Assessing Maternal and Fetal Exposure to Chemicals during the Second Trimester

Investigator: Tracey Woodruff, PhD, MPH
Sponsor: NIH National Institute of Environmental Health Science

Location(s): United States


A large and growing base of science demonstrates that exposure to chemicals that can alter the function of the endocrine system during specific periods of fetal development can result in health consequences that manifest in childhood and adulthood, for example, cancer, cardiovascular effects and diabetes. The latter connection has evolved into the fetal origin of adult disease hypothesis. Large national biomonitoring studies are reporting nearly ubiquitous exposure to numerous environmental contaminants in the US population - bisphenol A, phthalates, octylphenols, polybrominated diphenol ethers, perchlorate - raising the question of how people are being exposed. Furthermore, studies of mid-gestation fetal exposure confirm that the placenta does not act as a barrier to exogenous chemicals and also indicate that the fetus may experience higher levels of exposure than the mother. Thus, human fetal exposure to chemicals represents a previously unexplored, yet critical public health question. We propose to measure levels of exposure to the chemical Bisphenol A, a chemical shown to increase risk of adverse affects from fetal exposures. The data from this study will set the stage for subsequent studies to explore the effects of BPA on the development of specific organ systems. In addition, with the successful implementation of this pilot study, we will be poised to rapidly broaden our studies to explore the exposures and effects of other environmental contaminants.

The results of this study will substantially advance our understanding of human maternal and fetal exposures to Bisphenol A, including sources and predictors of exposure and hepatic metabolic transformation. Insights gained about the sources of exposure and the role of fetal metabolic phase II metabolism will be applicable to other environmental chemicals that have similar sources of exposure and are detoxified through the same pathways.