Removal of lead from gasoline and other environmental sources has decreased the median blood lead concentration ([BPb]) of children in the United States < 10 μg/dL: the current low level of concern [Centers for Disease Control and Prevention (CDC) 1991]. However, there is compelling cross-sectional and prospective epidemiological evidence that [BPb] in children ≤ 10 μg/dL causes cognitive decline (Canfield et al. 2003; Hu et al. 2006; Lanphear et al. 2005; Rothenberg et al. 2002; Winneke et al. 1990). Recently, Gilbert and Weiss (2006) suggested that the BPb action level in children should be 2 μg/dL. Developmental lead exposure also has been linked to a variety of neurological and neurodegenerative disorders in children and adolescents, including attention deficit hyperactivity disorder (ADHD) (Braun et al. 2006), auditory and language impairments (Dietrich et al. 1992; Rothenberg et al. 2000; Yuan et al. 2006), retinal deficits (Rothenberg et al. 2002), neuromotor dysfunction (Bhattacharya et al. 1990, 2006; Ris et al. 2004), and schizophrenia (Opler et al. 2004). Few studies, however, have examined the long-term effects of low-level gestational lead exposure (GLE) despite findings that children with prenatal lead exposure have reduced cognitive functions (Baghurst et al. 1992; Hu et al. 2006; Schnaas et al. 2006; Wasserman et al. 2000), neuromotor and visual motor dysfunction (Ris et al. 2004; Wasserman et al. 2000), and altered auditory and retinal function (Dietrich et al. 1992; Rothenberg et al. 2000, 2002; Wasserman et al. 2000). Maternal lead exposure results from inhalation, diet, and/or eating in lead-contaminated work areas (Correa et al. 2006; Min et al. 1996). Maternal skeletal bone lead from prior exposure mobilizes during pregnancy and lactation (Manton et al. 2003). Lead easily crosses the placental and mammary barriers (Bornschein et al. 1977; Korpela et al. 1986). Thus, the developing fetus and child are at risk, as evidenced by findings that fetal and maternal [BPb] are similar (Korpela et al. 1986). The adverse cognitive consequences of prenatal and postnatal exposure to moderate-level ([BPb] 11–39 μg/dL) and high-level ([BPb] ≥ 40 μg/dL) lead have been studied in rodents (Cory-Slechta 1997; Crofton et al. 1980; Kuhlmann et al. 1997; Wasserman et al. 2000). Several reports also link moderate-to-high-level lead exposure to altered motor activity (Crofton et al. 1980; Ma et al. 1999) and dopaminergic signaling (Antonio and Leret 2000; Cory-Slechta 1997). To date, there are no experimental studies on the effects and mechanisms of low-level GLE on neuromotor function, despite evidence that low-level lead exposure produces these deficits in children (vide supra). In this report we present a new model of human equivalent GLE and the sex-specific physiological, behavioral, and neurochemical abnormalities in year-old GLE mice. These studies were conducted because the long-term consequences of GLE are unknown and increasing evidence indicates that early developmental exposure to neurotoxicants accelerates age-related functional decline and/or produces delayed neurotoxicity (Barone et al. 1995; Basha et al. 2005; Landrigan et al. 2005; Newland and Rasmussen 2000; Rice and Barone 2000; Weiss 1990; Weiss et al. 2002). Sex differences were examined because a) early developmental lead exposure produces a heightened risk for attention, visual motor, and fine-motor deficits in males (Bhattacharya et al. 1990, 2006; Ris et al. 2004); b) male and female animals exhibit differences in exposure and susceptibility to chemicals and lead neurotoxicity (Cory-Slechta et al. 2004; Vahter et al. 2007); and c) this is an important and underexplored area of toxicology (Vahter et al. 2007). Our results show that GLE produced age-related, sex-specific, and non-monotonic dose–response alterations.