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A Polymorphism in the δ-Aminolevulinic Acid Dehydratase Gene May Modify the Pharmacokinetics and Toxicity of Lead

C. Mark Smith, Xi Wang, Howard Hu and Karl T. Kelsey
Environmental Health Perspectives
Vol. 103, No. 3 (Mar., 1995), pp. 248-253
DOI: 10.2307/3432544
Stable URL: http://www.jstor.org/stable/3432544
Page Count: 6
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Abstract

Associations between the presence of a constitutional variant of δ-aminolevulinic acid dehydratase (ALAD-2) and lead concentrations in blood and bone, as well as between this allele and indices of kidney function, were investigated among 691 members of a construction trade union. The average blood lead level in this group was 7.78 μg/dl. No significant difference was observed in blood lead concentration in ALAD-2 carriers compared to those homozygous for the more common ALAD-1 allel (7.78 (± 3.62 μg Pb/dl vs. 7.73 (± 3.48 μg Pb/dl, respectively; p = 0.73). Bone lead was measured in a subset of 122 of the study subjects. Patella minus tibia lead concentrations for each individual averaged 3.35 ± 11.99 μg Pb/g bone mineral in ALAD-1 homozygotes and 8.62 ± 9.47 μg Pb/g bone mineral in ALAD-2 carriers (p = 0.06). Comparisons of blood urea nitrogen (BUN) and uric acid by genotype indicated elevated levels among ALAD-2 individuals (p = 0.03 and 0.07, respectively). In logistic regression models accounting for other variables potentially associated with BUN and uric acid levels, BUN was significantly associated with blood lead levels (p = 0.01). Associations of BUN and uric acid levels with ALAD-2 were of borderline statistical significance in these models (p = 0.06 and 0.07). Taken together, these results suggest that the ALAD-2 genotype may influence the pharmacokinetic distribution and chronic renal toxicity of lead, perhaps due to differential binding of lead to the variant protein.

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