About

Daniel Hackman, PhD, is an associate professor at the USC Suzanne Dworak-Peck School of Social Work. His research examines how social and environmental contexts influence developmental trajectories of health and well-being across the lifecourse. He investigates the impact of socioeconomic, family, and neighborhood factors, particularly those in early childhood, on the development of cognitive, affective, and biological systems that contribute to healthy development. His focus includes executive function and stress reactivity at behavioral, physiological, and neurobiological levels. Hackman is also interested in social experiences and mechanisms that promote health and reduce risk processes, aiming to leverage this work to inform more effective policies and programs to address socioeconomic disparities. He employs a multi-method, interdisciplinary approach, often longitudinal, integrating tools from population health, psychology, neuroscience, and social work. Recently, he developed a virtual reality-based experimental model to test hypotheses concerning neighborhood effects on cognition, emotion, physiology, and health across development. Prior to USC, Hackman was a Robert Wood Johnson Health & Society Scholar at the University of Wisconsin-Madison. He completed his PhD in clinical psychology at the University of Pennsylvania and has experience as a policy advocate in the nonprofit sector focused on chronic disease prevention in childhood and adolescence.

Research topics

• Medicine
• Environmental health
• Ecology
• Chemistry
• Developmental psychology
• Environmental chemistry
• Psychology
• Psychiatry
• Neuroscience
• Demography
• Biology
• Environmental science

Selected publications

• The Relationship of School Modality With Stress and Mental Health During the COVID-19 Pandemic: Variation Across Sociodemographic Groups

  AERA Open · 2025-07-01

  articleOpen accessSenior authorCorresponding

  The COVID-19 pandemic and school closures adversely affected adolescents’ mental health and well-being, with the weight of evidence indicating worse outcomes for students attending school remotely or in a hybrid modality compared to fully in person. We leverage survey data from the Adolescent Brain Cognitive Development SM Study (ABCD Study ® ) collected from 6,245 adolescents (mean age = 13.2) during the 2020–2021 school year to investigate the moderating effects of race/ethnicity, household income, and neighborhood disadvantage on the relationship between 2020–2021 school modality and outcomes including perceived stress, sadness, and positive affect. For relatively advantaged students, our results corroborate prior findings that students in remote or hybrid schooling report worse mental health outcomes than students who attended fully in person. However, this pattern between schooling modality and mental health disappears or reverses for relatively disadvantaged students. Given substantial within-group variation, these findings underscore the importance of considering varied student needs in developing mental health supports.

  PublisherDOI

• Sources of outdoor air pollution exposure and child brain network development across the United States

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-25 · 1 citations

  preprintOpen access

  Abstract Ambient fine particulate matter (PM 2.5 ) pollution is a heterogeneous mixture of chemicals with documented neurotoxic effects. Developmental neuroimaging literature has linked childhood PM 2.5 exposure to alterations in brain morphology, microarchitecture, and function, with implications for cognition and psychopathology. However, the extant literature remains largely cross-sectional and often considers PM 2.5 a single pollutant, rather than a heterogeneous mixture of chemicals from different sources. This work addresses these gaps by leveraging estimates of exposure to six PM 2.5 sources derived from positive matrix factorization, and longitudinal neuroimaging data from a large, geographically-diverse sample of Adolescent Brain Cognitive Development Study youth ( N = 6,291) from across the United States (U.S.). To identify exposure-related differences in brain function and assess their geographical generalizability, we used a predictive modeling approach to assess both differences in functional brain network connectivity during childhood (9-11 years of age) and changes in functional brain network connectivity during the transition to adolescence (9-13 years of age) related to PM 2.5 exposure. Childhood PM 2.5 exposure from traffic emissions and industrial/residual fuel burning were linked to mixed patterns of both stronger and weaker connectivity of sensorimotor networks at ages 9-11 years. Conversely, childhood exposures to secondary pollutants (i.e., ammonium sulfates, nitrates) were linked to largely stronger connectivity of brain networks underlying higher-order cognition that decreased over the following two years. However, these patterns of exposure-related functional connectivity identified in youth across the U.S. better represented youth living in the northeast as compared to youth living in the west. Altogether, this work provides insights into the neurotoxicity of outdoor air pollution exposure in developing sensory and motor systems and potential for biomarkers of eventual psychopathology.

