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Background Prenatal alcohol exposure (PAE) is associated with postnatal iron deficiency (ID), which has been shown to exacerbate deficits in growth, cognition, and behavior seen in fetal alcohol spectrum disorders. However, the mechanisms underlying PAE-related ID remain unknown. Objectives We aimed to examine biochemical measures of iron homeostasis in the mother, placenta, neonate, and 6.5-month-old infant. Methods In a prenatally recruited, prospective longitudinal birth cohort in South Africa, 206 gravidas (126 heavy drinkers and 80 controls) were interviewed regarding alcohol, cigarette, and drug use and diet at 3 prenatal visits. Hemoglobin, ferritin, and soluble transferrin receptor (sTfR) were assayed twice during pregnancy and urinary hepcidin:creatinine was assayed once. Infant ferritin and hemoglobin were measured at 2 weeks and 6.5 months and sTfR was measured at 6.5 months. Histopathological examinations were conducted on 125 placentas and iron transport assays (iron regulatory protein-2, transferrin receptor-1, divalent metal transporter-1, ferroportin-1, and iron concentrations) were conducted on 63. Results In multivariable regression models, prenatal drinking frequency (days/week) was related to higher maternal hepcidin and to sequestration of iron into storage at the expense of erythropoiesis in mothers and neonates, as evidenced by a lower hemoglobin (g/dL)-to-log(ferritin) (ug/L) ratio [mothers: raw regression coefficient (β) = −0.21 (95% CI: −0.35 to −0.07); neonates: β = −0.15 (95% CI: −0.24 to −0.06)]. Drinking frequency was also related to decreased placental ferroportin-1:transferrin receptor-1 (β = −0.57 for logged values; 95% CI: −1.03 to −0.10), indicating iron-restricted placental iron transport. At 6.5 months, drinking frequency was associated with lower hemoglobin (β = −0.18; 95% CI: −0.33 to −0.02), and increased prevalences of ID (β = 0.09; 95% CI: 0.02–0.17) and ID anemia (IDA) (β = 0.13; 95% CI: 0.04–0.23). In causal inference analyses, the PAE-related increase in IDA was partially mediated by decreased neonatal hemoglobin:log(ferritin), and the decrease in neonatal hemoglobin:log(ferritin) was partially mediated by decreased maternal hemoglobin:log(ferritin). Conclusions In this study, greater PAE was associated with an unfavorable profile of maternal-fetal iron homeostasis, which may play mechanistic roles in PAE-related ID later in infancy. [ABSTRACT FROM AUTHOR]

Prenatal cigarette smoke exposure (PCSE) has been linked to problems in behavioral inhibition and attention deficit hyperactivity disorder in children in several epidemiological studies. We used event-related potentials (ERPs) to examine the effects of PCSE on neural correlates of inhibitory control of behavior. In a prospective longitudinal study on child development in the Canadian Arctic, we assessed 186 Inuit children (mean age = 11.3 years) on a visual Go/No-go response inhibition paradigm. PCSE was assessed through maternal recall. Potential confounders were documented from a maternal interview, and exposure to neurotoxic environmental contaminants was assessed from umbilical cord and child blood samples. PCSE was not related to behavioral performance on this simple response inhibition task. Nevertheless, this exposure was associated with smaller amplitudes of the N2 and P3 components elicited by No-go stimuli, suggesting an impairment in the neural processes underlying response inhibition. Amplitude of the No-go P3 component was also inversely associated with behavioral measures of externalizing problems and hyperactivity/impulsivity in the classroom. This study is the first to report neurophysiological evidence of impaired response inhibition in school-aged children exposed to tobacco smoke in utero . Effects were found on ERP components associated with conflict processing and inhibition of a prepotent response, indicating neurophysiological deficits that may play a critical role in the attention and behavior problems observed in children with PCSE. [ABSTRACT FROM AUTHOR]

Background Frequency and quantity of alcohol consumed by women are two important indicators of the risks associated with drinking during pregnancy. Some studies have compared the validity of maternal alcohol report obtained during and after pregnancy. However, to date none have examined alcohol use in a Native Canadian population, such as the Inuit. Effective measurement methods are necessary to better understand why children from some communities seem at increased risk of alcohol-related neurodevelopmental disorders. Methods Prospective and retrospective drinking interviews were obtained from a sub-sample of 67 women included in the Nunavik Child Development Study (NCDS), Nunavik, Canada (1995–2010; N = 248). Number of days of alcohol consumption and binge drinking (five drinks or more per episode) across pregnancy as well as ounces of absolute alcohol per day and per drinking day among users were collected using timeline follow-back interviews administered both during pregnancy and again 11 years after delivery. Consistency of alcohol reports over time, as well as significant differences for alcohol quantities described by users between interviews were examined. Sociodemographic characteristics associated with alcohol use reports were also assessed. Results The proportion of positive reports of alcohol and binge drinking during pregnancy was higher when women were interviewed prospectively during pregnancy than retrospectively. We observed a fair to moderate agreement of alcohol report between interview periods. By contrast, the number of binge drinking days during pregnancy was slightly higher among alcohol users when documented retrospectively. Conclusions Our findings endorse the conclusion that prospective alcohol measures provide more reliable ascertainment and likely generate more valid information about the proportion of children prenatally exposed to alcohol in the Inuit population. [ABSTRACT FROM AUTHOR]