Citation

Davidson PW, Myers GJ, Weiss B, Shamlaye CF, Cox C. Neurotoxicology 2006; 27(6): 1106-1109.

Affiliation

University of Rochester School of Medicine and Dentistry, United States.

Copyright

(Copyright © 2006, Elsevier Publishing)

DOI

10.1016/j.neuro.2006.03.024

PMID

16687174

Abstract

Evidence from an outbreak of methyl mercury (MeHg) poisoning in Iraq suggested that adverse effects of prenatal exposure on child development begin to appear at or above 10ppm measured in maternal hair. To test this hypothesis in a fish-eating population, we enrolled a cohort of 779 children (the main cohort) in the Seychelles Child Development Study (SCDS). The cohort was prenatally exposed to MeHg from maternal fish consumption, and the children started consuming fish products at about 1 year of age. Prenatal exposure was measured in maternal hair and recent postnatal exposure in the child's hair. The cohort has been examined six times over 11 years using extensive batteries of age-appropriate developmental tests. Analyses of a large number of developmental outcomes have identified frequent significant associations in the appropriate direction with numerous covariates known to affect child development, but only one adverse association between prenatal MeHg exposure and a developmental endpoint. Because such results could be ascribed to chance, there is no convincing evidence for an association between prenatal exposure and child development in this fish-eating population. Secondary analyses have generally supported the primary analyses, but more recently have suggested that latent or delayed adverse effects might be emerging at exposure above 10-12ppm as the children mature. This suggests that the association between prenatal exposure and child development may be more complex than originally believed. This paper reviews the SCDS main cohort study results and presents our current interpretations.

Language: en