Environmental lead exposure as a risk for childhood aplastic anemia

Concern about environmental lead exposure as a significant public health threat has increased as evidence has accumulated regarding adverse health effects at successively lower levels. Aplastic anemia is a hematological disorder of unknown etiology with a high lethality rate. Lead is a known toxicant for the hematopoietic system. Oxidative stress appears to be the possible mode of lead toxicity. We evaluated the effects of blood lead level on oxidative stress parameters in children suffering from aplastic anemia disease. Seventeen children with aplastic anemia disease (15 male and 2 female, age 3-12 y) were recruited in the study group. Fifty one healthy children (45 male and 6 female, age 3-12 y) having normal blood profiles and not suffering from any chronic disease(s) were used as controls. Blood lead level and oxidative stress parameters were determined. Mean blood lead level was significantly higher while delta-aminolevulinic acid dehydratase (delta-ALAD) activity, a biomarker for lead exposure was significantly lower in the study group as compared to the control group (p < 0.05 for each). Thiobarbituric acid reactive species (TBARS), a marker of lipid peroxidation, was significantly higher while the antioxidant glutathione (GSH) level was significantly lower in the study group as compared to the control group (p < 0.05 for each). Activity of the antioxidant enzyme catalase (CAT) was significantly higher in the study group than in the control group (p < 0.05). There was a significant negative correlation of blood lead levels with delta-ALAD (r = -0.45; p < 0.05) and GSH (r = -0.32; p < 0.05), and a positive correlation with TBARS (r = 0.41; p < 0.05) and CAT (r = 0.37; p < 0.05). Although a causal pathway cannot be determined from this study, our results indicated that lead induces oxidative stress in children suffering from aplastic anemia. Lead-induced oxidative stress as an underlying mechanism for aplastic anemia warrants further research.