Associations of Subtypes of Hemoglobin with Delta-Aminolevulinic Acid Dehydratase Genotype and Dimercaptosuccinic Acid-Chelatable Lead Levels

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Abstract
Hemoglobin in erythrocytes may be an important intravascular site of lead binding. We examined associations of hemoglobin subtypes A1 and A2 with δ-aminolevulinic acid dehydratase (ALAD) genotype, a protein that is another important site of erythrocyte lead binding. After oral administration of dimercaptosuccinic acid (DMSA-chelatable lead), we also examined 4-h lead excretion, which provides an estimate of bioavailable lead stores. We randomly selected 57 South Korean current lead battery manufacturing workers from two plants (N = 290 employees) and from two ALAD genotype strata (ALAD1–1 and ALAD1–2). These workers voluntarily administered 5 mg/kg oral DMSA. We frequency-matched subjects with ALAD1–1 (n = 38) to subjects with ALAD1–2 (n = 19) with respect to duration of employment in the lead industry. Blood lead levels ranged from 11 to 53 μg/dl (mean ± standard deviation, 25.4 ± 10.2 μg/dl). After administration of oral DMSA, workers excreted a mean lead level of 85.4 (standard deviation, 45.0 μg; range, 16.5–184.1 μg). Hemoglobin A1 and A2 ranged from 3.7% to 9.9% and 1.6% to 5.9%, respectively (mean ± standard deviation, 6.2 ± 1.0% and 2.7 ± 0.8%, respectively). Subjects with ALAD1–1 had elevated mean hemoglobin A1 levels (adjusted p = .05). In addition, higher hemoglobin A1 levels were associated with higher DMSA-chelatable lead levels (adjusted p = .03). This, as well as the results of prior research, suggest that both ALAD and hemoglobin A1 may be important lead-binding sites that influence urinary lead excretion after administration of DMSA.