Neighborhood Disadvantage and Autism Spectrum Disorder in a Population With Health Insurance.

Importance: Family socioeconomic status has been associated with autism spectrum disorder (ASD) diagnoses. Less is known regarding the role of neighborhood disadvantage in the United States, particularly when children have similar access to health insurance. Objective: To evaluate the association between neighborhood disadvantage and the diagnosis of ASD and potential effect modification by maternal and child demographic characteristics. Design, Setting, and Participants: This cohort study examined a retrospective birth cohort from Kaiser Permanente Southern California (KPSC), an integrated health care system. Children born in 2001 to 2014 at KPSC were followed up through KPSC membership records. Electronic medical records were used to obtain an ASD diagnosis up to December 31, 2019, or the last follow-up. Data were analyzed from February 2022 to September 2023. Exposure: Socioeconomic disadvantage at the neighborhood level, an index derived from 7 US census tract characteristics using principal component analysis. Main Outcomes and Measures: Clinical ASD diagnosis based on electronic medical records. Associations between neighborhood disadvantage and ASD diagnosis were determined by hazard ratios (HRs) from Cox regression models adjusted for birth year, child sex, maternal age at delivery, parity, severe prepregnancy health conditions, maternal race and ethnicity, and maternal education. Effect modification by maternal race and ethnicity, maternal education, and child sex was assessed. Results: Among 318 372 mothers with singleton deliveries during the study period, 6357 children had ASD diagnoses during follow-up; their median age at diagnosis was 3.53 years (IQR, 2.57-5.34 years). Neighborhood disadvantage was associated with a higher likelihood of ASD diagnosis (HR, 1.07; 95% CI, 1.02-1.11, per IQR = 2.70 increase). Children of mothers from minoritized racial and ethnic groups (African American or Black, Asian or Pacific Islander, Hispanic or Latinx groups) had increased likelihood of ASD diagnosis compared with children of White mothers. There was an interaction between maternal race and ethnicity and neighborhood disadvantage (difference in log-likelihood = 21.88; P < .001 for interaction under χ24); neighborhood disadvantage was only associated with ASD among children of White mothers (HR, 1.17; 95% CI, 1.09-1.26, per IQR = 2.00 increase). Maternal education and child sex did not significantly modify the neighborhood-ASD association. Conclusions and Relevance: In this study, children residing in more disadvantaged neighborhoods at birth had higher likelihood of ASD diagnosis among a population with health insurance. Future research is warranted to investigate the mechanisms behind the neighborhood-related disparities in ASD diagnosis, alongside efforts to provide resources for early intervention and family support in communities with a higher likelihood of ASD.

Air pollution and age-dependent changes in emotional behavior across early adolescence in the U.S.

Recent studies have linked air pollution to increased risk for behavioral problems during development, albeit with inconsistent findings. Additional longitudinal studies are needed that consider how emotional behaviors may be affected when exposure coincides with the transition to adolescence - a vulnerable time for developing mental health difficulties. This study investigates if annual average PM2.5 and NO2 exposure at ages 9-10 years moderates age-related changes in internalizing and externalizing behaviors over a 2-year follow-up period in a large, nationwide U.S. sample of participants from the Adolescent Brain Cognitive Development (ABCD) Study®. Air pollution exposure was estimated based on the residential address of each participant using an ensemble-based modeling approach. Caregivers answered questions from the Child Behavior Checklist (CBCL) at the baseline, 1-year follow-up, and 2-year follow-up visits, for a total of 3 waves of data; from the CBCL we obtained scores on internalizing and externalizing problems plus 5 syndrome scales (anxious/depressed, withdrawn/depressed, rule-breaking behavior, aggressive behavior, and attention problems). Zero-inflated negative binomial models were used to examine both the main effect of age as well as the interaction of age with each pollutant on behavior while adjusting for various socioeconomic and demographic characteristics. Against our hypothesis, there was no evidence that greater air pollution exposure was related to more behavioral problems with age over time.

Sex-specific effects in how childhood exposures to multiple ambient air pollutants affect white matter microstructure development across early adolescence.

