ABSTRACT
Lead (Pb2+) is a ubiquitous environmental neurotoxicant with a long history of exposure in children (Needleman, 1998; Mielke, 1999). The developing brain is highly susceptible to Pb2+ exposure and long-term deficits in cognitive function are the principal effects of Pb2+-induced neurotoxicity (Bellinger et al., 1987; McMichael et al., 1988; Bellinger et al., 1992; Winneke et al., 1994; Lanphear et al.,
2000). Despite significant efforts during the last two decades to reduce Pb2+ levels in the environment, one in twenty children living in the United States exhibit blood Pb2+ levels (>10 µg/dL) known to produce long-term deficits in cognitive function (Pirkle et al., 1994; 1998). The most prominent route of exposure at the present time is from Pb2+ found in the dust and soils in homes that were built prior to the 1970s in which leaded paint was used (Lanphear et al., 1999). A recent report by the United States Surgeon General indicates that “lead poisoning poses one of the greatest environmental threats to children in America” (Satcher, 2000). This environmental problem is not exclusive to the United States; in fact, emerging data from other industrialized and developing nations suggest that many more children are exposed to even higher levels of Pb2+ from contamination of their living environment (LopezCarrillo et al., 1996; Romieu et al., 1997; Factor-Litvak et al., 1999; Kaul et al., 1999; Gao et al., 2001; Rubin et al., 2002). Therefore, the effect of Pb2+ exposure on the cognitive development of children is a worldwide environmental health problem with significant social and economic consequences (Grosse et al., 2002; Landrigan et al., 2002). The overwhelming evidence of this environmental catastrophe underscores the need for understanding the molecular bases of Pb2+-induced learning impairments in order to devise useful intervention strategies to ameliorate its neurotoxic effects.
