Influence of bone-lead stores on the observed effectiveness of lead hazard intervention

Lead hazard interventions have reduced children's blood-lead concentrations, but do not eliminate lead altogether from the bloodstream. Several studies suggest that blood-lead concentrations, measured 6 to 12 months after such interventions, decline by approximately 25%. The Environmental Protection Agency is preparing to promulgate a rule prescribing residential lead levels in paint, dust, and soil that constitute a lead-based paint hazard. Such a rule will prompt interventions of primary prevention character (i.e., precluding exposure before it occurs) rather than the secondary prevention character interventions (i.e., alleviating exposure after it has adversely affected the resident child) documented in the literature. It is important to attempt to estimate the efficacy achieved from the primary prevention interventions prompted by the rule's promulgation. As bone-lead stores represent the principal confounding factor to relating secondary prevention results to primary prevention, this paper addresses the impact of lead stored in bone, which may later be released to the blood and other parts of the child's body. A simple, but thoroughly documented, modeling exercise is presented to estimate the maximum length of time for which bone-lead stores alone could account for continuing elevated blood-lead levels observed in children following an intervention. The approach is based on a two-compartment model for the transfer of lead between blood and bone tissues within the body and the elimination of lead from the body. Modeling results suggest that bone-lead mobilization can impact blood-lead levels of young children for considerably long periods following an intervention. These results may explain the seemingly contradictory fact that low declines in blood-lead concentrations are observed despite the significant reduction in residential dust-, paint-, and soil-lead levels observed following lead hazard interventions. An intervention which reduces a 5-year-old child's total lead exposure by 50% might, due to mobilized bone-lead stores, produce only a 25% decline in the child's blood-lead concentrations measured 12 months following the intervention. The results also suggest, however, that those intervention strategies for which less than 25% declines were observed 12 months following the intervention likely eliminated less than 50% of the children's total lead exposure.