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Furthermore, the effect estimates of blood and bone lead were not attenuated when assessed simultaneously, suggesting that both contribute independently to IHD.
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If lead exposure caused longer survival with PD, then this could bias our results, but this seems unlikely, and bone lead was not associated with PD duration in our data.
Bone lead was positively associated with blood lead only among postmenopausal women who were not using ERT, and this was true both for trabecular (patella) and cortical (tibia) bone lead.
In industrialized societies, accumulation of bone lead is many times greater than that observed in cultures that do not use lead (Drasch 1982).
In this study, tibia bone lead was more strongly associated with pulse pressure than was patella bone lead (data not shown).
Bone lead was measured in the tibia and patella.
Bone lead levels were not significantly associated with physical growth.
Bone lead concentration was not available in these data.
Tibia bone lead concentration was not associated with CCI scores in the overall population (Table 3).
The participants for the present study were a subgroup of the NAS cohort who underwent at least one KXRF bone lead measurement and were not on antihypertensive therapy at the time of this measurement.
Moreover, blood lead levels were not associated with tooth loss, suggesting that bone lead concentrations are a better indicator of the risk of tooth loss posed by cumulative long-term environmental lead exposure.
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