 Arsenic is a known human carcinogen and systemic toxin, but its developmental neurotoxicity has not been as well studied. This review provides evidence that prenatal and early postnatal exposure to arsenic can lead to reduced brain weight, decreased numbers of neurons, and alterations in neurotransmitter systems. Animal and in vitro studies suggest that oxidative stress may be a mechanism of arsenic neurotoxicity. Epidemiological studies indicate that early life exposure is associated with deficits in intelligence and memory, which may manifest later in life. Sex, concomitant exposures, and timing of exposure appear to modify the developmental neurotoxicity of arsenic. No behavioral outcomes were observed in four epidemiological studies. Future prospective birth cohort studies will allow for more precise definition of the developmental consequences of arsenic exposure in early life. This article was authored by Molly Tolins, Matheros Ruchirawot, and Philip Landrigan.