ISEE-551 Objective: The delta-aminolevulinic acid dehydratase (ALAD) polymorphism has been shown in some studies to alter the impact of lead on kidney function and other health outcomes, which may be due to associated effects on lead binding and tissue distribution kinetics. We evaluated the modifying influence of the ALAD polymorphism on the interrelations between erythrocyte lead, urine lead, and bone lead, and ALAD interaction with bone and erythrocyte lead in association with plasma lead among older community-exposed men. Materials and Methods: Information on ALAD genotype, lead levels in blood, bone (measured using K-shell x-ray fluorescence), and urine were collected for 727 Normative Aging Study participants. We created a structural equation model (SEM) to simultaneously evaluate the association between erythrocyte lead (estimated from whole blood lead) and bone lead, and between urine lead with erythrocyte lead by ALAD genotype (1–2/2–2 vs. 1–1). A second SEM assessed the relation between a latent plasma lead covariate, using urine lead as a surrogate measure, and bone and erythrocyte lead among ALAD 1–2 and 1–1 carriers. Potential predictors of lead levels in urine, erythrocytes, and bone were included in the SEMs. Results: Of the 727 participants, 16% (113) were heterozygous (1–2) and 1% (7) were homozygous (2–2) for the ALAD-2 allele, respectively. Among both ALAD 1–2/2–2 and 1–1 carriers, patella bone lead was associated with higher erythrocyte lead (P<0.05). We observed significant associations between erythrocyte lead and higher urine lead (P<0.05), and between erythrocyte lead and higher plasma lead (P<0.05), respectively, which did not vary with respect to ALAD genotype. Conclusions: The results of this study do not provide evidence that the ALAD genotype modifies the association between erythrocyte lead and plasma lead. These findings should be confirmed in populations with different exposure profiles and account for potential temporal changes in the internal distribution of lead.