Thesis Research


My thesis work focuses on maternal exposure to per- and polyfluoralkyl substances (called PFAS), which are manmade chemicals present in commercial household products like nonstick cookware, carpets, furniture, and food packaging. Humans exposure occurs through contaminated drinking water, food, and indoor dust. Exposure to these chemicals are widespread, and many studies have shown that 95-99% of the U.S. population has detectable levels of PFAS in their blood.

Importantly, many epidemiological studies have associated maternal exposure to these compounds with adverse pregnancy and birth outcomes, including preeclampsia, thyroid hormone disruption, and fetal growth restriction. My work asks how PFAS exposure may cause these complications. I am investigating the hypothesis that PFAS exposure affects the normal development and function of the placenta, leading to adverse pregnancy outcomes. The placenta is critical for a healthy pregnancy, as it supplies nutrients, removes waste, and acts as a communicative interface between mother and child. Interruptions of these essential processes may manifest in pregnancy complications such as those linked to PFAS exposure.

This research motivates me because it informs public health guidance and policy, which contributes to my career goals of developing and utilizing scientific research to improve public health for vulnerable populations around the world.

Determine the effects of PFAS exposure on trophoblast function and identify the dysregulated underlying biological pathways.

The development of the placenta begins in early embryogenesis, and requires trophoblast cells on the blastocyst to proliferate and differentiate into subtypes, which each play distinct roles in the function of the placenta throughout gestation. Using a novel human placental stem cell model, I am able to evaluate the effects of PFAS exposure on trophoblast differentiation and function. Then, using RNA sequencing and DNA methylation analyses, I can determine which biological pathways underlying cellular dysfunction and investigate if altered DNA methylation has a regulatory effect on gene expression.

Evaluate in vivo effects of maternal PFAS exposure on placental development and adverse pregnancy and health outcomes.

To understand if maternal PFAS exposure during pregnancy disrupts placentation and leads to adverse health outcomes, I evaluate relevant health and functional endpoints in an in vivo rabbit model. The rabbit is the requisite non-rodent model in regulatory toxicity testing and is also used in many developmental studies. Importantly, its placentation and pregnancy closely resemble humans. In my ongoing studies, female rabbits receive either control or PFAS-contaminated drinking water before and during pregnancy, and I assess pregnancy and health outcomes of the mothers and their offspring to determine effects of PFAS exposure.