Research

Role of PAH exposures associated with superfund site proximity in preterm birth etiology through placental transcriptomics and metagenomics

Master
Content

The preterm birth rate (PTB) in the United States persists as one of the highest rates among industrialized nations. Because the recurrence risk of preterm birth approximates as high as 40-50 percent, identification of the potential causative etiology is essential to improving maternal and child health. PTB rates have clear racial and ethnic disparities which have existed for decades, being increased in non-Hispanic black women compared with non-Hispanic white and Hispanic women. While the reasons for this disparity are likely multifaceted and include genetic factors, the role of environmental exposures has been hypothesized as being a potential underlying cause.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been implicated in adverse pregnancy, fetal and neonatal outcomes including preterm birth. Ambient PAH exposure, as well as that from tobacco smoke, has been shown to reduce birthweight and increase the risk for small for gestational age infants. Despite these known associations, little is understood about the environmental sources, tissue deposition, and the underlying mechanisms of action which link prenatal PAH exposure with subsequent adverse perinatal outcomes. Due to its public health impact and relatively high prevalence in the general population (9-11 percent), the rate and occurrence of spontaneous PTB in association with environmental PAH exposures is an important area of study.

Heading

Project Objectives

Content
  • To measure PAHs from serum and placenta to find biomarkers of PAH exposure and their association with preterm birth. Using mass spec technology we will measure levels of 16 PAHs from placenta tissue to determine how levels of PAHs are associated with PTB.
  • To use multi’omics analysis to determine molecular networks disrupted by PAH exposure in the placenta which may contribute to PTB. RNA-Seq and whole genome methylated DNA analyses will be performed on placenta tissue to determine mechanisms that may contribute to PTB with PAH exposure.
  • To utilize wearable environmental exposure monitoring devices to determine the contribution of PAH and other exposures to PTB. Pregnant women will be enrolled to wear silicone wristbands for one week. These bands absorb chemicals through the skin and yield information on exposure to environmental toxins. The data from these wristbands will be combined with health outcomes data to determine
Heading

Investigators and Trainees

Terms
Kjersti

Item Term
Kjersti Aagaard, M.D., Ph.D.

Item Definition

Project Role?
Institution: Baylor College of Medicine

Melissa

Item Term
Melissa Suter, Ph.D.

Item Definition

Project Role?
Institution: Baylor College of Medicine

Sohini

Item Term
Sohini Banerjee, Ph.D.

Item Definition

Postdoctoral Fellow, Kjersti Aagaard Lab
Institution: Baylor College of Medicine

Heading

Related Publications

Content

Suter MA, Aagaard KM, Coarfa C, Robertson M, Zhou G, Jackson BP, Thompson D, Putluri V, Putluri N, Hagan J, Wang L, Jiang W, Lingappan K, Moorthy B. Association between elevated placental polycyclic aromatic hydrocarbons (PAHs) and PAH-DNA adducts from Superfund sites in Harris County, and increased risk of preterm birth (PTB). Biochem Biophys Res Commun. 2019 Aug 20;516(2):344-349. doi: 10.1016/j.bbrc.2019.06.049. Epub 2019 Jun 14. PMID: 31208719; PMCID: PMC6637943.

Antony KM, Hemarajata P, Chen J, Morris J, Cook C, Masalas D, Gedminas M, Brown A, Versalovic J, Aagaard K. Generation and validation of a universal perinatal database and biospecimen repository: PeriBank. J Perinatol. 2016 Nov;36(11):921-929. doi: 10.1038/jp.2016.130. Epub 2016 Sep 15. PMID: 27629376.

Vizuete W, Sexton KG, Nguyen H, Smeester L, Aagaard KM, Shope C, Lefer B, Flynn JH, Alvarez S, Erickson MH, Fry RC. From the Field to the Laboratory: Air Pollutant-Induced Genomic Effects in Lung Cells. Environ Health Insights. 2016 Feb 18;9 (Suppl 4):15-23. doi: 10.4137/EHI.S15656. PMID: 26917966; PMCID: PMC4760675.