Burden of Environmental Adversity Associated With Psychopathology, Maturation, and Brain Behavior Parameters in...

Low socioeconomic status (L-SES) and the experience of traumatic stressful events (TSEs) are environmental factors implicated in behavioral deficits, abnormalities in brain development, and accelerated maturation. However, the relative contribution of these environmental factors is understudied.

To compare the association of L-SES and TSEs with psychopathology, puberty, neurocognition, and multimodal neuroimaging parameters in brain maturation.

The Philadelphia Neurodevelopmental Cohort is a community-based study examining psychopathology, neurocognition, and neuroimaging among participants recruited through the Children's Hospital of Philadelphia pediatric network. Participants are youths aged 8 to 21 years at enrollment with stable health and fluency in English. The sample of 9498 participants was racially (5298 European ancestry [55.8%], 3124 African ancestry [32.9%], and 1076 other [11.4%]) and economically diverse. A randomly selected subsample (n = 1601) underwent multimodal neuroimaging. Data were collected from November 5, 2009, through December 30, 2011, and analyzed from February 1 through November 7, 2018.

The following domains were examined: (1) clinical, including psychopathology, assessed with a structured interview based on the Schedule for Affective Disorders and Schizophrenia for School-Age Children, and puberty, assessed with the Tanner scale; (2) neurocognition, assessed by the Penn Computerized Neurocognitive Battery; and (3) multimodal magnetic resonance imaging parameters of brain structure and function.

A total of 9498 participants were included in the analysis (4906 [51.7%] female; mean [SD] age, 14.2 [3.7] years). Clinically, L-SES and TSEs were associated with greater severity of psychiatric symptoms across the psychopathology domains of anxiety/depression, fear, externalizing behavior, and the psychosis spectrum. Low SES showed small effect sizes (highest for externalizing behavior, 0.306 SD; 95% CI, 0.269 to 0.342), whereas TSEs had large effect sizes, with the highest in females for anxiety/depression (1.228 SD; 95% CI, 1.156 to 1.300) and in males for the psychosis spectrum (1.099 SD; 95% CI, 1.032 to 1.166). Both were associated with early puberty. Cognitively, L-SES had moderate effect sizes on poorer performance, the greatest being on complex cognition (-0.500 SD 95% CI, -0.536 to -0.464), whereas TSEs were associated with slightly better memory (0.129 SD; 95% CI, 0.084 to 0.174) and poorer complex reasoning (-0.109 SD; 95% CI, -0.154 to -0.064). Environmental factors had common and distinct associations with brain structure and function. Structurally, both were associated with lower volume, but L-SES had correspondingly lower gray matter density, whereas TSEs were associated with higher gray matter density. Functionally, both were associated with lower regional cerebral blood flow and coherence and with accelerated brain maturation.

Low SES and TSEs are associated with common and unique differences in symptoms, neurocognition, and structural and functional brain parameters. Both environmental factors are associated with earlier completion of puberty by physical features and brain parameters. These findings appear to underscore the need for identifying and preventing adverse environmental conditions associated with neurodevelopment.