Causes of lead toxicity in a Nigerian city.

BACKGROUND: Up to 70% of young Nigerian children have been reported to have blood lead concentrations > or =10 microg/dl. AIMS: To better elucidate risk factors for lead toxicity among Nigerian families with children at risk for lead toxicity. METHODS: Two geographic wards in Jos, Nigeria were selected for study, one previously reported to have a high mean blood lead level (37 (SD 13) microg/dl) and one with a lower mean blood lead level (17 (SD 10) microg/dl) in young children. Data pertaining to potential risk factors for lead exposure were collected from children and adults in 34 households. RESULTS: The mean (SD) blood lead concentration of 275 subjects, aged 3 weeks to 90 years, was 8.7 (5.7) microg/dl (range 1-34 microg/dl); 92 (34%) had concentrations > or =10 microg/dl. In multivariate analysis, an age of 5 years and under, flaking house paint, residence near a gasoline seller, male gender, increasing maternal and paternal education, and use of a lead ore eye cosmetic were independently associated with greater blood lead concentration. Vehicle ownership was associated with reduced lead concentration. Compared with the low-lead ward, residence in the high-lead ward remained significantly associated with greater lead values, indicating that additional factors likely contribute to lead exposure. CONCLUSION: Although the cause of increased lead levels in Jos appears to be multi-factorial, several remediable sources contribute to lead exposure in Nigeria.

Absence of vitamin D deficiency in young Nigerian children.

OBJECTIVE: To determine the prevalence of vitamin D deficiency in young Nigerian children residing in an area where nutritional rickets is common. STUDY DESIGN: A randomized cluster sample of children aged 6 to 35 months in Jos, Nigeria. RESULTS: Of 218 children evaluated, no child in the study had a 25-hydroxyvitamin D (25-OHD) concentration <10 ng/mL (the generally held definition of vitamin D deficiency). Children spent an average of 8.3 hours per day outside of the home. Twenty children (9.2%) had clinical findings of rickets. Children with clinical signs of rickets were more likely to be not currently breast fed and have significantly lower serum calcium concentrations than those without signs of rickets (9.1 vs 9.4 mg/dL, respectively, P =.01). Yet, 25-OHD levels were not significantly different between those children with clinical signs of rickets and those without such clinical signs. CONCLUSION: Vitamin D deficiency was not found in this population of young children in whom clinical rickets is common. This is consistent with the hypothesis that dietary calcium insufficiency, without preexisting vitamin D deficiency, accounts for the development of clinical rickets in Nigerian children.

PIP: Deficiencies of either calcium or vitamin D can cause nutritional rickets. Findings are reported from a study conducted to assess the prevalence of vitamin D deficiency in young Nigerian children living in an area where nutritional rickets is common. A random sample of 218 children aged 6-35 months in Jos, Nigeria, was evaluated. The children were of mean age 22 months. No child had a 25-hydroxyvitamin D (25-OHD) concentration of less than 10 ng/ml, the generally held definition of vitamin D deficiency. Children spent an average of 8.3 hours/day outside of the home, and 20 children (9.2%) had clinical findings of rickets. Children with clinical signs of rickets were more likely to be not currently breast-fed and have significantly lower serum calcium concentrations than those with no signs of rickets. 25-OHD levels were not significantly different between children with clinical signs of rickets and those without such clinical signs. The failure to find vitamin D deficiency in this population of young children in whom clinical rickets is common is consistent with the hypothesis that dietary calcium insufficiency, without preexisting vitamin D deficiency, accounts for the development of rickets in Nigerian children.