter and are not considered in detail here. 

The developing fetus and the growing child are at greater risk than adults are from exposur es to neurotoxic chemicals. Relatively little is known about developmental neurotoxic effects of single chemicals and even less about the effects of chanical mixtures. 

To the best of our knowledge, no studies with child and adolescent depressed cohorts have examined hippocampal volume. The one study that examined hippocampal volume in children and adolescents with PTSD (n = 43), about half of whom met criteria for comorbid MDD, failed to find evidence of hippocampal atrophy (De Beilis et ah, 1999). This finding is not surprising, as most of the children and adolescents in the study had not experienced more than one episode of depression, and hippocampal atrophy was found to be correlated with total lifetime duration of illness in the prior adult studies cited (Sheline et ah, 1996 Brem-ner et ah, 2000). Developmental factors may also account for the discrepant findings in child and adult studies. For example, age-dependent changes in sensitivity to some forms of N-methyl-D-aspartate (NMDA) receptor blockade neurotoxicity in corticolimbic regions have been reported in preclinical studies, with cell death minimal or absent prepuberty and reaching peak in early adulthood (Father et ah, 1995). 

Included for discussion in both the child and adult neurotoxicity sections are some critical topics which inform continuing or new directions for the topic. The topics include effect persistence or irreversibility, late life and tardive effects from earlier developmental exposures, and the putative lack of a measured threshold to neurotoxicity versus PbB. 

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