Like many malaria halo endemic developing countries, Uganda is faced with several health -threatening diseases including anemia. A majority (60%) of the Uganda’s urban dwellers live in slums such as Katanga  in Kampala capital city where social disadvantages remain a big problem . Due to the poor urban planning of Kampala city, there are no gazetted residential areas so people live in or next to industries, workshops, motor garages, metal crafts yards, battery recycling plants, motor garages, mosquito breeding grounds, and landfills which predisposes them to lead intoxication. There are reports of elevated lead levels in water sources, soils, foodstuffs and air around Kampala city . According to the study done by , Plasmodium malaria accounts for up to 40% of all outpatient visits, 25% of all hospital admissions, and 14% of all hospital deaths [4, 5] despite the government efforts to curb its transmission . 53% of the children in this area especially those under the age of 5 years have been reported to be anemic [3, 5] and this could be due to high malaria prevalence in this area.
Although, malaria infections remain the key cause of the high prevalence of anemia, there are maybe other neglected cofounders like Lead poisoning resulting from contaminated air, soils, water sources, urban-grown foodstuffs and Leaded paints [2, 6, 7, 8, 9]. Because both lead pollution and malaria geographically overlap, and produce similar hematological outcomes their co-existence in this area may affect the child’s health.
Lead exposure accounts for an individual’s blood lead level (BLL) and is more evident in developing fetus by directly affecting the hematopoietic system. Erythrocytes are the major sink of over 99% of the Lead present in the blood and with over 80% is bound to δ-aminolevulinic acid dehydratase (δ-ALAD) a cytosolic enzyme. This enzyme is believed to catalyze the formation of porphobilinogen from δ-aminolevulinic acid (ALA) [9, 10].
During lead intoxication, BL is believed to limit the iron transfer from endosomes toward the cytoplasm and to reduce the lifespan of circulating erythrocytes by increasing the fragility of cell membranes [11, 12].
Blood lead further triggers a reduction in red blood cells (RBC) production by specifically inhibiting Ferrochelatase a mitochondrial enzyme that catalyzes the insertion of iron into protoporphyrin during heme formation. Aminolevulinic acid synthetase (ALAS) a mitochondrial enzyme that catalyzes the formation of aminolevulinic acid (ALA) from succinyl CoA and glycine is also affected by BL [13, 14].
In a normal heme synthesis system, the rate of iron formation and utilization is well balanced and equilibrium is altered by insufficiency of iron. High malaria burden, overproduction of protoporphyrin and decreased ferrochelatase activity due to Lead poisoning could be responsible for the high anemia scourge.
During malaria anemia, Lead becomes even more concentrated in red blood cells causing deleterious effects on several essential cellular processes, including inhibition of protein synthesis. Malaria due to Plasmodium infections becomes fatal by causing severe anemia to the host though other symptoms may occur depending on the species.
Malarial anemia is caused by massive erythrocytes lysis due to elevated parastemia resulting in parasitized red cells rupture. Because of increased parasite density in the host system, there are intrinsic and extrinsic changes to the red blood cells. This persistent situation in turn activates the splenic and other macrophages for phagocytosis  and resulting into anemia.
Both iron deficiency due to malaria and BL are each capable of inhibiting heme synthesis at the final step but low cellular iron concentrations during iron deficiency enhance Lead’s inhibition on synthetic reactions because of its high affinity for the side chains of some amino acids than iron.
Ferrochelatase is specifically sensitive to low iron levels in the presence of Lead poisoning  and zinc instead of iron is incorporated into protoporphyrin (PPN) resulting in elevated levels of zinc protoporphyrin (ZPP).
Zinc protoporphyrin or FEP concentrations have been used to measure of heme synthesis inhibition, and increased levels are an indicator of iron deficiency as a heme synthesis disorders .
Since red cells are at the Centre of anemia pathogenesis, elevated malaria parasite density and BLL could produce severe anemia among children. The severity of anemia status is dependent on the host's age and nutrition status . The combined aftermath of these two processes in malaria-endemic regions may result in severe anemia. This work, therefore, aimed at finding the association between blood lead levels and Plasmodium parasite density and anemia status among the study group. In this study, reduced hemoglobin (Hb) concentration was considered an index of anemia while the FEB/Hb ratio as an impaired heme synthesis index due to Lead poisoning.