Abstract

The dominant exposure sources of lead, an ubiquitously present metal, include, in many geographical regions, leaded gasoline, water, paint, and industrial emissions. These sources may cause exposure via inhalation and ingestion. At inhalation, 10–60% of the particles with a of size 0.01–5 μm will be deposited in the alveolar region. Gastrointestinal absorption in adults is ∼10–20%. Lead accumulates in bone and teeth. The skeleton contains >90% of the total body burden in adults, less in children. Turnover in bone is slow, the half-time in trabecular bone being ∼1 year compared to decades in cortical bone. Other compartments in blood and soft tissues have a half-time of ∼1 month. Excretion is mainly through urine and feces. Lead toxicity may affect several organ systems, e.g., the hematopoietic system, the peripheral and central nervous system, the kidneys, the gastrointestinal tract, the cardiovascular system, and the reproducytive system. Lead is an animal carcinogen, but conclusive evidence for carcinogenesis in humans is lacking. Lead determinations in blood (B-Pb) is presently the prevailing indicator of lead exposure and risk. However, serum/plasma levels of lead may be more suitable as such an index, mainly because of the nonlinearity of B-Pb in relation to both exposure and effects. Other, less frequently used indices include lead concentrations in urine, mobilization tests, and disturbances of heme metabolism. During the last two decades in vivo determination of lead in bone, e.g., tibia, calcaneus, and finger bone, by X-ray fluorescence has been used for biological monitoring of long-term exposure. Recent data indicate that there is an accumulation of lead in finger bone, which is related to both time of exposure and B-Pb. In a three-dimensional model, lead in finger bone and the exposure time may be used for retrospective estimation of previous B-Pb, reflecting the historic lead exposure. Such estimates will be of particular value in cross-sectional studies of long-term health effects in lead-exposed populations. J. Trace Elem. Exp. Med. 11:289–301, 1998. © 1998 Wiley-Liss, Inc.

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