Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 μm (PM2.5) may increase the risk for Alzheimer’s disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer’s disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer’s disease associated with exposure. Participants included older females (n = 998; aged 73–87) enrolled in both the Women’s Health Initiative Study of Cognitive Aging and the Women’s Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999–2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1–3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005–06; MRI-2: 2009–10). Subjects were assigned Alzheimer’s disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer’s disease), developed by supervised machine learning and validated with data from the Alzheimer’s Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 μg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1–3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer’s disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1–3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer’s disease risk, independent of cerebrovascular damage.

Objective Neighborhood greenspace improves mental health of urban-dwelling populations, but its putative neurobehavioral benefits in adolescents remain unclear. We conducted a prospective study on urban-dwelling adolescents to examine the association between greenspace in residential neighborhood and aggressive behaviors. Method Participants (n = 1,287) of the Risk Factors for Antisocial Behavior Study, a multi-ethnic cohort of twins and triplets born in 1990–1995 and living in Southern California, were examined in 2000–2012 (aged 9 to 18 years) with repeated assessments of their aggressive behaviors by the parent-reported Child Behavior Checklist. Normalized Difference Vegetation Index (NDVI) derived from satellite imagery was used as a proxy for residential neighborhood greenspace aggregated over various spatiotemporal scales prior to each assessment. Multilevel mixed-effects models were used to estimate the effects of greenspace on aggressive behaviors, adjusting for within-family/within-individual correlations and other potential confounders. Results Both short-term (1- to 6-months) and long-term (1- to 3-years) exposures to greenspace within 1,000-meters surrounding residences were associated with reduced aggressive behaviors. The benefit of increasing vegetation over the range (~0.12 in NDVI) commonly seen in urban environments was equivalent to approximately 2 to 2.5 years of behavioral maturation. Sociodemographic factors (e.g., age, gender, race/ethnicity, and socioeconomic status) and neighborhood quality did not confound or modify these associations, and the benefits remained after accounting for temperature. Conclusion Our novel findings support the benefits of neighborhood greenspace in reducing aggressive behaviors of urban-dwelling adolescents. Community-based interventions are needed to determine the efficacy of greenspace as a preemptive strategy to reduce aggressive behaviors in urban environments.

Outdoor air pollution has been recognized as a novel environmental neurotoxin. Studies have begun to use brain Magnetic Resonance Imaging (MRI) to investigate how air pollution may adversely impact developing brains. A systematic review was conducted to evaluate and synthesize the reported evidence from MRI studies on how early-life exposure to outdoor air pollution affects neurodevelopment. Using PubMed and Web of Knowledge, we conducted a systematic search, followed by structural review of original articles with individual-level exposure data and that met other inclusion criteria. Six studies were identified, each sampled from 3 cohorts of children in Spain, The Netherlands, and the United States. All studies included a one-time assessment of brain MRI when children were 6–12 years old. Air pollutants from traffic and/or regional sources, including polycyclic aromatic hydrocarbons (PAHs), nitrogen dioxide, elemental carbon, particulate matter (<2.5 or <10 μm), and copper, were estimated prenatally (n = 1), during childhood (n = 3), or both (n = 2), using personal monitoring and urinary biomarkers (n = 1), air sampling at schools (n = 4), or a land-use regression (LUR) modeling based on residences (n = 2). Associations between exposure and brain were noted, including: smaller white matter surface area (n = 1) and microstructure (n = 1); region-specific patterns of cortical thinness (n = 1) and smaller volumes and/or less density within the caudate (n = 3); altered resting-state functional connectivity (n = 2) and brain activity to sensory stimuli (n = 1). Preliminary findings suggest that outdoor air pollutants may impact MRI brain structure and function, but limitations highlight that the design of future air pollution-neuroimaging studies needs to incorporate a developmental neurosciences perspective, considering the exposure timing, age of study population, and the most appropriate neurodevelopmental milestones.

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Mounting evidence indicates that early-life exposure to particulate air pollutants pose threats to children’s cognitive development, but studies about the neurotoxic effects associated with exposures during adolescence remain unclear. We examined whether exposure to ambient fine particles (PM2.5) at residential locations affects intelligence quotient (IQ) during pre-/early- adolescence (ages 9–11) and emerging adulthood (ages 18–20) in a demographically-diverse population (N = 1,360) residing in Southern California. Increased ambient PM2.5 levels were associated with decreased IQ scores. This association was more evident for Performance IQ (PIQ), but less for Verbal IQ, assessed by the Wechsler Abbreviated Scale of Intelligence. For each inter-quartile (7.73 μg/m3) increase in one-year PM2.5 preceding each assessment, the average PIQ score decreased by 3.08 points (95% confidence interval = [-6.04, -0.12]) accounting for within-family/within-individual correlations, demographic characteristics, family socioeconomic status (SES), parents’ cognitive abilities, neighborhood characteristics, and other spatial confounders. The adverse effect was 150% greater in low SES families and 89% stronger in males, compared to their counterparts. Better understanding of the social disparities and sexual dimorphism in the adverse PM2.5–IQ effects may help elucidate the underlying mechanisms and shed light on prevention strategies.