Intimate partner violence exposure, salivary cortisol, and childhood asthma

Neuroendocrine alterations may help explain health differences between intimate partner violence (IPV) exposed children and non-exposed children. We sought to determine the feasibility of having families, recruited at a child asthma visit, collect at home and return via mail child salivary samples, and whether socio-demographic variables were associated with sample return. For those returning samples, we examined whether past-year IPV exposure was associated with total cortisol output (AUC) and the magnitude of the cortisol awakening response (CAR), and whether these cortisol values were associated with asthma control.

Fifty-five families with an asthmatic child of any age were recruited from 2 pediatric asthma clinics. At the time of the visit, parents completed a survey packet which included a modified version of the Conflict Tactics Scale to assess IPV. Parents were given supplies to collect 3 child salivary cortisol samples (awakening, 30-min after awakening, bedtime) at home on a typical day, and return them via mail. Medical records also were abstracted.

Fifty-three percent (n=29) returned child salivary samples. Families who returned samples typically returned them within 2 weeks, most commonly before we made a reminder call. Parental male sex was associated (p=.06) with increased rate of return at the trend level. In multivariable models, a 1-unit increase in IPV was significantly associated with a .93 SD increase in root-transformed total cortisol output (AUC) (un-standardized beta=2.5; SE .59; p=.001). The odds of uncontrolled asthma were marginally higher for every nmol/l increase in CAR (OR 1.04; 95% CI 1.0, 1.1; p=.06).

This study provides support for the feasibility of obtaining a moderate return of salivary specimens from a convenience sample. Findings that IPV was associated with elevated total cortisol output and uncontrolled asthma was marginally associated with cortisol awakening response suggest that future studies should investigate whether cortisol mediates the IPV-child asthma relationship.