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Objectives To investigate current lead (Pb) exposure in children living in Andean Ecuadorian communities. Blood Pb (PbB) and zinc protoporphyrin (ZPP) levels were used respectively as biomarkers of acute and chronic Pb poisoning. The current PbB-ZPP levels were compared with previous pediatric PbB-ZPP levels recorded over years in the study area. Design and Methods Samples of whole blood were collected from 22 Andean children of Quechua and Mestizo backgrounds and measured for PbB concentrations by graphite furnace atomic absorption spectroscopy. ZPP/heme ratio and ZPP whole blood (ZPP WB) levels were measured with a hematofluorometer. Results The mean PbB level for children in the current study group was 14.5 μg/dL, which was significantly lower than the mean PbB level of 41.1 μg/dL found in the same study area in the 1996–2000 test period, and lower than the 22.2 μg/dL mean level found in the 2003–2007 period. The current mean ZPP/heme ratio was 102.1 μmol/mol, and the mean ZPP WB level was 46.3 μg/dL, both lower than values previously found in children in the study area. Conclusion While the current pediatric PbB-ZPP levels in the study area remain elevated in some children, the overall levels indicate a decline relative to levels observed in the same Pb-contaminated area in the period between 1996 and 2007. The elevated ZPP levels suggest a history of chronic Pb exposure, and potential iron deficiency in some children. The overall reduction in PbB-ZPP levels suggests a positive outcome of a Pb-exposure education and prevention program, and the therapeutic intervention of succimer chelation therapy.

A four-day-old boy with a positive result in newborn-screening testing was referred to the hospital for further evaluation. He was the product of a 39-week gestation and appeared well at birth. His laboratory results included the following plasma findings: ammonia, 109 g/dL (reference interval, 20 -65 g/dL); citrulline, 169 mol/L (reference interval, 2-50 mol/L); and leucine, 278 mol/L (reference interval, 32-153 mol/L). Also found were increases in homocysteine and ␥-aminobutyric acid. The amino acid spectrum is shown below (Fig. 1). QUESTIONS 1. What class of genetic disorders did this patient most likely have? 2. What enzyme deficiency was suggested by the patient's amino acid profile, and how did you reach the conclusion?The answers are on the next page. The patient's plasma sample was analyzed on a Hitachi L-8800 amino acid analyzer after removing proteins by treatment with 40 g/L sulfosalicylic acid/internal standard solution, centrifugation, and filtration. The amino acids were separated by high-resolution ion-exchange chromatography and then subjected to postcolumn ninhydrin derivatization; detection was by spectrophotometry at 570 nm and 440 nm. The areas under the curves were calculated by using the manufacturer's software for final quantification. Hcys, homocysteine; ␥-ABA, ␥-aminobutyric acid; AEC, S-2-aminoethyl-L-cysteine; 3-M Histidine, 3-methylhistidine.