  PublisherOA PDFDOI

• Within- and between-study site variations in ambient air pollution exposure at ages 9-10 years in the Adolescent Brain Cognitive Development (ABCD) Study

  2025-06-25

  preprintOpen access

  Minority and socioeconomically disadvantaged populations are disproportionately exposed to elevated levels of air pollution. This environmental injustice exhibits distinct patterns and predictors across regions of the United States, which we investigate by leveraging baseline data (2016-2018) from the Adolescent Brain Cognitive Development (ABCD) Study, the largest longitudinal study of child brain development in the United States. Specifically, we examine within- and between-site variability in exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) among 9- to 10-year-old participants. Using geocoded residential addresses and hybrid spatiotemporal models, air pollution exposure disparities were estimated by site, and by family- and neighborhood-level socioeconomic metrics within each site. Results indicate substantial variation in race/ethnicity- and class-based gaps in air pollution exposure across the 21 ABCD study sites. Overall, Hispanic/Latinx and Black children experienced higher average levels of PM2.5 and NO2 compared to their white counterparts, while children in neighborhoods with lower socioeconomic status exhibited elevated exposure regardless of race or ethnicity. Within-site disparities highlighted local environmental injustices, as well, with notable differences in pollution levels across neighborhoods at different levels of disadvantage. Elevated air pollution exposure in minoritized communities aligns with well-documented systemic inequities in built environment conditions and institutional resources, exacerbating health disparities. This study highlights the importance of integrating environmental justice into public health and policy initiatives, leveraging the multisite design of the ABCD Study to provide insights for promoting health equity in child and adolescent development within and across regions in the United States.

  PublisherOA PDFDOI

• Fine particulate matter air pollution and longitudinal gray matter development changes during early adolescence: variation by neighborhood disadvantage level

  Environment International · 2025-05-29 · 2 citations

  articleOpen access

  exposure was independently associated with greater age-related cortical thinning in the frontal regions, cingulate, and insula, but smaller age-related cortical thickening in temporal regions. Findings have policy implications for air quality improvements alongside investment in disadvantaged neighborhoods to bolster adolescent brain development.

  PublisherDOI

• Outdoor Air Pollution Is Related to Amygdala Subregion Volume and Apportionment in Early Adolescence

  Biological Psychiatry Global Open Science · 2025-06-03 · 1 citations

  articleOpen access

  Outdoor air pollution exposure is associated with structural and functional brain differences, and an increased risk for psychopathology. Although the neural mechanisms remain unclear, air pollutants may impact mental health by altering brain regions implicated in psychopathology, such as the amygdala. Here, we examine the association between ambient air pollution exposure and amygdala subregion volumes in 9–10-year-olds. Cross-sectional data from 4,473 (55.4% male) Adolescent Brain Cognitive Development SM (ABCD) Study® participants were leveraged. Air pollution exposure was estimated based on each participant’s primary residential address. Using the CIT168 atlas, we quantified total amygdala and 9 subregion volumes from T1- and T2-weighted images. We investigated associations between criteria pollutants (i.e., fine particulate matter [PM 2.5 ], nitrogen dioxide, and ground-level ozone), 15 PM 2.5 components, and amygdala subregion volumes and relative volume fractions using both single-pollutant linear mixed-effects regression and partial least squares correlation (PLSC) co-exposure modeling approaches. No significant associations were detected using single-pollutant models. Rather, in examining mixtures of exposures with PLSC, one latent dimension (52% variance explained) captured a positive association between calcium and several basolateral subregions. Latent dimensions were also identified for amygdala relative volume fractions (ranging from 30% to 82% variance explained), with PM 2.5 and component co-exposure associated with increases in lateral, but decreases in medial and central, relative volume fractions. Fine particulate matter and its components are associated with distinct amygdala differences, potentially playing a role in risk for adolescent mental health problems.