Ambient air pollution is ubiquitous, yet questions remain as to how it might impact the developing brain. Large changes occur in the brain's white matter (WM) microstructure across adolescence, with noticeable differences in WM integrity in male and female youth. Here we report sex-stratified effects of fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) on longitudinal patterns of WM microstructure from 9-13 years-old in 8,182 (49% female) participants using restriction spectrum imaging. After adjusting for key sociodemographic factors, multi-pollutant, sex-stratified models showed that one-year annual exposure to PM2.5 and NO2 was associated with higher, while O3 was associated with lower, intracellular diffusion at age 9. All three pollutants also affected trajectories of WM maturation from 9-13 years-old, with some sex-specific differences in the number and anatomical locations of tracts showing altered trajectories of intracellular diffusion. Concentrations were well-below current U.S. standards, suggesting exposure to these criteria pollutants during adolescence may have long-term consequences on brain development.

Prenatal air pollution, maternal immune activation, and autism spectrum disorder.

BACKGROUND: Autism Spectrum Disorder (ASD) risk is highly heritable, with potential additional non-genetic factors, such as prenatal exposure to ambient particulate matter with aerodynamic diameter < 2.5 µm (PM2.5) and maternal immune activation (MIA) conditions. Because these exposures may share common biological effect pathways, we hypothesized that synergistic associations of prenatal air pollution and MIA-related conditions would increase ASD risk in children. OBJECTIVES: This study examined interactions between MIA-related conditions and prenatal PM2.5 or major PM2.5 components on ASD risk. METHODS: In a population-based pregnancy cohort of children born between 2001 and 2014 in Southern California, 318,751 mother-child pairs were followed through electronic medical records (EMR); 4,559 children were diagnosed with ASD before age 5. Four broad categories of MIA-related conditions were classified, including infection, hypertension, maternal asthma, and autoimmune conditions. Average exposures to PM2.5 and four PM2.5 components, black carbon (BC), organic matter (OM), nitrate (NO3-), and sulfate (SO42-), were estimated at maternal residential addresses during pregnancy. We estimated the ASD risk associated with MIA-related conditions, air pollution, and their interactions, using Cox regression models to adjust for covariates. RESULTS: ASD risk was associated with MIA-related conditions [infection (hazard ratio 1.11; 95% confidence interval 1.05-1.18), hypertension (1.30; 1.19-1.42), maternal asthma (1.22; 1.08-1.38), autoimmune disease (1.19; 1.09-1.30)], with higher pregnancy PM2.5 [1.07; 1.03-1.12 per interquartile (3.73 µg/m3) increase] and with all four PM2.5 components. However, there were no interactions of each category of MIA-related conditions with PM2.5 or its components on either multiplicative or additive scales. CONCLUSIONS: MIA-related conditions and pregnancy PM2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM2.5 exposure with ASD risk.

Effects of ambient fine particulates, nitrogen dioxide, and ozone on maturation of functional brain networks across early adolescence.

BACKGROUND: Air pollution is linked to neurodevelopmental delays, but its association with longitudinal changes in brain network development has yet to be investigated. We aimed to characterize the effect of PM2.5, O3, and NO2 exposure at ages 9-10 years on changes in functional connectivity (FC) over a 2-year follow-up period, with a focus on the salience (SN), frontoparietal (FPN), and default-mode (DMN) brain networks as well as the amygdala and hippocampus given their importance in emotional and cognitive functioning. METHODS: A sample of children (N = 9,497; with 1-2 scans each for a total of 13,824 scans; 45.6% with two brain scans) from the Adolescent Brain Cognitive Development (ABCD) Study® were included. Annual averages of pollutant concentrations were assigned to the child's primary residential address using an ensemble-based exposure modeling approach. Resting-state functional MRI was collected on 3T MRI scanners. First, developmental linear mixed-effect models were performed to characterize typical FC development within our sample. Next, single- and multi-pollutant linear mixed-effect models were constructed to examine the association between exposure and intra-network, inter-network, and subcortical-to-network FC change over time, adjusting for sex, race/ethnicity, income, parental education, handedness, scanner type, and motion. RESULTS: Developmental profiles of FC over the 2-year follow-up included intra-network integration within the DMN and FPN as well as inter-network integration between the SN-FPN; along with intra-network segregation in the SN as well as subcortical-to-network segregation more broadly. Higher PM2.5 exposure resulted in greater inter-network and subcortical-to-network FC over time. In contrast, higher O3 concentrations resulted in greater intra-network, but less subcortical-to-network FC over time. Lastly, higher NO2 exposure led to less inter-network and subcortical-to-network FC over the 2-year follow-up period. CONCLUSION: Taken together, PM2.5, O3, and NO2 exposure in childhood relate to distinct changes in patterns of network maturation over time. This is the first study to show outdoor ambient air pollution during childhood is linked to longitudinal changes in brain network connectivity development.

