Air pollution exposure during pregnancy and childhood, cognitive function, and emotional and behavioral problems in adolescents.

BACKGROUND: Exposure to air pollution may impact neurodevelopment during childhood, but current evidence on the association with cognitive function and mental health is inconclusive and primarily focusses on young children. Therefore, we aim to study the association of exposure to air pollution during pregnancy and childhood, with cognitive function and emotional and behavioral problems in adolescents. METHODS: We used data from 5170 participants of a birth cohort in Rotterdam, the Netherlands. Concentrations of fourteen air pollutants at participant's home addresses were estimated during pregnancy and childhood, using land use regression models. We included four cognitive domains (processing speed, working memory, fluid reasoning and verbal intelligence quotient (IQ)) and an estimated full-scale IQ. Internalizing, externalizing, and attention problems were self- and parent-reported. We used linear regression models to assess the association of each air pollutant, with cognitive function and emotional and behavioral problems, adjusting for socioeconomic status and lifestyle characteristics. Then, we performed multipollutant analyses using the Deletion/Substitution/Addition (DSA) algorithm. RESULTS: Air pollution exposure was not associated with full-scale IQ, working memory, or processing speed. Higher exposure to few air pollutants was associated with higher fluid reasoning and verbal IQ scores (e.g. 0.22 points of fluid reasoning (95%CI 0.00; 0.44) per 1 µg/m3 increase in organic carbon during pregnancy). Higher exposure to some air pollutants was also associated with less internalizing, externalizing, and attention problems (e.g. -0.27 internalizing problems (95% CI -0.52; -0.02) per each 5 ng/m3 increase in copper during pregnancy). CONCLUSIONS: Higher exposure to air pollution during pregnancy and childhood was not associated with lower cognitive function or more emotional and behavioral problems in adolescents. Based on previous literature and biological plausibility, the observed protective associations are probably explained by negative residual confounding, selection bias, or chance and do not represent a causal relationship.

Lifetime prevalence and temporal trends of incidence of child's mental disorder diagnoses in Catalonia, Spain.

INTRODUCTION: Most mental disorders have its onset during childhood, but less than one third of affected children seek professional help. The aim of this study is to (1) estimate the lifetime prevalence of mood, anxiety, conduct, and eating disorder diagnoses in 18-year-olds in 2017 and (2) the temporal trends of incidence diagnosis rates in 2009-2017 in children aged 2-18 in Catalonia, Spain. MATERIAL AND METHODS: We used a registry-based cohort including all children aged 2-18 living in Catalonia in 2009-2017, from the Catalan Health Service. Cases were identified with ICD-9 codes. Lifetime prevalence was calculated for 2017, and annual incidence for 2009-2017. Temporal trends were analyzed with multivariate negative binomial regression models. RESULTS: Lifetime prevalence of diagnoses was highest for conduct disorders (5.05%), followed by anxiety (4.37%), mood (3.07%), and eating disorders (2.11%). Median age of diagnosis was 16 years for mood, anxiety and eating disorders, and 15 years for conduct disorders. Comorbidity was present in 20.74% of those diagnosed with a mental disorder. Annual incidence rates for all disorders increased in 2011-2013/2014, and then stabilized. However, incidence rate of anxiety diagnoses in 13-18-year-old children doubled between 2016 and 2017. CONCLUSIONS: Lifetime prevalence of diagnoses are lower than the expected rates of mental disorders based on interview/survey European studies. Further research is needed into the factors underlying (1) the underdiagnoses of mental disorders in children and (2) the increasing trend of anxiety disorder diagnoses in older children.

Exposure to traffic-related air pollution and noise during pregnancy and childhood, and functional brain connectivity in preadolescents.

BACKGROUND: The amount of people affected by traffic-related air pollution and noise is continuously increasing, but limited research has been conducted on the association between these environmental exposures and functional brain connectivity in children. OBJECTIVE: This exploratory study aimed to analyze the associations between the exposure to traffic-related air pollution and noise during pregnancy and childhood, and functional brain connectivity amongst a wide-swath of brain areas in preadolescents from 9 to 12 years of age. METHODS: We used data of 2,197 children from the Generation R Study. Land use regression models were applied to estimate nitrogen oxides and particulate matter levels at participant's homes for several time periods: pregnancy, birth to 3 years, 3 to 6 years, and 6 years of age to the age at magnetic resonance imaging (MRI) assessment. Existing noise maps were used to estimate road traffic noise exposure at participant's homes for the same time periods. Resting-state functional MRI was obtained at 9-12 years of age. Pair-wise correlation coefficients of the blood-oxygen-level-dependent signals between 380 brain areas were calculated. Linear regressions were run and corrected for multiple testing. RESULTS: Preadolescents exposed to higher levels of NO2, NOx, and PM2.5 absorbance, from birth to 3 years, and from 3 to 6 years of age showed higher correlation coefficients among several brain regions (e.g. from 0.16 to 0.19 higher correlation coefficient related to PM2.5 absorbance exposure, depending on the brain connection). Overall, most identified associations were between brain regions of the task positive and task negative networks, and were mainly inter-network (20 of 26). Slightly more than half of the connections were intra-hemispheric (14 of 26), predominantly in the right hemisphere. Road traffic noise was not associated with functional brain connectivity. CONCLUSIONS: This exploratory study found that exposure to traffic-related air pollution during the first years of life was related to higher functional brain connectivity predominantly in brain areas located in the task positive and task negative networks, in preadolescents from 9 to 12 years of age. These results could be an indicator of differential functional connectivity in children exposed to higher levels of air pollution.

Air pollution, white matter microstructure, and brain volumes: Periods of susceptibility from pregnancy to preadolescence.

Air pollution exposure during early-life is associated with altered brain development, but the precise periods of susceptibility are unknown. We aimed to investigate whether there are periods of susceptibility of air pollution between conception and preadolescence in relation to white matter microstructure and brain volumes at 9-12 years old. We used data of 3515 children from the Generation R Study, a population-based birth cohort from Rotterdam, the Netherlands (2002-2006). We estimated daily levels of nitrogen dioxide (NO2), and particulate matter (PM2.5 and PM2.5absorbance) at participants' homes during pregnancy and childhood using land-use regression models. Diffusion tensor and structural brain images were obtained when children were 9-12 years of age, and we calculated fractional anisotropy and mean diffusivity, and several brain structure volumes. We performed distributed lag non-linear modeling adjusting for socioeconomic and lifestyle characteristics. We observed specific periods of susceptibility to all air pollutants from conception to age 5 years in association with lower fractional anisotropy and higher mean diffusivity that survived correction for multiple testing (e.g., -0.85 fractional anisotropy (95%CI -1.43; -0.27) per 5 µg/m3 increase in PM2.5 between conception and 4 years of age). We also observed certain periods of susceptibility to some air pollutants in relation to global brain and some subcortical brain volumes, but only the association between PM2.5 and putamen survived correction for multiple testing (172 mm3 (95%CI 57; 286) per 5 µg/m3 increase in PM2.5 between 4 months and 1.8 year of age). This study suggested that conception, pregnancy, infancy, toddlerhood, and early childhood seem to be susceptible periods to air pollution exposure for the development of white matter microstructure and the putamen volume. Longitudinal studies with repeated brain outcome measurements are needed for understanding the trajectories and the long-term effects of exposure to air pollution.