  PublisherDOI

• Sleep moderates how prenatal and childhood pollutant exposure impacts white matter microstructural integrity in adolescence

  npj Biological Timing and Sleep · 2025-11-04

  articleOpen access

  Air pollution is a ubiquitous neurotoxicant linked to altered structural brain connectivity. Sleep may offer neuroprotection through its roles in brain waste clearance and immune regulation. Using Fitbit-derived sleep data and multi-shell diffusion MRI from 2178 children (ages 10–13) in the ABCD Study®, we examined whether sleep moderated associations between prenatal and childhood exposure to PM2.5, NO2, and O3 and white matter microstructure. Restriction spectrum imaging yielded restricted normalized isotropic (RNI) and directional (RND) metrics, averaged across tracts. Pollution exposure was estimated at prenatal and childhood (ages 9–10) residences. Linear mixed-effects models tested sleep-by-pollution interactions on RNI/RND. Childhood NO2 and prenatal O3 interacted with sleep duration and efficiency, respectively, to influence RND. Among children with similar pollutant exposure, those with longer sleep duration and higher sleep efficiency had lower RND than peers with poorer sleep. This suggests that healthy sleep may buffer adverse effects of air pollution on white matter integrity.

  PublisherOA PDFDOI

• Ambient Pollution Components and Sources are Associated with Hippocampal Architecture and Memory in Pre-Adolescents

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-09

  preprintOpen access

  Background: Ambient air pollution poses significant risks to brain health. Hippocampal structure and function are particularly vulnerable, yet the extent to which they are associated with air pollution in children remains unclear. We therefore conducted multi-pollutant mixture analyses to examine how air pollution influences hippocampal architecture and memory performance in late childhood. Methods: , and ozone exposures, and measures of hippocampal microstructure and volume in children aged 9-11 years (n = 7,940) We adjusted for demographic, socioeconomic, and neuroimaging confounds. We also tested whether air pollutants were associated with hippocampal-dependent list-learning memory performance to examine functional implications of air pollution exposure. Shared variance refers to the proportion of total covariance between variable sets captured by each latent dimension in the multivariate relationship. Findings: In the first latent dimension, greater exposure to organic carbon and ozone was associated with differential hippocampal diffusion (72% of shared variance), whereas the second latent dimension linked elemental carbon and iron to hippocampal diffusion (24% of shared variance). Source-based analyses identified biomass burning and traffic pollution as key contributors (61% and 32% variance, respectively). Volumetric analyses revealed higher copper and zinc exposure correlated with smaller hippocampal subregion volumes (left head, right body, tail; 77% variance), whereas lower nickel levels correlated with smaller right head volume (12% variance). Higher industrial and traffic pollutants were also associated with smaller hippocampal volumes (75% variance). We found two latent dimensions (67% and 23% variance, respectively) showing poorer learning, immediate recall, and mnemonic interference performance linked to higher calcium, elemental carbon, and zinc, and organic carbon, alongside lower copper exposure. Finally, hippocampal diffusion (higher free water/lower hindered extracellular diffusion; 83% variance) and smaller tail volumes (96% variance) were linked to poorer RAVLT recall. Interpretation: These results underscore the complex relationship between air pollution exposure and hippocampal architecture and cautions that such structural changes may either presage or reflect subtle differences in neurocomputational mechanisms associated with learning and memory performance in children. Funding: U.S. National Institute of Environmental Health Sciences.

  PublisherOA PDFDOI

• Sleep duration and efficiency moderate the effects of prenatal and childhood ambient pollutant exposure on global white matter microstructural integrity in adolescence