Air pollution and emotional behavior in adolescents across the U.S.

Recent studies have linked air pollution to increased risk for behavioral problems during development, albeit with inconsistent findings. Additional longitudinal studies are needed that consider how emotional behaviors may be affected when exposure coincides with the transition to adolescence - a vulnerable time for developing mental health difficulties. This study examines how annual average PM2.5 and NO2 exposure at ages 9-10 years relates to internalizing and externalizing behaviors over a 2-year follow-up period in a large, nationwide U.S. sample of participants from the Adolescent Brain Cognitive Development (ABCD) Study®. Air pollution exposure was estimated based on the residential address of each participant using an ensemble-based modeling approach. Caregivers answered questions from the Child Behavior Checklist (CBCL) at baseline and annually for two follow-up sessions for a total of 3 waves of data; from the CBCL we obtained scores on internalizing and externalizing problems plus 5 syndrome scales (anxious/depressed, withdrawn/depressed, rule-breaking behavior, aggressive behavior, and attention problems). Zero-inflated negative binomial models were used to examine both the main effect of age as well as the interaction of age with each pollutant on behavior while adjusting for various socioeconomic and demographic characteristics. Overall, the pollution effects moderated the main effects of age with higher levels of PM2.5 and NO2 leading to an even greater likelihood of having no behavioral problems (i.e., score of zero) with age over time, as well as fewer problems when problems are present as the child ages. Albeit this was on the order equal to or less than a 1-point change. Thus, one year of annual exposure at 9-10 years is linked with very small change in emotional behaviors in early adolescence, which may be of little clinical relevance.

Ambient fine particulate exposure and subcortical gray matter microarchitecture in 9- and 10-year-old children across the United States.

Neuroimaging studies showing the adverse effects of air pollution on neurodevelopment have largely focused on smaller samples from limited geographical locations and have implemented univariant approaches to assess exposure and brain macrostructure. Herein, we implement restriction spectrum imaging and a multivariate approach to examine how one year of annual exposure to daily fine particulate matter (PM2.5), daily nitrogen dioxide (NO2), and 8-h maximum ozone (O3) at ages 9-10 years relates to subcortical gray matter microarchitecture in a geographically diverse subsample of children from the Adolescent Brain Cognitive Development (ABCD) Study℠. Adjusting for confounders, we identified a latent variable representing 66% of the variance between one year of air pollution and subcortical gray matter microarchitecture. PM2.5 was related to greater isotropic intracellular diffusion in the thalamus, brainstem, and accumbens, which related to cognition and internalizing symptoms. These findings may be indicative of previously identified air pollution-related risk for neuroinflammation and early neurodegenerative pathologies.

Location matters: Regional variation in association of community burden of COVID-19 with caregiver and youth worry.

Our study characterized associations between three indicators of COVID-19's community-level impact in 20 geographically diverse metropolitan regions and how worried youth and their caregivers in the Adolescent Brain Cognitive Development℠ Study have been about COVID-19. County-level COVID-19 case/death rates and monthly unemployment rates were geocoded to participants' addresses. Caregivers' (vs. youths') COVID-19-related worry was more strongly associated with COVID-19's community impact, independent of sociodemographics and pre-pandemic anxiety levels, with these associations varying by location. Public-health agencies and healthcare providers should avoid adopting uniform "one-size-fits-all" approaches to addressing COVID-19-related emotional distress and must consider specific communities' needs, challenges, and strengths.

Cumulative Neighborhood Risk and Subsequent Internalizing Behavior among Asian American Adolescents.

Neighborhood disadvantage is a developmental context that may contribute to Asian American adolescent internalizing problems, yet there is a dearth of longitudinal studies as well as examination of cultural protective factors. Co-ethnic density, or the proportion of individuals of the same racial/ethnic background in the neighborhood that is often cited as a protective factor for racial/ethnic minority groups, has not been adequately examined in Asian American youth. This study examined the longitudinal association between cumulative neighborhood risk and internalizing behavior, and the moderating role of sex and co-ethnic density using an Asian American subsample (N = 177; 45.2% female; ages 10-12, 14-15; Cambodian, Chinese, Filipino, Hmong, Japanese, Korean, Laotian, Samoan, Vietnamese, and other ethnic backgrounds) of a longitudinal panel study over a span of 6 years. Cumulative neighborhood risk during early adolescence (ages 10-14) was significantly associated with internalizing behavior at mid-adolescence (age 15) controlling for prior levels of internalizing behavior. There was no evidence of moderation by co-ethnic density or sex, indicating that reducing neighborhood disadvantage may be a promising preventive measure to address mental health problems for both sexes of Asian American adolescents.

