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BACKGROUND: Exposure to methylmercury was shown to decrease neural stem cell populations, whereas aerobic fitness has beneficial effects on the adult brain that relies on improved neurogenesis in the hippocampus. OBJECTIVES: We examined the association between aerobic fitness and neurocognitive outcomes at young adult age, along with the potential moderating effect of prenatal exposure to methylmercury. Methods: At age 22 years, 262 members of a Faroese birth cohort, established in 1986-1987, underwent a graded exercise test of aerobic fitness to measure maximal oxygen uptake (V[O.sub.2MaX]). Their prenatal methylmercury exposure had been assessed from the mercury concentration in cord blood. We estimated cross-sectional associations between V[O.sub.2Max] and multiple measures of neurocognitive function. In addition, we compared groups with low and high prenatal methylmercury exposure. RESULTS: A 1 standard deviation (SD) increase in V[O.sub.2Max] was associated with better scores on short-term memory and cognitive processing speed by 0.21 SD (95% CI: -0.04, 0.46) and 0.28 SD (95% CI: 0.02, 0.54), respectively. In the group with lower prenatal methylmercury exposure, a 1 SD increase in V[O.sub.2Max] was associated with increased scores on cognitive processing speed by 0.45 SD (95% CI: 0.08, 0.81) and with a slightly lesser benefit in short-term memory. No such association was observed in the group with high prenatal methylmercury exposure. CONCLUSIONS: Higher aerobic capacity was associated with better performance in short-term memory and processing speed. However, prenatal methylmercury exposure seemed to attenuate these positive associations., Background Adult neurogenesis occurring in the dentate gyrus of the hippocampus is a dynamic process regulated by both intrinsic and extrinsic factors (Aimone et al. 2014). Neurogenesis can be affected [...]

OBJECTIVES. To examine possible effects on blood pressure, neurological function, and neurobehavioral tests in school-aged children with and without prenatal pesticide exposure in an area where stunting is common. METHODS. In a community of Northern Ecuador with intensive floriculture and a high female employment rate, we invited 79 children attending the 2 lowest grades of a public school for clinical examinations. In addition to a thorough physical examination, we administered simple reaction time, Santa Ana dexterity test, Stanford-Binet copying, and Wechsler Intelligence Scale for Children-Revised Digit Spans forward. Maternal interview included detailed assessment of occupational history to determine pesticide exposure during pregnancy. Recent and current pesticide exposure was assessed by erythrocyte acetylcholine esterase activity and urinary excretion of organophosphate metabolites. RESULTS. All eligible children participated in the study, but 7 children were excluded from data analysis due to other disease or age >9 years. A total of 31 of the remaining 72 children were classified as stunted based on their height for age. Maternal occupational history revealed that 37 children had been exposed to pesticides during development. After confounder adjustment, prenatal pesticide exposure was associated with a higher systolic blood pressure than in the controls. On neurological examination, 14 exposed children and 9 controls showed [greater than or equal to] 1 abnormalities. Of 5 neurobehavioral tests, the Stanford-Binet copying test showed a lower drawing score for copying designs in exposed children than in controls. Stunting was associated with a lower score on this test only, and both risk factors remained statistically significant in a multiple regression analysis with adjustment for demographic and social confounders. Increased excretion of dimethyl and diethyl metabolites of organophosphates was associated with increased reaction time and no other outcomes. CONCLUSION. Prenatal pesticide exposure may cause lasting neurotoxic damage and add to the adverse effects of malnutrition in developing countries. The effects differ from those due to acute pesticide exposure. KEY WORDS. blood pressure, maternal exposure, neuropsychological tests, neurotoxicity syndromes, organophosphorus compounds, prenatal exposure, delayed effects., URL: [...]

Background: Exposure to methylmercury was shown to decrease neural stem cell populations, whereas aerobic fitness has beneficial effects on the adult brain that relies on improved neurogenesis in the hippocampus. Objectives: We examined the association between aerobic fitness and neurocognitive outcomes at young adult age, along with the potential moderating effect of prenatal exposure to methylmercury. Methods: At age 22 years, 262 members of a Faroese birth cohort, established in 1986–1987, underwent a graded exercise test of aerobic fitness to measure maximal oxygen uptake (VO2Max). Their prenatal methylmercury exposure had been assessed from the mercury concentration in cord blood. We estimated cross-sectional associations between VO2Max and multiple measures of neurocognitive function. In addition, we compared groups with low and high prenatal methylmercury exposure. Results: A 1 standard deviation (SD) increase in VO2Max was associated with better scores on short-term memory and cognitive processing speed by 0.21 SD (95% CI: –0.04, 0.46) and 0.28 SD (95% CI: 0.02, 0.54), respectively. In the group with lower prenatal methylmercury exposure, a 1 SD increase in VO2Max was associated with increased scores on cognitive processing speed by 0.45 SD (95% CI: 0.08, 0.81) and with a slightly lesser benefit in short-term memory. No such association was observed in the group with high prenatal methylmercury exposure. Conclusions: Higher aerobic capacity was associated with better performance in short-term memory and processing speed. However, prenatal methylmercury exposure seemed to attenuate these positive associations. Citation: Oulhote Y, Debes F, Vestergaard S, Weihe P, Grandjean P. 2017. Aerobic fitness and neurocognitive function scores in young Faroese adults and potential modification by prenatal methylmercury exposure. Environ Health Perspect 125:677–683; http://dx.doi.org/10.1289/EHP274

The article presents the possibility of using structural equation models for combining information from different studies in environmental epidemiology. The study involves combining two data from two birth cohorts assessing the long-term effects of prenatal exposure to methyl mercury (MeHg) on childhood cognitive performance. Results revealed that mercury's effect on childhood performance is statistically significant.