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-16

  preprintOpen access

  Abstract Background Air pollution is a ubiquitous neurotoxicant associated with alterations in structural connectivity. Good habitual sleep may be an important protective lifestyle factor due to its involvement in the brain waste clearance and its bidirectional relationship with immune function. Wearable multisensory devices may provide more objective measures of sleep quantity and quality. We investigated whether sleep duration and efficiency moderated the relationship between prenatal and childhood pollutant exposure and whole-brain white matter microstructural integrity at ages 10-13 years. Methods We used multi-shell diffusion-weighted imaging data collected on 3T MRI scanners and objective sleep data collected with Fitbit Charge 2 from the 2-year follow-up visit for 2178 subjects in the Adolescent Brain Cognitive Development Study®. White matter tracts were identified using a probabilistic atlas. Restriction spectrum imaging was performed to extract restricted normalized isotropic (RNI) and directional (RND) signal fraction parameters for all white matter tracts, then averaged to calculate global measures. Sleep duration was calculated by summing the time spent in each sleep stage; sleep efficiency was calculated by dividing sleep duration by time spent in bed. Using an ensemble-based modeling approach, air pollution concentrations of PM 2.5 , NO 2 , and O 3 were assigned to each child’s residential addresses during the prenatal period (9-month average before birthdate) as well as at ages 9- 10 years. Multi-pollutant linear mixed effects models assessed the associations between global RNI and RND and sleep-by-pollutant interactions, adjusting for appropriate covariates. Results Sleep duration interacted with childhood NO 2 exposure and sleep efficiency interacted with prenatal O 3 exposure to affect RND at ages 10-13 years. Longer sleep duration and higher sleep efficiency in the context of higher pollutant exposure was associated with lower RND compared to those with similar pollutant exposure but shorter sleep duration and lower sleep efficiency. Conclusions Low-level air pollution poses a risk to brain health in youth, and healthy sleep duration and efficiency may increase resilience to its harmful effects on white matter microstructural integrity. Future studies should evaluate the generalizability of these results in more diverse cohorts as well as utilize longitudinal data to understand how sleep may impact brain health trajectories in the context of pollution over time.

  PublisherOA PDFDOI

• The potential effects of hypothetical PM2.5 interventions on childhood autism in different neighborhood socioeconomic contexts

  American Journal of Epidemiology · 2025-02-06

  articleOpen access

  Particulate air pollution is associated with autism spectrum disorder (ASD), with disadvantaged neighborhoods potentially increasing vulnerability due to stress or other social determinants of health. Understanding the impact of air pollution interventions on ASD incidence across neighborhood disadvantage levels can guide policies to protect vulnerable populations. We examined 2 sets of hypothetical particulate matter (PM)2.5 interventions: percentage reduction and regulatory standards as thresholds, to assess their potential effects on ASD cumulative incidence. Using G-computation under a counterfactual framework, we estimated changes in the cumulative incidence of ASD by age 5 under hypothetical interventions compared to observed exposures. Our study involved a birth cohort of 318 298 children born between 2001-2014 in Southern California, with 4548 diagnosed with ASD by age 5. Pregnancy average PM2.5 and neighborhood disadvantage were assigned to residential addresses. Adjusted Cox regression models were applied to estimate ASD cumulative incidence. Reducing pregnancy average PM2.5 by 30% or below 9 μg/m3 would have prevented 10.6 (95% CI, 3.6-19.2) and 12.5 (2.7-23.6) ASD cases per 10 000 children, respectively. The decreases in ASD cumulative incidence under hypothetical interventions were similar across neighborhood disadvantage levels. These findings suggest that reducing ambient PM2.5 levels to meet or surpass current standards could help prevent ASD.

  PublisherOA PDFDOI

• Sources and components of fine air pollution exposure and brain morphology in preadolescents

  The Science of The Total Environment · 2025-04-23 · 3 citations

  article
  PublisherDOI

Frequent coauthors

• Megan M. Herting

  36 shared

• Rob McConnell

  University of Southern California

  31 shared

• Martha J. Farah

  University of Pennsylvania

  26 shared

• Jiu‐Chiuan Chen

  University of Southern California

  22 shared

• Joel Schwartz

  Harvard University

  19 shared

• Carlos Cardenas‐Iniguez

  University of Southern California

  16 shared

• Kiros Berhane

  Columbia University

  16 shared

• Devyn L. Cotter

  University of Southern California

  15 shared

Awards & honors

• Robert Wood Johnson Foundation Health and Society Scholar (2…