Resilience to COVID-19: Socioeconomic Disadvantage Associated With Positive Caregiver-Youth Communication and Youth Preventative Actions.

Socioeconomic disadvantage is associated with larger COVID-19 disease burdens and pandemic-related economic impacts. We utilized the longitudinal Adolescent Brain Cognitive Development Study to understand how family- and neighborhood-level socioeconomic disadvantage relate to disease burden, family communication, and preventative responses to the pandemic in over 6,000 youth-caregiver dyads. Data were collected at three timepoints (May-August 2020). Here, we show that both family- and neighborhood-level disadvantage were associated with caregivers' reports of greater family COVID-19 disease burden, less perceived exposure risk, more frequent caregiver-youth conversations about COVID-19 risk/prevention and reassurance, and greater youth preventative behaviors. Families with more socioeconomic disadvantage may be adaptively incorporating more protective strategies to reduce emotional distress and likelihood of COVID-19 infection. The results highlight the importance of caregiver-youth communication and disease-preventative practices for buffering the economic and disease burdens of COVID-19, along with policies and programs that reduce these burdens for families with socioeconomic disadvantage.

Neighborhood poverty, intergenerational mobility, and early developmental health in a population birth cohort.

Living in a neighborhood with high levels of intergenerational mobility is associated with better childhood cognition and behavior as well as adult health. Nevertheless, it is unclear if such differences originate earlier, and thus if neighborhood intergenerational mobility is associated with health differences at birth. To address this question, we examined whether neighborhood intergenerational mobility, independent of neighborhood poverty, was associated with low birth weight (LBW) in a population-based cohort of singleton children born in California in 2017 (n = 426,873). Although increased neighborhood mobility was associated with a decreased likelihood of LBW, it was no longer associated with LBW (OR = 0.98, CI = 0.96, 1.00) after adjusting for neighborhood poverty. Meanwhile, neighborhood poverty was associated with LBW (OR = 1.04, CI = 1.02, 1.05) after accounting for mobility, with the odds of LBW 9.4% higher among children born where neighborhood poverty was in the 90th percentile compared with children born where neighborhood poverty was in the 10th percentile. Findings indicate that neighborhood poverty, but not intergenerational mobility, is a robust and independent correlate of increased LBW births, and thus early developmental health. These findings also suggest that the role of neighborhood intergenerational mobility in child and adult health outcomes may emerge later in development, independent of LBW, or that the role of neighborhood intergenerational mobility in LBW may be indirectly mediated through exposure to neighborhood poverty.

School Climate, Cortical Structure, and Socioemotional Functioning: Associations across Family Income Levels.

School climates are important for children's socioemotional development and may also serve as protective factors in the context of adversity. Nevertheless, little is known about the potential neural mechanisms of such associations, as there has been limited research concerning the relation between school climate and brain structure, particularly for brain regions relevant for mental health and socioemotional functioning. Moreover, it remains unclear whether the role of school climate differs depending on children's socioeconomic status. We addressed these questions in baseline data for 9- to 10-year-olds from the Adolescent Brain and Cognitive Development study (analytic sample for socioemotional outcomes, n = 8887), conducted at 21 sites across the United States. Cortical thickness, cortical surface area, and subcortical volume were derived from T1-weighted brain magnetic resonance imaging. School climate was measured by youth report, and socioemotional functioning was measured by both youth and parent report. A positive school climate and higher family income were associated with lower internalizing and externalizing symptoms, with no evidence of moderation. There were no associations between school climate and cortical thickness or subcortical volume, although family income was positively associated with hippocampal volume. For cortical surface area, however, there was both a positive association with family income and moderation: There was an interaction between school climate and income for total cortical surface area and locally in the lateral orbitofrontal cortex. In all cases, there was an unexpected negative association between school climate and cortical surface area in the lower-income group. Consequently, although the school climate appears to be related to better socioemotional function for all youth, findings suggest that the association between a positive school environment and brain structure only emerges in the context of socioeconomic stress and adversity. Longitudinal data are needed to understand the role of these neural differences in socioemotional functioning over time.

