The effects of lead on the cognitive development of children, behavioral effects, reasons for the child’s exquisite sensitivity, and the long-term prognosis of lead toxicity are reviewed at the Center for Trace Element Studies and Environmental Neurotoxicology, Staten Island, NY. The direct neurotoxic effects of lead include apoptosis, and damage to neurotransmitter storage, mitochondria, cerebrovascular endothelial cells, astroglia and oligodendroglia. The ability of lead to substitute for calcium is a common factor in the mechanism of lead toxicity. Lead suppresses Ca-dependent release of acetylcholine, dopamine and amino acid neurotransmitters. Indirect neurotoxic effects include iron deficiency anemia, disruption of the blood-brain-barrier (BBB), disruption of thyroid hormone transport to the brain, substitution for zinc in zinc-mediated processes, and altered regulation of gene transcription.
A greater proportion of ingested lead is absorbed from the gastrointestinal tract of children than of adults, and the BBB permits more circulating lead to reach the brain of children less than 5 years of age. In contrast to IQ tests, more specific neuropsychological tests (eg attention, visuomotor integration, reaction time etc) are more sensitive to the effects of brain damage resulting from low levels of lead toxicity, and may be expected to uncover subtle cognitive signs of toxicity. Cognitive deficits due to lead are found to persist in to adulthood. Factors influencing the vulnerability of children to lead include socioeconomic status, dietary factors, genetic factors, and lead concentrations. Even with blood lead levels lower than 5 mcg/dl, there is an inverse relation between lead level and arithmetic and reading scores (Lanphear et al, 2000). The present threshold at which blood lead levels are considered to be unacceptable (10 mcg/dl) is too high. Once in the brain, lead cannot be removed by chemical chelating agents (Rogan et al, 2001), and the deleterious effects of lead on the developing brain cannot be prevented. The only prevention of adverse toxicity is prevention of lead ever entering the body. 
COMMENT. There are accumulating research data showing that toxic effects of lead on learning and behavior occur at levels of lead much lower than the currently accepted threshold of 10 mcg/dl adopted in 1991. It may be argued that there is no ‘safe’ level of lead.