Kinetics of lead in blood after the end of occupational exposure.

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

“…Lead levels in cortical bone may be a better indicator of long-term cumulative exposure than lead in trabecular bone, possibly because lead in trabecular bone may exchange more actively with lead in blood than does cortical bone. This is consistent with estimates of a longer elimination half-time of lead in cortical bone, compared to trabecular bone (Borjesson et al 1997;Brito et al 2005;Nilsson et al 1991;Schutz et al 1987). Longitudinal measures of bone lead over a 3-year period showed no significant decline in cortical bone lead, whereas trabecular bone lead declined by approximately 15% (Kim et al 1997).…”

“…Lead in blood has a much shorter retention half-time than lead in bone (days compared to years); therefore, PbB concentration provides a marker for more recent exposure, while lead in bone appears to reflect longer-term cumulative exposures (Borjesson et al 1997;Nilsson et al 1991;Schutz et al 1987). Lead in tooth enamel is thought to reflect exposures in utero and during early infancy, during which development of tooth enamel and coronal dentine is completed.…”

Bone lead as a biological marker in epidemiologic studies of chronic toxicity: conceptual paradigms.

“…Blood lead levels also reflect the mobilization of lead from the skeleton back into the circulation. This has been reported in the occupational setting (12), clinical studies (13), among women with community exposure (14), among pregnant women (15), and among adults undergoing joint replacement (16 In the latter case, the error associated with using blood lead as a proxy for a biologically more relevant biomarker of lead dose would, under most circumstances, result in weak correlations and small effect estimates in linear regression analyses (18).…”

Chelated lead and bone lead.

“…Again, this possibility indicates that the bone lead levels per se relate to chelated urinary lead in a complex way and that looking for correlations without being able to take into account exposure history (ie, using a metabolic model) is unlikely to be fruitful. For example, it is possible that the 10-20070 of chelated lead that can be correlated with bone lead may be associated with that part of the blood lead known to have a long residence time (28). In other words, a fraction of the blood lead can be considered to be deriving from the bone lead pool.…”