What causes racial disparities in very preterm birth? A biosocial perspective

Abstract

Very preterm birth (<32 weeks' gestation) occurs in approximately 2% of livebirths but is a leading cause of infant mortality and morbidity in the United States. African-American women have a 2-fold to 3-fold elevated risk compared with non-Hispanic white women for reasons that are incompletely understood. This paper reviews the evidence for the biologic and social patterning of very preterm birth, with attention to leading hypotheses regarding the etiology of the racial disparity. A systematic review of the literature in the MEDLINE, CINAHL, PsycInfo, and EMBASE indices was conducted. The literature to date suggests a complex, multifactorial causal framework for understanding racial disparities in very preterm birth, with maternal inflammatory, vascular, or neuroendocrine dysfunction as proximal pathways and maternal exposure to stress, racial differences in preconceptional health, and genetic, epigenetic, and gene-environment interactions as more distal mediators. Interpersonal and institutionalized racism are mechanisms that may drive racially patterned differences. Current literature is limited in that research on social determinants and biologic processes of prematurity has been generally disconnected. Improved etiologic understanding and the potential for effective intervention may come with better integration of these research approaches.

Figure 1

Traditional conceptual framework for explaining the association of race with very preterm (VPT) birth (<32 weeks’ gestation). SES, socioeconomic status.

Figure 2

Alternative conceptual framework for understanding the association of race with very preterm (VPT) birth (<32 weeks’ gestation). HPA, hypothalamic-pituitary-adrenal axis; SES, socioeconomic status.