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The pattern of results suggested a linear effect, with increasing lead dose producing progressively slower learning and an increased incidence of "impaired" individuals.
Existing research on the lead dose range associated with nephrotoxicity in the occupational setting is inconsistent and primarily cross-sectional in design.
The lead dose levels were adjusted biweekly to gradually elevate the blood lead level of each monkey to a target of 1.69 1.93 μmol/L (35 40 μg/dL).
Results: The number of transfusions per patient was 4.2 ± 2.8 (mean ± SD) with 15.7 ± 1.9 mL/kg packed red blood cells for a lead dose of 1.56 ± 1.77 μg/dL.
In several of the longitudinal studies, change in cognitive function was explicitly modeled in relation to preceding lead dose or in relation to change in lead dose.
Associations between lead dose and NAG were unchanged, and uric acid was inversely associated with RBP.
The strong associations of cumulative lead dose with race/ethnicity and socioeconomic status raises methodologic concerns.
The daily lead dose from the supplements at 100% compliance was about 3 microg Pb.
Therefore, the associations between lead dose and uric acid may be due to the same process causing inverse associations between lead dose and renal function in those with the ALAD2 allele.
However, effect modification by ALAD genotype on associations between lead dose and uric acid was most consistent with the observed effect modification by this genotype on associations between lead dose and renal function.
Studies that used bone lead levels as a direct indicator of retained cumulative lead dose are summarized below.
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