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Prenatal stress has long been associated with risk for behavioral problems throughout childhood (Hentges et al., 2019). Recent work points to atypical cortical functioning in infancy as being a mechanism from which risk from prenatal stress exposure is transmitted (Humphreys et al., 2020; Demers et al., 2021), with continuing long-term effects on neurodevelopment (Craig et al., 2014; Sandman et al., 2015; Sandman et al., 2018) and associated neuropsychiatric risk (Van den Bergh et al., 2018). However, few investigations have focused on the effects of prenatal stress on cortical functioning in early childhood, a period of peak developmental plasticity. Doing so can help future scientists develop neurodevelopmentally-informed early interventions to mitigate risk for affective problems later in childhood. To uncover these neural risk mechanisms, the present study tested this question in the context of a natural experiment in which pregnant women were exposed to stress associated with a natural disaster, specifically, Hurricane Harvey in Houston, Texas. At a baseline assessment, we assessed mothers’ (n = 772) stress at the time of the natural disaster and mental health functioning using validated instruments as described in recent work (Paquin et al., 2021). A sub-sample (n=47) of pregnant mothers and children were followed prospectively and participated in a laboratory session when children reached 24 months of age. EEG was recorded “at rest” during this session using a 64 channel array, as following standard paradigms. Specifically, children sat in a quiet alert state in an EEG recording chamber while watching a wheel full of brightly colored bingo balls spinning for 2-minutes. EEG activity will be processed according to standard practices using the Harvard Automated Processing Processing Pipeline for Electroencephalography (HAPPE) Pipeline (Gabbard et al., 2018). Mothers also reported on child behavior using the Child Behavior Checklist (CBCL) (Achenbach & Rescorla 2001). In line with previous work, (Marshall & Fox, 2004), we hypothesize that children whose mothers indicated higher levels of stress during pregnancy would show more immature or delayed patterns of cortical maturation, as indicated by relatively higher proportions of low-frequency (theta) activity and lower proportions of high-frequency (alpha) when compared with children whose mother reported less prenatal stress. We also expect children with higher prenatal stress exposure to show relatively lower peak alpha frequencies over the resting period than children whose mothers’ reported less stress during pregnancy. Thus, we expect that profiles of more immature or delayed cortical maturation would be associated with higher CBCL scores, suggesting that these children are at greater risk for temperamental difficulties later in life.