The current approach in toxicological risk assessment relies on traditional toxicity testing such as evaluation of clinical signs or pathological changes. This approach effectively provides concentrations to which an animal can be exposed without expecting any adverse outcome. However, it does not provide precise information on where, how and when toxicity occurs, as well as whether any long-term and trans-generational effects that may occur. To address this shortcoming, a new branch of toxicology recently appeared, helped by the development of technology: toxicogenomic. This field of research focuses on the global genome impact of a toxicant and provides information regarding the molecular pathways affected. Thus, toxicogenomic is complementary to classical methods. The objective of this thesis was to demonstrate that the preimplantation porcine embryo is an effective toxicogenomic model to evaluate the chlorination by-products and ethanol at environmentally-relevant concentrations. To conduct our experiments, we integrated the sensitivity of the preimplantation porcine embryo to powerful transcriptomic and epigenomic microarrays developed in our laboratory. The advantage of the early embryo is its capacity to express a plethora of pathways whilst serving as a relevant model for human. The result is a toxicogenomic screening system that better identifies the mode of action of toxicants that induce adverse health outcomes. We exposed embryos to either 0.2% ethanol or chlorination by-products found in drinking water, bromodichloromethane (BDCM) and dichloroacetic acid (DCAA). The concentrations used were similar to human exposure. Our results suggest that the preimplantation embryo is vulnerable to the toxicants present in its environment and that the adaptive mechanisms it activates are compatible with the adverse outcomes observed in human exposed in utero. All tested products induced a decreased in embryonic survival and significant modification in the transcriptomic profile. However, each product induced specific pathways, suggesting a different mode of action and demonstrating the plasticity of the embryonic response. In summary, the results presented in this thesis provide information on the mechanisms activated by the embryo in order to survive following exposure to toxicants and give insight on the mode of action of these molecules. These results support the use of toxicogenomic tools combined to sensitive animal model in risk assessment.