Maternal Intimate Partner Violence Exposure and Autonomic Reactivity: Associations With Positive Parenting.

Intimate partner violence (IPV) can negatively impact parenting, posing a threat both to the wellbeing of mothers and their young children. Parenting may also be influenced by emotion regulation (ER), which can support parents' ability to navigate relational challenges or buffer against the influence of adverse experiences on parenting. Changes in maternal respiratory sinus arrhythmia (RSA) during parent-child interactions have been conceptualized as a psychophysiological index of ER. Competing theoretical models posit that RSA response may mediate or moderate the relation between IPV and parenting or may be independently associated with parenting, however, there is little prior evidence concerning these hypothesized associations. This study examined these associations in a sample of 125 low-income maltreating and comparison mothers and their 3- to 5-year-old children. Dyads completed a moderately challenging laboratory task, and positive parenting and maternal RSA were measured during the task. Maternal verbal IPV exposure, but not physical IPV, was associated with less positive parenting, while greater maternal RSA activation over the task was associated with more positive parenting. Maternal RSA activation did not mediate or moderate the relationship between IPV exposure and parenting, and this association did not differ by whether or not the mother had perpetrated child maltreatment. Consequently, verbal IPV exposure and greater RSA activation independently predicted positive parenting. Results suggest that interventions for IPV-exposed mothers of young children may benefit from ensuring psychological safety and improving maternal ER to promote positive parenting for at-risk children.

Evidence of susceptibility to autism risks associated with early life ambient air pollution: A systematic review.

BACKGROUND: Many studies have found associations between early life air pollution exposure and subsequent onset of autism spectrum disorder (ASD). However, characteristics that affect susceptibility remain unclear. OBJECTIVE: This systematic review examined epidemiologic studies on the modifying roles of social, child, genetic and maternal characteristics in associations between prenatal and early postnatal air pollution exposure and ASD. METHODS: A systematic literature search in PubMed and Embase was conducted. Studies that examined modifiers of the association between air pollution and ASD were included. RESULTS: A total of 19 publications examined modifiers of the associations between early life air pollution exposures and ASD. In general, estimates of effects on risk of ASD in boys were larger than in girls (based on 11 studies). Results from studies of effects of family education (2 studies) and neighborhood deprivation (2 studies) on air pollution-ASD associations were inconsistent. Limited data (1 study) suggest pregnant women with insufficient folic acid intake might be more susceptible to ambient particulate matter less than 2.5 µm (PM2.5) and 10 µm (PM10) in aerodynamic diameter, and to nitrogen dioxide (NO2). Children of mothers with gestational diabetes had increased risk of ozone-associated ASD (1 study). Two genetic studies reported that copy number variations may amplify the effect of ozone, and MET rs1858830 CC genotype may augment effects of PM and near-roadway pollutants on ASD. CONCLUSIONS: Child's sex, maternal nutrition or diabetes, socioeconomic factors, and child risk genotypes were reported to modify the effect of early-life air pollutants on ASD risk in the epidemiologic literature. However, the sparsity of studies on comparable modifying hypotheses precludes conclusive findings. Further research is needed to identify susceptible populations and potential targets for preventive intervention.

Ambient air pollution associated with lower academic achievement among US children: A nationwide panel study of school districts.

BACKGROUND: Ambient air pollution is an important environmental exposure and has been linked with impaired cognitive function. Few studies have investigated its impact on children's academic performance on a nationwide level. We hypothesize that higher ambient air pollution concentrations will be associated with lower average academic test scores. METHODS: We investigated three prevalent ambient air pollutants: PM2.5, NO2 and ozone, and their associations with the average academic test scores, at the Geographic School District (GSD) level, of the third to eighth grade students in the United States from 2010 to 2016. We applied multivariate linear regression and controlled for urbanicity, socioeconomic status, student racial/ethnic compositions, and individual intercepts for each district-grade level and each year. RESULTS: We found that an interquartile range increase in PM2.5 concentrations was associated with a 0.007 (95% confidence interval: 0.005, 0.009) SD lower average math test scores, and a 0.004 (95% confidence interval: 0.002, 0.005) SD lower average English language/arts test scores. Similar associations were observed for NO2 and ozone on math, and for NO2 on English language/arts. The magnitudes of these associations are equivalent to the effects of short-term reductions of thousands of dollars in district median household income. The reductions in test scores were larger for GSDs with higher socioeconomic status, though most associations remained negative at all socioeconomic levels. CONCLUSIONS: Our results show that ambient air pollution within a GSD is associated with lower academic performance among children. Further improving air quality may benefit children's overall academic achievement and socioeconomic attainment across the lifespan.

