Associations between adverse childhood experiences, mitochondrial DNA copy number and atopic disease in children

Exposure to adverse childhood experiences (ACEs) chronically activates the neuroendocrine stress response, which can perturb mitochondrial DNA and may drive risk of atopic disease among children. We sought to examine the association between ACEs and mitochondrial DNA copy number (mtDNAcn), a measure of mitochondrial DNA abundance, and to characterize associations between mtDNAcn and atopic disease (atopic dermatitis, rhinitis and asthma) in a pediatric population.

We performed cross-sectional analyses in a sample of 226 children enrolled in the Pediatric ACEs Screening and Resiliency Study who were recruited during well-child visits. Caregivers reported whether their child was exposed to ACEs or ever diagnosed with asthma, atopic dermatitis, or allergic rhinitis. MtDNAcn was measured in buccal swabs using qPCR. Multivariate linear and logistic regression analyses were used to measure associations with ACEs, mtDNAcn and atopic disease.

Children in our study were predominantly non-Hispanic Black, female, with a mean age of 5.6 years (SD = 3.6), and most caregivers had completed high school. We found that greater ACEs exposure was associated with a decrement in children's mtDNAcn. We also observed mtDNAcn was inversely associated with odds of children having atopic dermatitis but not associated with asthma or allergic rhinitis.

Our results suggest that greater exposure to ACEs is associated with lower mtDNAcn in children, and that having lower mtDNAcn is associated with greater odds of atopic dermatitis. Future work should measure other biomarkers of mitochondrial stress to understand this potential mechanistic relationship between adverse childhood experiences and atopic disease in children.