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Prenatal risk including substance exposure is increasingly linked to deficits in regulatory processes from infancy into childhood. Less is known about regulation during adolescence when neural rewiring may either exacerbate or ameliorate the earlier effects of prenatal risk. The regulatory system is complex and is reflected in autonomic (ANS) systems. The sympathetic branch (SNS) of the ANS can be measured via pre-ejection period (PEP) and skin conductance levels (SCL) while the parasympathetic branch (PNS) is commonly measured by respiratory sinus arrhythmia (RSA). For SCL, PEP and RSA, measures of baseline of reactivity (change during environmental challenge) have been used to assess autonomic regulation. Although existing studies have found sex differences in autonomic regulation among substance-exposed infants, missing from this literature are tests of possible moderation of prenatal risk with postnatal environmental risk and biological sex to autonomic functioning in early school age and early adolescence.
This study investigated hypothesized pathways from early risk (i.e., prenatal cocaine and other substance exposure; PCE) to autonomic functioning during kindergarten and early adolescence. The sample included 216 mother-child dyads (49% boys) from a prospective study of prenatal cocaine exposure (116 cocaine-exposed, 100 non-cocaine exposed). Assessments occurred in early-infancy (1 month), late-infancy (7-13 months), toddler age (24 months), early-preschool age (36 months), late-preschool age (48 months), kindergarten age (60 months) and EA (Myears = 13.26, SD = .83; see Table 1). PCE was ascertained by a combination of self-report, maternal hair, and urine toxicology assessments at delivery. Postnatal environmental risk was a composite of maternal postnatal substance use, psychopathology, violence exposure, and caregiving instability from birth to 48 months. Autonomic reactivity was assessed during a frustration task in kindergarten and during the Trier Social Stress Task (TSST) in early adolescence (12-14 years). Change in RSA from baseline to frustration (Kindergarten) or TSST (adolescence) were calculated and standardized to index parasympathetic reactivity. Changes in SCL during kindergarten and changes in PEP during early adolescence were standardized and used to assess sympathetic reactivity.
Path analysis was used to examine the direct effects of cocaine and other substance exposure during pregnancy on reactivity at kindergarten age and in early adolescence. Interactions between prenatal exposure, postnatal environmental risk, and sex were also explored. The model provided an adequate fit to the data. Results indicated an interaction of PCE and postnatal environmental risk on both kindergarten age and early adolescent RSA reactivity (see Figure 1). However, the direction of effects were different at the two time points. There were also significant sex differences. In particular, cocaine exposed females or females that experienced higher rates of postnatal environmental risk had less optimal parasympathetic reactivity at early adolescence; whereas cocaine exposed males with higher rates of postnatal environmental risk had less optimal parasympathetic reactivity at early school age. These findings underscore the importance of examining sex differences as well as the role of postnatal environmental risk when examining developmental pathways to autonomic functioning. Results also highlight the possibility of differential pubertal effects for boys vs. girls for the development of regulatory processes.
Pamela Schuetze, State University of New York Buffalo State University
Presenting Author
Stephanie Godleski, Rochester Institute of Technology
Non-Presenting Author
Madison Rachel Kelm, Pennsylvania State University, University Park
Non-Presenting Author
Rina D. Eiden, The Pennsylvania State University
Non-Presenting Author