Resilience to COVID-19: Socioeconomic Disadvantage Associated With Higher Positive Parent-youth Communication and Youth Disease-prevention Behavior.

Socioeconomic disadvantage is associated with larger COVID-19 disease burdens and pandemic-related economic impacts. We utilized the longitudinal Adolescent Brain Cognitive Development Study to understand how family- and neighborhood-level socioeconomic disadvantage relate to disease burden, family communication, and preventative responses to the pandemic in over 6,000 youth-parent/caregiver dyads. Data were collected at three timepoints (May to August 2020). Here, we show that both family- and neighborhood-level disadvantage were associated with parents’ reports of greater family COVID-19 exposure risk and diagnoses, less perceived exposure risk, more frequent parent-youth conversations about COVID-19 risk/prevention and reassurance, and greater youth preventative behaviors. More disadvantaged families may be adaptively incorporating more protective strategies to reduce emotional distress and likelihood of COVID-19 infection. The results highlight the importance of parent-youth communication and disease-preventative practices for buffering the economic and disease burdens of COVID-19, along with policies and programs that reduce these burdens for families with socioeconomic disadvantage.

Association of Local Variation in Neighborhood Disadvantage in Metropolitan Areas With Youth Neurocognition and Brain Structure.

Importance: Neighborhood disadvantage is an important social determinant of health in childhood and adolescence. Less is known about the association of neighborhood disadvantage with youth neurocognition and brain structure, and particularly whether associations are similar across metropolitan areas and are attributed to local differences in disadvantage. Objective: To test whether neighborhood disadvantage is associated with youth neurocognitive performance and with global and regional measures of brain structure after adjusting for family socioeconomic status and perceptions of neighborhood characteristics, and to assess whether these associations (1) are pervasive or limited, (2) vary across metropolitan areas, and (3) are attributed to local variation in disadvantage within metropolitan areas. Design, Setting, and Participants: This cross-sectional study analyzed baseline data from the Adolescent Brain and Cognitive Development (ABCD) Study, a cohort study conducted at 21 sites across the US. Participants were children aged 9.00 to 10.99 years at enrollment. They and their parent or caregiver completed a baseline visit between October 1, 2016, and October 31, 2018. Exposures: Neighborhood disadvantage factor based on US census tract characteristics. Main Outcomes and Measures: Neurocognition was measured with the NIH Toolbox Cognition Battery, and T1-weighted magnetic resonance imaging was used to assess whole-brain and regional measures of structure. Linear mixed-effects models examined the association between neighborhood disadvantage and outcomes after adjusting for sociodemographic factors. Results: Of the 11 875 children in the ABCD Study cohort, 8598 children (72.4%) were included in this analysis. The study sample had a mean (SD) age of 118.8 (7.4) months and included 4526 boys (52.6%). Every 1-unit increase in the neighborhood disadvantage factor was associated with lower performance on 6 of 7 subtests, such as Flanker Inhibitory Control and Attention (unstandardized Β = -0.5; 95% CI, -0.7 to -0.2; false discovery rate (FDR)-corrected P = .001) and List Sorting Working Memory (unstandardized Β = -0.7; 95% CI, -1.0 to -0.3; FDR-corrected P < .001), as well as on all composite measures of neurocognition, such as the Total Cognition Composite (unstandardized Β = -0.7; 95% CI, -0.9 to -0.5; FDR-corrected P < .001). Each 1-unit increase in neighborhood disadvantage was associated with lower whole-brain cortical surface area (unstandardized Β = -692.6 mm2; 95% CI, -1154.9 to -230.4 mm2; FDR-corrected P = .007) and subcortical volume (unstandardized Β = -113.9 mm3; 95% CI, -198.5 to -29.4 mm3; FDR-corrected P = .03) as well as with regional surface area differences, primarily in the frontal, parietal, and temporal lobes. Associations largely remained after adjusting for perceptions of neighborhood safety and were both consistent across metropolitan areas and primarily explained by local variation in each area. Conclusions and Relevance: This study found that, in the US, local variation in neighborhood disadvantage was associated with lower neurocognitive performance and smaller cortical surface area and subcortical volume in young people. The findings demonstrate that neighborhood disadvantage is an environmental risk factor for neurodevelopmental and population health and enhancing the neighborhood context is a promising approach to improving the health and development of children and adolescents.

