A common feature among children with autism is a larger brain size at birth and a slower rate of increase in brain size after birth. Many factors contribute to the size of the brain and these include the number of cells, the amount of cellular material (myelin, dendrites), and the size of ventricles. Many studies have been conducted examining the genes regulating these factors but fewer studies have been concerned with environmental factors. In autism, for example, the preponderance of research has been directed to mutations, polymorphisms, and gene-gene interactions. Yet, studies have shown a direct link between the environment and autism. Furthermore, population studies have revealed the importance of environment-gene interactions. The question posed in our study is whether environmental chemicals affect brain size. More specifically, the studies are directed to understanding the effect of methyl mercury and cadmium on cell number. These chemicals kill cells and many studies have been published delineating the mechanism of cell death. In contrast, the studies here will examine whether very low concentrations of these chemicals protect cells. The number of cells in the brain, or any organ, depends on proliferation and cell death. There are a number of factors that will promote cell death depending on the type of cell. In the brain, for example, neurons die during normal development under conditions such as growth factor withdrawal or diminished nutrients. Cell death occurs through apoptosis, which is a complex and orderly process that enables the surrounding tissue to remain healthy. Chemicals that kill cells at high concentrations might induce protection at low concentrations. Indeed, mild hypoxia has been shown to pre-condition cells resulting in a higher resistance to apoptosis induced by intense hypoxia. The experiments described here will test the hypothesis that apoptosis is impeded by exposure to low concentrations of cadmium and methyl mercury through the induction of the anti-apoptotic protein hairless.