The mercury concentration in blood or scalp hair has been widely used as a biomarker for methlimercury exposure. Becasue of the increased risks associated with exposures during prenatal and early postnatal development, biomarker results must be interpreted with regard to the age-dependent susceptibillity. The authors compared regression coefficients for five sets of exposure biomarkers in 917 children from the Faroe Islands examined at birth, 1 year, and 7 years. Outcome varibales were the results of neuropsychologic exemination carried out in 1993–1994 at age 7 years. After adjustment for covariates, the cord-blood concentration showed the clearest associations with deficits in language, atention, and memory. Fine-moteor function deficits were particularly associated with the maternal hair mercury at parturition. Mercury concentrations in the child‘s blood and hair at age 7 years were significant predicors only of performance on memory for visuopatial information. These flndings emphaisze the usefulness of the cord-blood mercury concentration as a main risk indicator. They also support the notion that the greatest susceptibility to methlymercury neurotoxicity occurs during late gestation, while early postnatal vulnerability is less, and they suggest that the time-dependent susceptibility may vary for different brain functions. Am J Epidemiol 1999; 149; 301–5. [ABSTRACT FROM PUBLISHER]

The potential of structural equation models for combining information from different studies in environmental epidemiology is explored. For illustration we synthesize data from two birth cohorts assessing the effects of prenatal exposure to methylmercury on childhood cognitive performance. One cohort was the largest by far, but a smaller cohort included superior assessment of the PCB exposure which has been considered an important confounder when estimating the mercury effect. The data were analyzed by specification of a structural equation model for each cohort. Information was then pooled based on a joint likelihood function with key parameters constrained to be equal in the different models. Modeling assumptions were chosen to obtain a meaningful biological interpretation of the joint effect parameters. Measurement errors in mercury variables were taken into account by viewing observed variables as indicators of latent variables. Adjustments for measurement error were also included for confounder variables. In particular, this example illustrates how to properly utilize that one study provided superior information about a confounder. A final more advanced model pooled information across different outcomes to gain power and to avoid multiple testing problems. In this model, the mercury effect remained statistically significant, while the effect of PCB was less certain.

Exposure to methylmercury from marine mammals and other seafood may affect the development of the central nervous system. In a traditional Inuit community in Qaanaaq, Greenland, mercury concentrations in cord blood and maternal hair have been examined in connection with all births. We examined 43 children at age 7–12 years with a battery of neurobehavioral tests. The average mercury concentration in hair was 5.0 μ/g and 1.5 μ/g in children and mothers, respectively. Clinical neurological examination did not reveal any obvious deficits. However, neuropsychological tests showed possible exposure-associated deficits, though only in a few cases reaching statistical significance. In conjunction with data from other studies, peak latencies on brainstem auditory evoked potentials tended to be prolonged at increased exposure levels. The data from the present study therefore appears in accordance with other evidence that prenatal or early postnatal exposures to methylmercury may cause subtle neurobehavioral deficits.

Hit Reaction Time latencies (HRT) in the Continuous Performance Test (CPT) measure the speed of visual information processing. The latencies may involve different neuropsychological functions depending on the time from test initiation, i.e., first orientation, learning and habituation, then cognitive processing and focused attention, and finally sustained attention as the dominant demand. Prenatal methylmercury exposure is associated with increased reaction time (RT) latencies. We therefore examined the association of methylmercury exposure with the average HRT at age 14 years at three different time intervals after test initiation. A total of 878 adolescents (87% of birth cohort members) completed the CPT. The RT latencies were recorded for 10 min, with visual targets presented at 1000 ms intervals. After confounder adjustment, regression coefficients showed that CPT-RT outcomes differed in their associations with exposure biomarkers of prenatal methylmercury exposure: During the first 2 min, the average HRT was weakly associated with methylmercury (beta (SE) for a ten-fold increase in exposure, (3.41 (2.06)), was strongly for the 3-to-6 min interval (6.10 (2.18)), and the strongest during 7-10 min after test initiation (7.64 (2.39)). This pattern was unchanged when simple reaction time and finger tapping speed were included in the models as covariates. Postnatal methylmercury exposures did not affect the outcomes. Thus, these findings suggest that sustained attention as a neuropsychological domain is particularly vulnerable to developmental methylmercury exposure, indicating probable underlying dysfunction of the frontal lobes. When using CPT data as a possible measure of neurotoxicity, test results should therefore be analyzed in regard to time from test initiation and not as overall average reaction times., (Copyright © 2010 Elsevier Inc. All rights reserved.)