Early childhood poverty and adult executive functioning: Distinct, mediating pathways for different domains of executive functioning.

Executive functioning in adulthood is associated with early-in-life disadvantage. Furthermore, distinct and independent underlying processes account for differences in specific domains of adult executive functioning. The duration of poverty from birth to age 9 is associated with reduced adult inhibitory control assessed by the Flanker task (n = 233, M = 23.52 years). This effect is largely explained by lower levels of maternal responsiveness in adolescence. Early poverty also related to worse working memory in adulthood, and this effect is partially explained by elevated allostatic load during adolescence, an index of chronic physiological stress.

Fine particulate matter exposure during childhood relates to hemispheric-specific differences in brain structure.

BACKGROUND: Emerging findings have increased concern that exposure to fine particulate matter air pollution (aerodynamic diameter ≤ 2.5 µm; PM2.5) may be neurotoxic, even at lower levels of exposure. Yet, additional studies are needed to determine if exposure to current PM2.5 levels may be linked to hemispheric and regional patterns of brain development in children across the United States. OBJECTIVES: We examined the cross-sectional associations between geocoded measures of concurrent annual average outdoor PM2.5 exposure, regional- and hemisphere-specific differences in brain morphometry and cognition in 10,343 9- and 10- year-old children. METHODS: High-resolution structural T1-weighted brain magnetic resonance imaging (MRI) and NIH Toolbox measures of cognition were collected from children at ages 9-10 years. FreeSurfer was used to quantify cortical surface area, cortical thickness, as well as subcortical and cerebellum volumes in each hemisphere. PM2.5 concentrations were estimated using an ensemble-based model approach and assigned to each child's primary residential address collected at the study visit. We used mixed-effects models to examine regional- and hemispheric- effects of PM2.5 exposure on brain estimates and cognition after considering nesting of participants by familial relationships and study site, adjustment for socio-demographic factors and multiple comparisons. RESULTS: Annual residential PM2.5 exposure (7.63 ± 1.57 µg/m3) was associated with hemispheric specific differences in gray matter across cortical regions of the frontal, parietal, temporal and occipital lobes as well as subcortical and cerebellum brain regions. There were hemispheric-specific associations between PM2.5 exposures and cortical surface area in 9/31 regions; cortical thickness in 22/27 regions; and volumes of the thalamus, pallidum, and nucleus accumbens. We found neither significant associations between PM2.5 and task performance on individual measures of neurocognition nor evidence that sex moderated the observed associations. DISCUSSION: Even at relatively low-levels, current PM2.5 exposure across the U.S. may be an important environmental factor influencing patterns of structural brain development in childhood. Prospective follow-up of this cohort will help determine how current levels of PM2.5 exposure may affect brain development and subsequent risk for cognitive and emotional problems across adolescence.

Systemic inflammation is associated with differential neural reactivity and connectivity to affective images.

Systemic inflammation is increasingly appreciated as a predictor of health and well-being. Further, inflammation has been shown to influence and be influenced by affective experiences. Although prior work has substantiated associations between inflammatory and affective processes, fewer studies have investigated the neurobiological correlates that underlie links between systemic, low-grade inflammation and affective reactivity. Thus, the current study examined whether markers of systemic inflammation (i.e. interleukin-6, C-reactive protein) are associated with differential patterns of neural activation and connectivity in corticolimbic regions in response to affective images. We investigated this question in a sample of 66 adults (44 women, M age = 54.98 years, range = 35-76) from the Midlife in the United States study. Higher levels of inflammation were associated with lower activity in limbic regions (i.e. amygdala, hippocampus, anterior insula, temporal pole) when viewing positive (vs neutral) images. Higher levels of inflammation were also associated with greater connectivity between the hippocampus and the medial prefrontal cortex in response to positive images. Inflammatory markers were not associated with significant differences in activation or connectivity to negative images. These findings highlight the utility of health neuroscience approaches in demonstrating that physiological processes such as inflammation are related to how our brains respond to affective information.