Abstract

The aim of this paper was to assess the endogenous release of lead from bone to blood, in 204 exposed subjects resuming their duties after a 10-month strike in a primary lead smelter in 1991. In vivo¹⁰⁹Cd K X-ray Fluorescence (¹⁰⁹Cd K XRF) was used to measure the bone lead concentration in tibia and calcaneus in the smelter, in 1994 and five years later. The 1994 data were used to derive the post-strike bone lead concentrations retrospectively from the significant association between bone lead and the cumulative blood lead index (CBLI). When a linear model was used to predict the current blood lead upon the level of lead in bone, structural analysis of the data produced slopes for tibia (2.0, 95% CI 1.66–2.54) and calcaneus (0.19, 95% CI 0.16–0.23) that were significantly higher than those predicted by the commonly used simple linear regression method, for tibia (0.73, 95% CI 0.58–0.88) and calcaneus (0.08, 95% CI 0.06–0.09). This suggests that more lead than previously predicted by regression is released from bone to blood. Furthermore, the structural analysis of the data produced an estimation of the contribution of the bone lead stores to the bloodstream that was more consistent with the 1999 epidemiological data than did the regression estimation. Moreover, a non-linear relationship between tibia lead and blood lead was suggested from the assumption checking procedures for regression. When a non-linear regression model was fit to the data, the method produced estimates of important parameters in human lead kinetics, namely the blood lead saturation constant, showing a good agreement with current knowledge of lead metabolism. Finally, the likelihood of a non-linear bone lead release seems to be supported by the recently described dependence of the half-life of lead in bone on age and intensity of occupational exposure.