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Author Notes:

Ramkumar Menon, PhD, Women's and Children's Center, Department of Epidemiology Rollins School of Public Health, Emory University, 1518 Clifton Rd NE, Atlanta, GA 30322, USA. E-mail: rmenon3@emory.edu

The authors have stated explicitly that there are no conflicts of interest in connection with this article.


Research Funding:

This article follows a four-part seminar series on causes of racial disparities in preterm birth held in the fall of 2009 at the Rollins School of Public Health, Emory University, Atlanta, GA. The series and this work are supported in part by the National Institute of Health Reproductive, Perinatal, and Pediatric Health Training grant T32 HD052460.

Ramkumar Menon is also supported by Grants from March of Dimes, New York, NY, USA (21-FY08–557) to study genetic and biomarker differences in preterm birth racial disparity.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Obstetrics & Gynecology
  • African American
  • health disparities
  • infant health
  • infection
  • prematurity

An overview of racial disparities in preterm birth rates: caused by infection or inflammatory response?


Journal Title:

Acta Obstetricia et Gynecologica Scandinavica


Volume 90, Number 12


, Pages 1325-1331

Type of Work:

Article | Post-print: After Peer Review


Infection has been hypothesized to be one of the factors associated with spontaneous preterm birth (PTB) and with the racial disparity in rates of PTB between African American and Caucasian women. However, recent findings refute the generalizability of the role of infection and inflammation. African Americans have an increased incidence of PTB in the setting of intraamniotic infection, periodontal disease, and bacterial vaginosis compared to Caucasians. Herein we report variability in infection- and inflammation-related factors based on race/ethnicity. For African American women, an imbalance in the host proinflammatory response seems to contribute to infection-associated PTB, as evidenced by a greater presence of inflammatory mediators with limited or reduced presence of immune balancing factors. This may be attributed to differences in the genetic variants associated with PTB between African Americans and Caucasians. We argue that infection may not be a cause of racial disparity but in association with other risk factors such as stress, nutritional deficiency, and differences in genetic variations in PTB, pathways and their complex interactions may produce differential inflammatory responses that may contribute to racial disparity. © 2011 Nordic Federation of Societies of Obstetrics and Gynecology.

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