Environmental factors such as pollutants are associated with diabetes incidence. Of particular interest is exposure to persistent organic pollutants (POPs) during critical stages of fetal development. TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is a potent ligand of the aryl hydrocarbon receptor, which leads to induction of cytochrome P450 (CYP) 1A1 enzymes. We hypothesize that POPs such as TCDD accumulate in the pancreas, thereby eliciting stress on developing beta cells through induction of CYP1A1. Here, I exposed rodent alpha and beta cell lines to TCDD in vitro, but did not observe induction of Cyp1a1 gene expression or enzyme activity, meaning that this pathway is not activated in immortalized pancreatic endocrine cell lines. I also differentiated human embryonic stem cells toward pancreatic cell fate in vitro to study how TCDD exposure impacts human beta cell development. I concluded that TCDD might impede normal development of beta cells, potentially through induction of CYP1A1 and other embryonic lineages.