(Gaithersburg, MD, USA) . Blood manganese accuracy was verified by participating in pro- ficiency testing with the Wadsworth Center of New York Trace Elements in Whole Blood Program (Albany, NY, USA). The level of con- cern for blood lead is 10 µg/dL (CDC 2002). Although there is no blood level of concern for metallic mercury exposure, long-term effects, largely neurological, have been noted at total blood mercury levels < 1.0 µg/L (Agency for Toxic Substances and Disease Registry 1999). Investigators used the reference range of 7.7–12.1 µg/L from Tietz Textbook of Clinical Chemistry for blood manganese (Milne 1999). Although some heavy metals, such as mercury, are better evaluated using urine biomarkers, logistical constraints precluded collection of urine specimens. Environmental sampling. Places where children ate or slept, which were identified by the eldest mother in each compound, were targeted for environmental sampling in each surveyed compound. Samples of soil were swept, placed in a plastic bag, and analyzed for lead content using a portable, hand-held X-ray fluorescence spectrometer (XRF) (Innov-XSystems, Woburn, MA, USA and Thermo-Scientific Niton, Billerica, MA, USA) in an uncontaminated area away from the villages. A certified industrial hygienist or environmental engineer also assessed each village and took XRF readings throughout the villages using U.S. Environmental Protection Agency (EPA) method 6200 to determine areas of high contamination (U.S. EPA 2007). Inside the villages, priority for XRF assess- ment and analysis was given to areas poten- tially affected by ore processing. The limit of detection for lead by XRF was approximately 40 ppm, whereas the upper reporting limit was 100,000 ppm. Samples of processed ore were also collected and analyzed for lead using XRF. After XRF analysis, a subset of soil and ore samples was sent to the U.S. Geological Survey (USGS) for further analysis using inductively coupled plasma mass spectroscopy to verify XRF field results and to perform mineralogy analysis to determine the chemical composition of the samples. The U.S. EPA’s Lead: Renovation, Repair, and Painting Program (U.S. EPA 2008) defines a soil lead hazard as bare soil containing total lead ≥ 400 ppm in a child’s play area or 1,200 ppm in bare soil in other parts of a yard where a child lives (U.S. EPA 2008). U.S. EPA standards were used to cat- egorize XRF soil lead results from surveyed compounds into three groups: ≤ 400 ppm, 401–1,200 ppm, and > 1,200 ppm. A lim- ited number of water samples were collected by a certified industrial hygienist. Water was drawn up in a bucket, and the sampling bottle was immediately submerged to obtain the sample. Water samples were stabilized Environmental Health Perspectives • volume 120 | number 4 | April 2012 with 1 mL nitric acid. Unfortunately, no field blanks were taken. Water samples were sent to a commercial environmental testing labora- tory in the United States and analyzed using U.S. EPA method 200.8 for lead, arsenic, and manganese. The U.S. EPA action level of 15 ppb for drinking water was the reference standard for water results (U.S. EPA 1991). Statistical analysis. Data from the household survey, blood lead results, and environmental sample results were entered into Epi-Info version 3.5.1 (CDC, Atlanta, GA, USA). Statistical analyses were per- formed using SAS software (SAS Institute Inc., Cary, NC, USA). Univariate analyses, including calculation of daily and overall under age 5 mortality rates (U5MR) were performed. The daily U5MR was calculated by taking the number of deaths per 10,000 children per day for the 6-month period of December 2009—May 2010. This rate was compared with the United Nations High Commissioner for Refugees (UNHCR) threshold of > 2.0/10,000/day, which indi- cates deteriorating conditions in a refugee relief situation (UNHCR 2007). To calcu- late the overall U5MR, the number of deaths was divided by the number of children alive in the compounds in the 12-month period of May 2009–May 2010 and multiplied by 1,000. This was compared with the U5MR per 1,000 live births for this region of north- western Nigeria (217 in 1,000 live births) as a way to crudely estimate excess mortality in the villages (NPC and ICF Macro 2009). Bivariate and multivariate logistic regres- sion was used to identify risk factors for child mortality from suspected lead poisoning. Using this outcome, compounds without any children < 5 years of age were excluded from bivariate and multivariate analyses. Risk fac- tors were grouped into demographic, ore pro- cessing, and other environmental risk factors. Demographic risk factors included age, sex, and village of residence. Ore-processing risk factors included whether members of the com- pound or a child’s mother participated in any of the six ore-processing activities. Investigators focused on maternal risk factors because chil- dren < 5 years of age in this population typi- cally spend the majority of time with their Acute childhood lead poisoning in Nigeria mothers in the compound. Environmental risk factors included proximity to ore-grinding activities, presence of ground material inside the compound, soil lead concentrations within the compound, primary water source, and his- tory of animal death (as a proxy for environ- mental contamination) within the compound. The outcome of interest was death of a child. Multicollinearity, intervariable correlation, the Hosmer–Lemeshow goodness-of-fit assess- ment, and the effect of each risk factor on the outcome were considered. Variables from bivariate analysis with a p-value < 0.1 were tested in the model using backward selection. Variables with a p-value of < 0.05 remained in the final model. Results Survey results. All 54 compounds identified in village A and 90% (65 of 72) of compounds in the central area of village B participated in the survey (n = 119). Responses from one compound in village A were excluded because data were incomplete. A total of 463 children < 5 years of age living in the sampled areas of the villages from May 2009 to May 2010 were included in this analysis. Data from all 118 surveyed compounds were used to calculate descriptive statistics regarding village demo- graphics and ore-processing activities. To cal- culate bivariate and multivariate statistics, only data from the 110 surveyed compounds with children < 5 years of age were used. The two villages were similar demographi- cally (Table 1). An average of 4.2 children < 5 years of age lived in each compound. From May 2009 to May 2010, 25% (118 of 463) of children < 5 years of age in the sur- veyed compounds were reported to have died and 82% (97 of 118) were reported to have had convulsions before death. A history of convulsions was reported in 17% (58 of 345) of the surviving children. Sixty-two (53%) of 110 surveyed compounds with children < 5 years of age reported that from one to eight children < 5 years of age had died from May 2009 to May 2010. Eighty-two percent of deaths occurred from December 2009 to May 2010, making the daily U5MR 12.1 per 10,000 children age < 5 years/day for the period in the villages. The approximate overall Table 1. Demographics of participating family compounds by village. Demographic Mean no. of married men per compound Mean no. of mothers per compound Mean no. of children < 5 years of age per compound Total no. of children < 5 years of age in participating compounds, as of May 2009 No. of children < 5 years of age living at time of survey (%) No. of children < 5 years of age who had died within previous 12 months before survey (%) No. of compounds with ≥ 1 pregnant women (%) aNumber of compounds. Village A (n = 53)a 3.1 3.7 4.8 259 181 (70) 78 (30) 26 (49) Village B (n = 65)a 2.1 3.0 3.1 204 164 (80) 40 (20) 24 (37) Both villages (n = 118)a 2.6 3.4 4.2 463 345 (75) 118 (25) 50 (42) 603