This pilot project will analyze the growth inhibiting effects of the herbicide metolachlor on non-target, human HepG2 cells. Metolachlor, a very commonly used herbicide in the United States, especially in the Midwest corn-belt, functions by inhibiting chlorophyll and protein synthesis in target plants. Herbicide exposure has led to detrimental effects in several organisms, notably affecting their growth and behavior, however, its mechanism of action in non-target organisms is not yet clear. The EPA does not currently have specific regulations for maximal limits allowed in drinking water. Growth studies from our lab demonstrate that increasing metolachlor concentrations and increasing time of exposure results in decreased growth of liver cells. The objective of this study is to elucidate a mechanism for decreased HepG2 cell growth after metolachlor exposure. Analyses will include assessing toxicity effects leading to necrosis, effects of apoptosis induction and alterations in cell cycle progression