Role of blood lead levels on the anemia status of malaria infected children of Katanga- Kampala

Abstract

Like many other African countries, Uganda is faced with simultaneous unfolding economical, demographic, environmental, urbanization and technological transitions. These transitions are coming with economic growth, massive urban poverty, health burden, environmental degradation and other social challenges. Environmental degradation for example is concentrating metal toxicants like Lead and breeding grounds for vectors associated with infectious diseases via anthropogenic activities. Increased number of mosquito habitats account for malaria infection while elevated environmental lead levels of environmental Lead account for blood Lead levels. Following exposure to both malaria infection and lead pollution, they target the red blood cells (RBC) with similar hematological outcomes. The malaria parasites destroy both infected and uninfected red cells, decrease bone marrow responses, impair iron metabolism and cause iron deficiency while blood Lead decrease heme biosynthesis, dyserythropoiesis, and iron dysregulation The present study, therefore, aimed at assessing the role of blood Lead levels on the anemia pathogenesis in urban Ugandan children aged between six to sixty months who live exposed to both environmental Lead and malaria infection (Katanga-Kampala, Uganda). Site-specific data on environmental Lead levels in water, soil and air were obtained, and used to predict blood lead levels of the target study participants (n =198). Following the blood lead levels predictions, blood samples were collected assayed for blood Lead levels, malaria parasite density, anemia and oxidative stress status, degree of inhibition on enzymes delta-aminolevulinic acid dehydratase (ALAD) and pyrimidine-5 nucleotidase (P5N) important for both heme biosynthesis and RBC integrity respectively. It was found that environmental Lead levels during both the rainy and dry seasons were 15±4.3 µg/L and 11±1.7 µg/L respectively (r = 0.39, R = 0.067, p-value = 0.03), predicted geometric (GM) blood Lead levels = 9.7µg/dL (mean), 78/198 (39.4%) samples had detectible B-Pb ions = 8.6 µg/dL, Hb = 8.3g/dL with a calculated mean health risk factor of (RQ) > 1, mean parasite density during the rainy seasons and dry season = 1.1x103 /µL blood and 1.7x103 /µL blood respectively (r = 0.52, R =0.23, p-value = 0.002). Correlation of parasite densities and environmental Lead levels during both the rainy and dry seasons was R = 0.0044 and P-value (two-tailed) = 0.61). Study participants anemia status (mean Hb levels) was 8.6 g/dL, mean ALAD enzyme activity = 3.96 U/dL blood, mean P5N activity = 7.1µm/h/g Hb while their ALA levels (17.5 µg/dL), and oxidative stress status (GSH/GSSH index) =22.4:1. Regression analysis and correlation between parasite density and Hb (r = -0.231, R2 = 0.15, Pvalue < 0.001), blood Lead levels and ALAD activity (r = - 0.34, P-value < 0.001), B-Pb, and Hb (r =-0.955, p=˂0.0001, R=0.913), B-Pb and P5N (r =-0.997, p=˂0.0001, R=0.993), P5N and Hb (r=0.961, p=˂0.0001, R=0.924). Delta-aminolevulinic acid (ALA) levels (17.5 µg/dL), reduced GSH/GSSH index mean value (22.4:1), redox status and blood Lead levels (R2 =0.33, P-value < 0.001). This study reports a strong and significant positive correlation between blood Lead levels, and hemoglobin levels during malaria infection. This study therefore, reports that concomitant exposure to both malaria infection and lead toxicity may pose serious health challenges and therefore, recommends a more detailed study on delta-aminolevulinic acid dehydratase polymorphism in relation to Lead toxicity susceptibility among Uganda‘s urban children.