TY - JOUR
T1 - Understanding Racial Disparities of Preterm Birth Through the Placenta
AU - Matoba, Nana
AU - Mestan, Karen K.
AU - Collins, James W.
N1 - Funding Information:
Drs. Matoba and Mestan conceptualized the manuscript, and drafted and reviewed the manuscript. Dr. Collins critically reviewed the manuscript for important intellectual content. All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work. The study was supported by Perinatal Origins of Disease Strategic Research Initiative of the Stanley Manne Children's Research Institute of Chicago.
Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2021/2
Y1 - 2021/2
N2 - The racial disparity associated with preterm birth is a public health concern in the United States. The placenta is the principal metabolic, respiratory, and endocrine organ of the fetus and a key route by which environmental exposures are transmitted from mother to offspring. Available at every delivery, it may serve as a marker of differences in prenatal exposures that manifest differently by race. Recently, we described differences in placental pathology between African-American and White preterm births: the prevalence of chronic inflammation was higher among African-American women's placentas compared with those of White women. Similarly, racial differences have been shown in placental malperfusion and placental weight. Social determinants such as poverty and stress from discrimination have been implicated in racial disparities in preterm birth. To date, however, the underlying biological mechanisms, whether through inflammatory, oxidative stress, or other pathways involving epigenetic programming, remain largely unknown. The placenta, complemented by maternal and umbilical cord blood biomarkers, may provide important information on the perinatal environment that explains the origins of racial disparities in preterm birth rates and subsequent health outcomes. This article reviews existing literature and current research gaps. Opportunities are discussed for future placental research that may reveal novel mechanisms leading to the development of new approaches in the prevention and management of preterm birth and its outcomes.
AB - The racial disparity associated with preterm birth is a public health concern in the United States. The placenta is the principal metabolic, respiratory, and endocrine organ of the fetus and a key route by which environmental exposures are transmitted from mother to offspring. Available at every delivery, it may serve as a marker of differences in prenatal exposures that manifest differently by race. Recently, we described differences in placental pathology between African-American and White preterm births: the prevalence of chronic inflammation was higher among African-American women's placentas compared with those of White women. Similarly, racial differences have been shown in placental malperfusion and placental weight. Social determinants such as poverty and stress from discrimination have been implicated in racial disparities in preterm birth. To date, however, the underlying biological mechanisms, whether through inflammatory, oxidative stress, or other pathways involving epigenetic programming, remain largely unknown. The placenta, complemented by maternal and umbilical cord blood biomarkers, may provide important information on the perinatal environment that explains the origins of racial disparities in preterm birth rates and subsequent health outcomes. This article reviews existing literature and current research gaps. Opportunities are discussed for future placental research that may reveal novel mechanisms leading to the development of new approaches in the prevention and management of preterm birth and its outcomes.
KW - placental pathology
KW - preterm birth
KW - racial disparity
KW - stress
UR - http://www.scopus.com/inward/record.url?scp=85099619281&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85099619281&partnerID=8YFLogxK
U2 - 10.1016/j.clinthera.2020.12.013
DO - 10.1016/j.clinthera.2020.12.013
M3 - Article
C2 - 33483135
AN - SCOPUS:85099619281
SN - 0149-2918
VL - 43
SP - 287
EP - 296
JO - Clinical Therapeutics
JF - Clinical Therapeutics
IS - 2
ER -