Pre-school child blood lead levels in a population-derived Australian birth cohort: the Barwon Infant Study.

OBJECTIVES: To investigate blood lead levels in an Australian birth cohort of children; to identify factors associated with higher lead levels. DESIGN, SETTING: Cross-sectional study within the Barwon Infant Study, a population birth cohort study in the Barwon region of Victoria (1074 infants, recruited June 2010 - June 2013). Data were adjusted for non-participation and attrition by propensity weighting. PARTICIPANTS: Blood lead was measured in 523 of 708 children appraised in the Barwon Infant Study pre-school review (mean age, 4.2 years; SD, 0.3 years). MAIN OUTCOME MEASURE: Blood lead concentration in whole blood (µg/dL). RESULTS: The median blood lead level was 0.8 µg/dL (range, 0.2-3.7 µg/dL); the geometric mean blood lead level after propensity weighting was 0.97 µg/dL (95% CI, 0.92-1.02 µg/dL). Children in houses 50 or more years old had higher blood lead levels (adjusted mean difference [AMD], 0.13 natural log units; 95% CI, 0.02-0.24 natural log units; P = 0.020), as did children of families with lower household income (per $10 000, AMD, -0.035 natural log units; 95% CI, -0.056 to -0.013 natural log units; P = 0.002) and those living closer to Point Henry (inverse square distance relationship; P = 0.002). Associations between hygiene factors and lead levels were evident only for children living in older homes. CONCLUSION: Blood lead levels in our pre-school children were lower than in previous Australian surveys and recent surveys in areas at risk of higher exposure, and no children had levels above 5 µg/dL. Our findings support advice to manage risks related to exposure to historical lead, especially in older houses.

Importance of accounting for sibling age when examining the association between family size and early childhood cognition, language and emotional behaviour: a birth cohort study.

OBJECTIVES: Larger sibships are associated with poorer cognitive and language outcomes but have different impacts on child emotional development. Previous studies have not taken into account sibling age, nor have impacts across multiple neurodevelopmental domains been considered in the same participant group. This study investigated the influence of family size indicators on early childhood cognitive, language and emotional-behavioural development. The effect of sibling age was considered by evaluating these relationships separately for different sibling age categories. DESIGN: Prospective birth cohort study. SETTING: Participants in the Barwon Infant Study were recruited from two major hospitals in the Barwon region of Victoria, Australia, between 2010 and 2013 (n=1074 children). PARTICIPANTS: The 755 children with any neurodevelopmental data at age 2-3 years excluding twins and those with an acquired neurodisability. OUTCOME MEASURES: Cognitive and language development was assessed using the Bayley Scales of Infant and Toddler Development, Third Edition, and emotional-behavioural development was measured with the Child Behaviour Checklist for Ages 1½-5. RESULTS: Greater household size was associated with a reduced cognitive development score (adjusted mean difference (AMD) -0.66 per extra household member; 95% CI -0.96 to -0.37; p<0.001) without age-specific differences. However, poorer expressive language was only observed for exposure to siblings between 2-6 and 6-10 years older. Having siblings 2-6 years older was associated with less internalising behaviour (AMD -2.1 per sibling; 95% CI -3.1 to -1.0; p<0.001). These associations persisted after multiple comparison adjustment. CONCLUSIONS: The influence of siblings on early childhood development varies substantially by sibling age and the neurodevelopmental outcome under study. Although family size alone appears important for cognitive development, age-specific findings emphasise the importance of sibling interaction in early childhood expressive language development and emotional behaviour.

Prenatal phthalate exposure, oxidative stress-related genetic vulnerability and early life neurodevelopment: A birth cohort study.

Prenatal phthalate chemicals may have adverse effects on brain development by various mechanisms including oxidant damage. However, birth cohort findings have been conflicting. This study aimed to (i) investigate the interplay between maternal prenatal phthalate levels, infant genetic vulnerability to oxidative stress, and child neurodevelopment and (ii) examine combined putative oxidant exposures. In a population-based birth cohort of 1064 women with prenatal recruitment in Victoria, Australia, maternal urine was collected at 36 weeks of pregnancy and phthalate metabolite concentrations measured. An unweighted genetic score for oxidative stress was made using a candidate gene approach. Cognition was assessed using the BAYLEY-III at two years (n = 678). Parents completed questionnaires for doctor diagnosed autism spectrum disorder (ASD) (1.4 %), ASD traits (4.9 %) and child inattention/hyperactivity (n = 791). Analyses included multiple linear and logistic regression. Higher prenatal phthalate levels and a higher oxidative stress genetic score were each associated with subsequent ASD. Several oxidative stress-related SNPs modified the association between prenatal phthalates and ASD and other outcomes. Consistent patterns were evident across gene score-phthalate combinations for cognition, ASD, ASD traits and inattention/hyperactivity. Other putative oxidant factors such as prenatal smoking further increased risk. Prenatal phthalate levels and infant oxidative stress-related genetic vulnerability are associated with adverse neurodevelopment. Combined exposures are important. Current recommendations and regulation on maternal phthalate exposure during pregnancy require re-evaluation.

Childhood adiposity, adult adiposity, and the ACE gene insertion/deletion polymorphism: evidence of gene-environment interaction effects on adult blood pressure and hypertension status in adulthood.

BACKGROUND: Genetic variants may modify the associations of adiposity measures with blood pressure (BP) and hypertension. The insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is an attractive candidate. AIMS: To examine interaction effects between I/D polymorphism and adiposity measures (BMI, waist circumference, waist-to-hip ratio, and skinfold thickness) during childhood and adulthood in relation to adult BP and hypertension. METHODS: Data were available for 4835 participants from three prospective cohort studies. Multivariable linear regression models for adult SBP and DBP, and multivariable logistic regression models for hypertension were fit that included interaction effects between child or adult adiposity and I/D polymorphism. RESULTS: Evidence for interaction effects on BP/hypertension were found across the three studies. Compared with childhood measures, the effect modification appeared to be more consistent when using adult adiposity. In particular, the adverse effects of greater adult waist circumference on increasing adult SBP and DBP appeared to be larger among carriers of ACE DD (or GG) [adjusted linear regression coefficients 0.26, 95% CI (0.21-0.31) and 0.28 (0.24-0.32) for SBP and DBP, respectively] and ID (or AG) genotypes [0.25 (0.21-0.29) and 0.25 (0.21-0.28), respectively], whereas those with II (or AA) genotypes had smaller effects [0.15 (0.09-0.21) and 0.19 (0.13-0.23)]. CONCLUSION: ACE genetic variation may modify the effect of adult adiposity on increasing BP and risk of hypertension in adulthood. Individuals with ACE DD (or GG) and/or ID (or AG) genotypes, compared with those with II (or AA) genotype, appear more vulnerable to the impact of excess adiposity.