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The infant mortality rate in USA exceeds that of most other developed nations, ranking 26th among Organisation for Economic Co-operation and Development countries.1 Non-Hispanic black infants in USA die more than twice as often as non-Hispanic white infants (11.4 vs 4.9 per 1000 live births).2 This disparity reflects disparities in preterm birth (PTB) rates, since two-thirds of infant mortality occurs in preterm infants.3 The PTB rate is 52% higher for black (13.8%) than white (9.0%) women. Efforts to reduce PTB and its disparities have failed (figure 1). We propose that racial disparities in PTB are a cumulative biosensor of exposures that vary by race, arising from long-standing inequities.
PTB disparities are not due to genetic sequence variation between racial groups
While some monogenic diseases track (incompletely) with race, such as sickle cell anaemia and cystic fibrosis, the vast majority of health conditions cannot be mapped to genetic variation between racial groups. Most human genetic variation is found within ancestral groups with only 5%–10% of gene frequencies differing between ancestral groups.4 Nonetheless, different frequencies of single nucleotide polymorphisms (SNPs) by race have led some investigators to search for genetic differences that cause racial disparities in PTB. However, SNPs explain an exceedingly small portion of PTB risk, and are often not replicated.5 6 Some strong evidence supports that disparities in birth outcomes are largely attributable to environmental, as opposed to genetic variation. One example is the phenomenon of erosion of immigrant health over generations. Birth weight (BWT) distributions of infants born to African-born black women and US-born white women nearly overlap, whereas infants born to US-born black women were substantially smaller.7 Indeed in a study of 27 states’ births in 2008, foreign-born black women had significantly lower odds of PTB than US-born black women even …
Contributors HHB conceived of the manuscript in collaboration with her coauthors and wrote the manuscript. Her coauthors critically edited and approved the final revised version of the manuscript.
Funding This work was funded by National Institute of Environmental Health Sciences (grant number:K23ES022242).
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
Patient consent for publication Not required.
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