Abstract
Background With rapid industrialization, urbanization, and population explosion in sub-Saharan Africa including Uganda, the population has experienced increased exposure to environmental lead subsequently causing elevated blood lead levels. Mean blood levels of 332µg/dL,120µg/dʟ, 25µg/dL,11µg/dL, and 10µg/dL in children under 18 years of age in Nigeria, DR Congo, South Africa, Sudan, and Uganda respectively. Susceptibility to lead toxicity correlates with one’s nutrition status, age, and genetics. This study expounded susceptibility to lead toxicity by relating blood lead levels, delta-aminolevulinic acid dehydratase (ALAD) enzyme activity, and genetic variations of proteins that code for ALAD in urban children of Uganda aged between 6 and 60 months. Methods A total of 198 blood samples were analyzed for blood lead levels (BLL), on an atomic absorption spectrophotometer whereas hemoglobin (Hb) levels, and ALAD enzyme activity, were analyzed on a spectrophotometer before DNA extraction, polymerase chain reaction, and restriction fragment length digestion for ALAD polymorphism. Results Geometric means of BLL (10.55µg/dL, SD = 7.4), Hb (7.85g/dL, SD = 1.3) and ALAD enzyme activity (37.15 units/L BLL, S.D = 9.7), corresponded to samples that coded for ALAD1 allele (99.05%) compared to the 0.05% that coded for ALAD2 with BLL (14.5µg/ dL, SD = 4.7), Hb (6.1 g/ dL), ALAD enzyme activity (33.8 units/L, SD=1.45). There was a significant relationship with a negative linear correlation between BLL, Hb (status, and ALAD enzyme activity in the three isozymes (ALAD1-1, ALAD1-2, and ALAD2-2) in the strength of ALAD1-1 (r = 0.42, p-value = 0.02) ˂ ALAD1-2 (r = 0.62, effective size = 0.43, p-value = ˂ 0.001) ˂ ALAD2-2 (r = 0.67, effective size = 0.86, p-value = ˂ 0.001). Conclusions Most of the study participants coded for the ALAD1 allele hence hoarded blood lead, which could result in delayed exposure and adverse effects later in their lives.
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