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Background Because of their geographical location and traditional lifestyle, Canadian Inuit children are highly exposed to polychlorinated biphenyls (PCBs) and lead (Pb), environmental contaminants that are thought to affect fetal and child growth. We examined the associations of these exposures with the fetal and postnatal growth of Inuit children. Methods We conducted a prospective cohort study among Inuit from Nunavik (Arctic Québec). Mothers were recruited at their first prenatal visit; children ( n =290) were evaluated at birth and at 8–14 years of age. Concentrations of PCB 153 and Pb were determined in umbilical cord and child blood. Weight, height and head circumference were measured at birth and during childhood. Results Cord blood PCB 153 concentrations were not associated with anthropometric measurements at birth or school age, but child blood PCB 153 concentrations were associated with reduced weight, height and head circumference during childhood. There was no association between cord Pb levels and anthropometric outcomes at birth, but cord blood Pb was related to smaller height and shows a tendency of a smaller head circumference during childhood. Interpretation Our results suggest that chronic exposure to PCBs during childhood is negatively associated with skeletal growth and weight, while prenatal Pb exposure is related to reduced growth during childhood. This study is the first to link prenatal Pb exposure to poorer growth in school-age children. [ABSTRACT FROM AUTHOR]

Despite several decades of research and prevention efforts, fetal alcohol spectrum disorders (FASD) remain the most common preventable cause of neurodevelopmental disabilities worldwide. Animal and human studies have implicated fetal alcohol-induced alterations in epigenetic programming as a chief mechanism in FASD. Several studies have demonstrated fetal alcohol-related alterations in methylation and expression of imprinted genes in placental, brain, and embryonic tissue. Imprinted genes are epigenetically regulated in a parent-of-origin-specific manner, in which only the maternal or paternal allele is expressed, and the other allele is silenced. The chief functions of imprinted genes are in placental development, somatic growth, and neurobehavior—three domains characteristically affected in FASD. In this review, we summarize the growing body of literature characterizing prenatal alcohol-related alterations in imprinted gene methylation and/or expression and discuss potential mechanistic roles for these alterations in the teratogenic effects of prenatal alcohol exposure. Future research is needed to examine potential physiologic mechanisms by which alterations in imprinted genes disrupt development in FASD, which may, in turn, elucidate novel targets for intervention. Furthermore, mechanistic alterations in imprinted gene expression and/or methylation in FASD may inform screening assays that identify individuals with FASD neurobehavioral deficits who may benefit from early interventions. [ABSTRACT FROM AUTHOR]

Given that their traditional lifestyle and diet still relies on fish and other marine species for sustenance, the Inuit are highly exposed to polychlorinated biphenyls (PCBs) and PCBs are increasingly linked to obesity. However, evidence is not consistent regarding which periods of exposure are most relevant. In this study, we examine whether in utero, childhood, and adolescent exposure to PCBs are related to physical growth at adolescence. Inuit adolescents from Canada (N=212) enrolled in a prospective longitudinal cohort study since birth were assessed for height, weight, body mass index (BMI), fat mass index (FMI) and fat free mass index (FFMI) at 18 years of age. PCB 153 concentrations were quantified in blood samples obtained at birth (umbilical cord), 11, and 18 years of age. Maternal anthropometrics were measured and those for the newborns collected from medical records. Data on biological mothers and participants' sociodemographic characteristics and food security were collected using interviews. Multiple linear regression analyses were used to test associations between PCB 153 concentrations and adolescent anthropometric measures. Cord PCB 153 was not related to height or FFMI at adolescence. By contrast, analyses showed that cord PCB 153 was related to higher BMI, FMI and marginally to weight in girls but not boys. Child PCB 153 was not related to height, weight or FFMI in adolescence. Child PCB 153 was related to lower BMI and FMI at adolescence in both sexes, particularly among those considered overweight or obese during childhood. Adolescent PCB 153 was not associated with any outcome. This study suggests that prenatal exposure to PCBs may have a long-term effect on growth in early adulthood among girls and identifies the peri-pubertal period as another window of sensitivity for the action of PCBs. Our findings also suggest that exposure to PCBs and body size be documented in multiple time periods from infancy to adulthood. • Prenatal exposure to PCBs may have a long-term effect on growth among girls. • Peri-pubertal period identified as a window of sensitivity for PCBs. • Exposure to PCBs and body size be documented in multiple time periods. [ABSTRACT FROM AUTHOR]

Lead (Pb) exposure is associated with adverse neurological development. Most notably, it has been observed through externalizing behavior symptoms, as observed among Inuit children from northern Québec. Evidence for a persistent neurological impact of early Pb exposure later in life is however scarce. Pb exposure may initiate a developmental cascade that increases the risk of long-term behavior problems. Testing for direct associations between childhood Pb concentrations and adolescent externalizing symptoms and substance use, as well as indirect associations through childhood behavior assessments. The study sample is a longitudinal cohort of Inuit children (n = 212) followed since birth. Blood Pb concentrations were measured during childhood (median age = 11.4 years) and adolescence (median age = 18.5 years). Externalizing/inattentive behavior were teacher-assessed through the Teacher Report Form and the Disruptive Behavior Disorders Rating Scale for children. At the adolescence follow-up, behavior problems were self-reported by filling Achenbach's Youth Self-Report, the Barkley Adult ADHD-IV Rating Scale, and the Diagnostics Interview Schedule for Children. Adolescent substance use was also self-assessed through the DEP-ADO. Direct and indirect associations of child Pb concentrations with adolescent outcomes were tested through mediation models. Child blood Pb concentrations were not directly associated with any adolescent outcomes. On the contrary, childhood Pb exposure was indirectly associated, through childhood externalizing behavior assessments, with adolescent externalizing behaviors, binge drinking, and cannabis use. These indirect associations held after controlling for adolescents' concurrent Pb blood concentrations. Our results highlight the indirect but lasting effects of child Pb exposure on adolescent behavior problems, and the importance of childhood externalizing behavior in this relationship. Adverse early-life environment put children on a riskier developmental trajectory, increasing their likelihood of lifelong psychological, social and health problems. • Child Pb associated with adolescent externalizing behavior and substance use. • These associations mediated by child externalizing behaviors. • Early-life impairments may put children on a riskier developmental trajectory. [ABSTRACT FROM AUTHOR]