Background Family socioeconomic status (SES) is an important source of child health disparities in the USA. Chronic stress is one way SES may impact children's physiology with implications for later health inequalities. These processes may work differently across childhood due to differences in exposure and susceptibility to stressors at different ages. We assess associations between family SES and one biomarker of chronic stress exposure—low-grade inflammation detected by elevated C reactive protein (CRP)—and evaluate differences in the associations by child age.
Methods We used nationally representative data from the National Health and Nutrition Examination Survey and Tobit regression models to estimate SES associations with CRP and the moderating effects of age for children age 2–18 years. Our sample was limited to CRP ≤10 mg/l to focus on low-grade inflammation (N=13 165).
Results Children whose parent had less than a high school degree had 35% higher CRP than those with a college graduate parent; and, poor children had 24% higher CRP than those with high family income, net of controls. When children's body mass index was accounted for, low education and poverty associations were reduced to 19% and 15%, respectively. Child age interactions were negative and significant for both parental education and family income.
Conclusions This study provides new evidence that SES is associated with low-grade inflammation in children, and that these associations may be particularly strong during early and mid-childhood. Future research should further our understanding of stressors related to low family SES that may lead to immune system dysregulation during childhood.
- Comm Child Health
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Contributors As the primary author, KKS conceptualised the study, conducted the data analysis, and was the main writer. AY contributed to writing and editing the paper.
Funding This research was funded in part by a K01 grant awarded to KKS (1 K01 HD 077063-01 A1) through the Eunice Kennedy Shriver National Institute for Child Health and Human Development (NICHD) of the National Institutes of Health (NIH). Support for this project was also provided through a seed grant awarded to KKS by the Ohio State University Institute for Population Research through a grant from the Eunice Kennedy Shriver NICHD of NIH, P2CHD058484.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.