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Background: Biological stress systems are immature in early childhood and vulnerable to early adversity, including poverty. Parents play a key role in buffering young children from biological stress (Gunnar & Talge, 2008). While this has been examined extensively with salivary cortisol measures of acute biological stress, less is known about the role of parenting quality and parental biological stress for long-term, cumulative cortisol exposure, which can be indexed via hair cortisol concentration (HCC). HCC has long term health implications, thus it is important to understand parental contributions to HCC levels in early childhood. Further, children’s biological stress systems may differ in their response to environmental risks and parental buffering. In particular, child emotion regulation may play a role in how reactive children are to their environments, given that children who are more adept at regulating the experience of emotion show better coping skills when faced with everyday stressors (Lengua, 2002).
Method: The current study investigated the association of parent HCC, socioeconomic status (SES), and parental sensitivity with child HCC, and examined whether child emotion regulation and reactivity moderated these associations. We collected hair samples from 86 preschool-aged children (44 females, Mage=3.54 years, SD=0.13 years) and their parents. Parent sensitivity during a parent-child interaction was coded using the Emotional Availability Scales (Pipp-Siegel & Biringen, 1998). Parents reported on their income, highest level of education, and occupation which was combined for an SES composite. Parents completed the Emotion Regulation Checklist (Shields & Cicchetti, 1997) which yielded two subscales, child emotion reactivity and emotion regulation.
Results: Child HCC was susceptible to poverty (r(85)=-.39,p<.001), such that lower SES was linked to higher cumulative biological stress. Child HCC was also associated with both parent HCC (r(84)=.58,p<.001) and parental sensitivity (r(86)=-.27,p=.01). Parents who had lower biological stress themselves and who were sensitive and responsive had children with lower cumulative cortisol exposure. Moderation analyses were conducted using ordinary least squares path analysis (Hayes, 2013). Emotion regulation moderated the association between parent HCC and child HCC such that parent HCC was closely tied to child HCC only for children who were emotionally dysregulated (F(5, 78)=9.44,p<.001;b4=-0.95,p =.006,CI:-1.61–-0.28). Emotion reactivity moderated associations of SES and parental sensitivity with child HCC. Emotionally reactive children were more vulnerable to socioeconomic adversity in terms of their HCC (F(5, 79)=4.84,p=.001; b4=-1.15,p=.02,CI:-2.13–-0.18), and child HCC also was more closely tied to parental sensitivity for these emotionally reactive children (F(5, 79)=3.23,p=.01;b4=-0.95,p=.006,CI:-1.61–-0.28),
Discussion: Results indicate that chronic biological stress in young children is both vulnerable to SES risks and responsive to protective parent factors. Environmental susceptibility differed based on child emotion regulation capacities. For emotionally dysregulated children, having a biologically well-regulated and sensitive parent was especially critical in buffering them from cumulative biological stress, and having a sensitive parent was crucial for emotionally reactive children. Children who are more emotionally regulated may also be more independent in regulating their biological stress, making them less vulnerable to SES risks but also less responsive to the protective effects of parental sensitivity.