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Objective: To investigate the effects of prenatal and postnatal lead exposure and polymorphisms in dopamine metabolism genes on neurocognitive development of Mexican children at 24 months (n = 220) and 48 months (n = 186) of age. Study design: We genotyped the dopamine transporter gene (DAT1; SLC6A3) variable nucleotide tandem repeat and the dopamine receptor D2 (DRD2) Taq1A single nucleotide polymorphism. Children were assessed at 24 months with Bayley Scales of Infant Development (Mental Development Index and Psychomotor Development Index) and at 48 months with McCarthy Scales of Children’s Abilities. Results: Blood lead concentration (BLL) in umbilical cord was 6.6 ± 3.3 μg/dL (measured in 1995-96), 8.1 ± 4.4 μg/dL at 24 months, and 8.1 ± 3.6 μg/dL at 48 months. Cord BLL was negatively associated with Mental Development Index (P < .01) and Psychomotor Development Index (P < .1), but not McCarthy scores. The 48-month BLL, but not the 24-month BLL, was negatively associated with children’s scores. Children with DRD2 TT genotype (variant) scored higher than children with CC genotype (wild type) on the Mental Development Index and McCarthy memory scale. Neither polymorphism modified the relationship between BLL (either prenatal or postnatal) and neurocognitive development. Conclusion: Lead exposure was adversely associated with neurocognitive measures, whereas the DRD2 Taq1A TT variant was positively associated with neurocognitive measures. We found no evidence of gene-environment interactions on developmental outcomes in early childhood. [Copyright &y& Elsevier]

Background: Recent evidence suggests that low-level environmental exposure to manganese adversely affects child growth and neurodevelopment. Previous studies have addressed the effects of prenatal exposure, but little is known about developmental effects of early postnatal exposure.Methods: We studied 448 children born in Mexico City from 1997 through 2000, using a longitudinal study to investigate neurotoxic effects of early-life manganese exposure. Archived blood samples, collected from children at 12 and 24 months of age, were analyzed for manganese levels using inductively coupled plasma mass spectrometry. Mental and psychomotor development were scored using Bayley Scales of Infant Development at 6-month intervals between 12 and 36 months of age.Results: At 12 months of age, the mean (SD) blood manganese level was 24.3 (4.5)microg/L and the median was 23.7 microg/L; at 24 months, these values were 21.1 (6.2) microg/L and 20.3 microg/L, respectively. Twelve- and 24-month manganese concentrations were correlated (Spearman correlation = 0.55) and levels declined over time ([beta] = -5.7 [95% CI = -6.2 to -5.1]). We observed an inverted U-shaped association between 12-month blood manganese and concurrent mental development scores (compared with the middle 3 manganese quintiles, for the lowest manganese quintile, [beta] = -3.3 [-6.0 to -0.7] and for the highest manganese quintile, [beta] = -2.8 [-5.5 to -0.2]). This 12-month manganese effect was apparent but diminished with mental development scores at later ages. The 24-month manganese levels were not associated with neurodevelopment.Conclusions: These results suggest a possible biphasic dose-response relationship between early-life manganese exposure at lower exposure levels and infant neurodevelopment. The data are consistent with manganese as both an essential nutrient and a toxicant. [ABSTRACT FROM AUTHOR]

Objective: To compare self-report and physician assessments of sexual maturation against serum hormone markers to evaluate the hypothesis that the validity of self-assessed sexual maturation is underestimated in traditional validation studies.Study Design: We adapted a self-assessment instrument that 248 Mexican children and adolescents, aged 8-13 years, completed. The participants were examined by a trained pediatrician and provided fasting blood samples for measurement of reproductive hormones (eg, testosterone, estradiol, sex hormone-binding globulin, inhibin B) and other hormones (eg, C-peptide, insulin-like growth factor 1, leptin, dehydroepiandrosterone sulfate) known to change during adolescence. Spearman correlations (r) were calculated among the average rank of all hormones and self-assessed and physician-assessed Tanner stage. The method of triads was used to assess the validity of self-reports by estimating correlations between self-assessments and true but unobservable sexual maturation based on all available data. Bootstrap sampling was used to construct 95% CIs.Results: The validity of self-reported genitalia staging for boys was modest (r = 0.50; 95% CI,  0.31-0.65) and inferior to physician assessment (r = 0.75; 95% CI, 0.56-0.93). Breast stage was well reported (r = 0.89; 95% CI, 0.79-0.97) and superior to physician assessment (r = 0.80; 95% CI, 0.70-0.89). Pubic hair stage reported by boys (r = 0.91; 95% CI, 0.79-0.99) and girls (r = 0.99; 95% CI, 0.96-1.00) was superior to physician assessment (r = 0.79; 95% CI, 0.57-0.97 and r = 0.91; 95% CI, 0.83-0.97, respectively).Conclusion: Self-assessment can be validly used in epidemiologic studies for evaluating sexual maturation in children; however, physician assessment may be necessary for accurate assessment of genitalia development in boys. [ABSTRACT FROM AUTHOR]