Environmental chemical exposures and mechanisms underlying human placental dysfunction and disease

March 30th, 2021; 12-1 pm


Assistant Professor Joshua Robinson, PhD

Postdoctoral Fellow Hao Chen, PhD


Speaker Biographies

Dr. Robinson is an Assistant Professor in the Center for Reproductive Sciences and the Department of Obstetrics, Gynecology & Reproductive Sciences at UCSF. His laboratory studies the toxicological consequences of environmental chemical exposures during early pregnancy and their mechanistic links with developmental disease. His background and training includes a Ph.D. in Toxicology from the University of Washington and postdoctoral training at the National Institute of Public Health and the Environment in the Netherlands and UCSF. As a project leader and the designated Faculty Developmental Investigator of the former UCSF Pregnancy Exposures to Environmental Chemicals (PEEC) Children’s Center (led by Dr. Tracey Woodruff), he will provide an overview of his collective group’s research studies focused in utilizing primary human placental cell/tissue models, systems biology, and in vivo biomarker approaches to study the relationship between environmental chemical exposures and human pregnancy complications.

Dr. Chen is a Postdoctoral Fellow in the laboratories of Dr. Joshua Robinson and Dr. Susan Fisher. He received a PhD in Pharmacology and Toxicology at UC Davis in 2017, and was recently awarded the NIH/NIEHS K99/R00 Award due to his early research efforts. He will present his initial findings from his project aimed at using proteomic-based approaches to understand the effects of environmental chemicals (PBDE, PFAS) exposures on human cytotrophoblast differentiation.


What is the problem and why is this important?

During pregnancy, we are exposed to thousands of chemicals in the environment. The majority of chemicals that we are exposed to lack information regarding their potential to cause developmental toxicity. Placental-mediated complications such as preterm birth and preeclampsia afflict a significant proportion of births and are associated with adverse birth outcomes and diseases which manifest later on in life. Our group is specifically interested in determining chemical exposures that alter placental development and underlie pregnancy complications.


What is the science behind it?

Toxicological and epidemiological studies suggest significant relationships between environmental chemical exposures and placental toxicity. For example, specific flame retardants (e.g., PBDEs) are associated with preterm birth in humans (in limited studies) and linked with changes in placental function and expression of molecular pathways in animal/cell models.


What is innovative/exciting about the science?

Our group utilizes primary placental cell/tissue models representative of early/mid pregnancy which enables us to examine the effects of environmental chemicals during a susceptible developmental window that precedes pregnancy complications.

We employ a combination of in vitro, in silico and omic-approaches to identify chemical exposures that contribute to toxicity in the human placenta.

As an extension of this work, we are investigating the relationship between human chemical levels and biomarkers of chemical exposure related to placental development and adverse pregnancy outcomes.


What should we do going forward about this problem?

Efforts are needed to identify chemicals linked with pregnancy complications and replace, reduce, or remove these hazardous chemicals from the environment, involving the work of basic researchers, epidemiologists, risk assessors, chemical regulators and stakeholders.


How does this work address environmental health needs and/or environmental justice?

Specific populations are exposed to disproportionate levels of chemicals (e.g., pesticides, heavy metals) due to several factors, including, geographical location, occupation, and socioeconomic status. We aim to elucidate relationships between specific environmental chemical exposures and pregnancy complications to inform community stakeholders and provide evidence for regulatory action.