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Several biological mechanisms have been identified, with different implications for the use of bone lead as an exposure measure.
A strength of our study is the use of bone lead measurements as biomarkers of cumulative lead exposure over many years.
However, despite these limitations, we believe our results are still valid given the longitudinal design of our study, the adjustment for several predictors and potential confounders, and the use of bone lead as a measure of cumulative prenatal lead exposure.
Details regarding the measurement of lead in bone using in vivo KXRF have been reviewed previously (Chettle et al. 1991; Todd et al. 1992a), as has the use of bone lead in epidemiologic studies (Hu et al. 1989, 1998; Landrigan and Todd 1994).
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This variability in the estimates of bone lead contribution calculated using two different sampling pairs is produced by the relative size of the analytical measurement error compared with the isotopic differences between blood and feces from two collection time points.
We used directed acyclic graphs and the example of bone lead and mortality (all-cause, cardiovascular, and ischemic heart disease) among 835 white men in the Normative Aging Study NASS) to illustrate potential bias related to recruitment into the NAS and the bone lead substudy.
Measurements of bone lead content in children could be used to establish empirical relationships between bone and blood lead levels in pediatric populations.
In industrialized societies, accumulation of bone lead is many times greater than that observed in cultures that do not use lead (Drasch 1982).
Repeated measurements of bone lead demonstrate the slow elimination of lead from bone.
Changes in the ratio of blood lead to bone lead with time would reflect the course of bone lead availability.
Thus, the approach used here, which assumes that the bone lead isotopic composition does not change with time, yields a minimum calculated value for the contribution of bone lead to blood.
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