Project Summary (2000-2005)

The overall goal of this project is to assess whether specific developmental toxicants (e.g. trichloroethylene (TCE) and (As) arsenic) perturb one or more developmental pathways leading to morphologic alterations resulting in specific birth defects. The main objective is to investigate the molecular pathways altered by TCE that cause cardiac malformations in rat embryos. Researchers hypothesize that analysis of biological markers at the molecular level provides a sensitive index of environmental exposure. Molecules critical to normal development can eventually be tested by genetic manipulation as a direct source of defects. The similarities and differences of a separate potential teratogen (As versus TCE) are being examined in the developing embryo. Preliminary data indicate that several markers of exposure to TCE and As are perturbed in both heart and lungs during development. One objective is to determine minimum exposure levels that result in altered gene expression and use the most sensitive markers for risk assessment.