Prenatal methyl mercury exposure in relation to neurodevelopment and behavior at 19 years of age in the Seychelles Child Development Study

E van Wijngaarden, S.W. Thurston, G.J. Myers, JJ STRAIN, B Weiss, T Zarcone, G.E. Watson, C.F. Zareba, E. M. McSorley, Maria S. Mulhern, Alison J. Yeates, J Henderson, J Gedeon, C.F. Shamlaye, P.W. Davidson

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39 Citations (Scopus)


Background: Fish are important sources of protein and contain a variety of nutrients, such as n-3 long-chainpolyunsaturated fatty acids (PUFA), essential for normal brain development. Nevertheless, all fish also containmethyl mercury (MeHg), a known neurotoxicant in adequate dosage. Our studies of the Seychelles Child DevelopmentStudy (SCDS) Main Cohort enrolled in 1989–1990 (n = 779) have found no consistent pattern ofadverse MeHg effects at exposures achieved by daily fish consumption. Rather, we have observed evidence ofimproved performance on some cognitive endpoints as prenatal MeHg exposure increases in the range studied.These observations cannot be related to MeHg and may reflect the role of unmeasured covariates such as essentialnutrients present in fish. To determine if these associations persist into young adulthood, we examined therelationship between prenatal MeHg exposure, recent PUFA exposure and subjects' neurodevelopment andbehavior at 19 years of age.Methods: We examined 533 participants using the following test battery: the Profile of Mood States—Bipolar(POMS-Bi); Finger Tapping; Kaufman Brief Intelligence Test (K-BIT);measures of FineMotor Control and ComplexPerceptual Motor Control; and Visual Spatial Contrast Sensitivity.We collected the following covariates:maternalIQ, family life course stressors, socioeconomic status, and subjects' recent postnatalMeHg, sex, and computer use.Primary analyses (based on N = 392–475) examined covariate-adjusted associations inmultiple linear regressionmodels with prenatal MeHg as the primary exposure measure. Secondary analyses additionally adjusted for totaln-6 and fish-related n-3 PUFA measured in the subjects' serum at the 19-year examination.Results: Study participants had amean prenatalMeHg exposure of 6.9 ppm, and a mean recent postnatal exposureof 10.3 ppm. Therewere no adverse associations between prenatalMeHg and any of themeasured endpoints. Forrecent postnatalMeHg exposure, however, adverse associationswere observed for Finger Tapping (non-dominanthand) among women and for the K-BIT Matrices for both sexes, with or without adjustment for PUFA.Conclusion: Our findings continue to provide no evidence for an adverse effect of prenatal MeHg exposure ondevelopment in a cohort that consumes fish daily. Observations for postnatal MeHg exposure will need to be confirmedusing more comprehensive exposure measures.
Original languageEnglish
Pages (from-to)19-25
JournalNeurotoxicology and Teratology
Publication statusPublished (in print/issue) - 14 Jun 2013


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