Advances in understanding the distribution and retention of lead in mineralized tissues are important for two reasons: first, bone lead may be a more accurate dosimeter of integrated absorption associated with chronic exposures, and second, bone lead may be a source of internal exposure to the host organism. Little attention has been paid to this second aspect, the remobilization of lead from bone. Mobilization of lead from bone is likely to occur during periods of altered mineral metabolism; since calciotropic factors determine the uptake and storage of lead in this compartment, changes in calcium-related regulatory factors are likely to affect lead compartmentation. Calcium metabolism changes drastically in humans during pregnancy and lactation; although relatively little is known of lead kinetics during these critical periods, it is likely that bone lead is mobilized and transferred to the more bioavailable compartment of the maternal circulation, with potential toxic effects on the fetus and the mother.

There is an urgent need to develop efficient and rapid strategies in order to characterize the potential health risks associated with nanomaterials, given the speed with which applications and uses are increasing. Use of standard toxicity methods will not be sufficient to meet this need. This article proposes the adoption of two novel guidances: the system’s biological approach to toxicity testing advocated by the US National Research Council and a nanobiological perspective that identifies key events at the nanoscale that are relevant to signal transduction and structural biology.

Mice were exposed to lead from birth by substituting solutions of lead acetate for the drinking water of their mothers. The suckling mice were thus exposed to lead through their mother's milk and, at weaning, directly through the drinking water. Controls received equal concentrations of sodium acetate. No deaths of offspring or mothers occurred during the first 90 days of exposure. It has been suggested recently that lead exposure may account for some incidences of behavior disorders in children. Levels of motor activity of individual offspring were measured from weaning until 70 days of age in specially designed activity cages. Lead-treated mice were more than three times as active as age-matched or size-matched controls.Treated and control animals were administered drugs currently used in the treatment and diagnosis of hyperactivity in children. All control animals responded as expected to all drugs used in this study. However, lead-treated mice responded paradoxically to d-and 1-amphetamine, methylphenidate, and phenobarbital. That is, the CNS stimulants suppressed their hyperactivity while phenobarbital exacerbated the lead-induced hyperactivity. These findings suggest that lead produces an animal model of hyperactivity which may have clinical relevance and which may explain some cases of hyperactivity in children.Clinical experience has shown a relationship between lead intoxication and behavioral disorders in children (1-4). These disorders are manifest as irritability, restlessness, and aggressiveness, but no experimental evidence has been previously advanced to support or deny the clinical experience. Although animal studies employing high levels of lead exposure have produced significant organ damage (5), encephalopathies (6, 7), and neuromuscular impairment (8,9), no behavioral dysfunction due to lead

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