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Despite the knowledge of clinical effects of lead, there has been a recent resurgence in concerns relative to its biochemical toxicity. Absorption of ingested lead from water, food, or lead-contaminated dust is the major source of exposures in non-occupationally exposed individuals. Following absorption, lead is distributed to two main compartments; the readily exchangeable “pools” represented by blood and soft tissue (including the brain) and a “deep tissue reservoir” represented by bone [1]. Over 95% of blood lead is contained within the erythrocytes [2]. While acute lead exposure (e.g. that seen after ingestion of metallic lead) is limited in distribution to the aforementioned readily exchangeable pools, chronic, persistent, lowlevel exposure; such as that associated with non-occupational exposure, will result in accumulation of lead. This, in turn, has the potential for producing chronic, subclinical lead poisoning capable of disrupting normal protein synthesis (e.g., heme) and altering cognitive and/or neurobehavioral function.
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