Summary of project:

Gestational brain development lays the foundation for life-long neural function. Unfortunately, the fetal brain is also vulnerable to environmental insults due to its poorly developed blood-brain barrier and the sensitivity of neural progenitor cells. Exposure to environmental contaminants, such as bisphenol A (BPA), an endocrine-disrupting chemical with estrogenic properties, have increasingly been associated with altered neurodevelopment. The vast majority (95%) of Canadians have detectable BPA in their urine, including pregnant women, and prenatal exposure to BPA is associated with increased anxiety and depression in children. Despite this evidence, Health Canada and agencies around the world declare BPA safe. Definitive evidence linking prenatal BPA exposure to changes in neural structure and function is required to change policy and enhance human health.  The aims of this study are to:

  1. Determine the brain morphometry and connectivity changes associated with high prenatal exposure to BPA in children.
  2. To use neuroimaging in mice to identify the phenotype of the circuits changed by BPA exposure.

This study will use a translational approach to determine the brain alterations associated with prenatal BPA exposure, validate these brain alterations in a mouse model of prenatal BPA exposure, and begin to determine the mechanisms via which these brain alterations are induced. Our results will shed valuable insight into the structural effects of prenatal BPA exposure on the brain – data that has never been collected in humans. In addition, we have the unique advantage of employing a parallel mouse model, which will provide valuable information about the underlying neurobiological changes induced by BPA exposure in utero. The combination of human and animal studies in this project can potentially provide the needed direct evidence (or, lack thereof) as to whether there are brain alterations in children with high levels of BPA exposure.