Outbreak of Fatal Childhood Lead Poisoning Related to Artisanal Gold Mining in Northwestern Nigeria, 2010

Article excerpt

BACKGROUND: In May 2010, a team of national and international organizations was assembled to investigate children's deaths due to lead poisoning in villages in northwestern Nigeria.

OBJECTIVES: Our goal was to determine the cause of the childhood lead poisoning outbreak, investigate risk factors for child mortality, and identify children < 5 years of age in need of emergency chelation therapy for lead poisoning.

METHODS: We administered a cross-sectional, door-to-door questionnaire in two affected villages, collected blood from children 2-59 months of age, and obtained soil samples from family compounds. Descriptive and bivariate analyses were performed with survey, blood lead, and environmental data. Multivariate logistic regression techniques were used to determine risk factors for childhood mortality.

RESULTS: We surveyed 119 family compounds. Of 463 children < 5 years of age, 118 (25%) had died in the previous year. We tested 59% (204/345) of children < 5 years of age, and all were lead poisoned [greater than or equal to] 10 pg/dL); 97% (198/204) of children had blood lead levels (BLLs) 45 pg/dL, the threshold for initiating chelation therapy. Gold ore was processed inside two-thirds of the family compounds surveyed. In multivariate modeling, significant risk factors for death in the previous year from suspected lead poisoning included the age of the child, the mother's work at ore-processing activities, community well as primary water source, and the soil lead concentration in the compound.

CONCLUSION: The high levels of environmental contamination, percentage of children < 5 years of age with elevated BLLs (97%, > 45 pg/dL), and incidence of convulsions among children before death (82%) suggest that most of the recent childhood deaths in the two surveyed villages were caused by acute lead poisoning from gold ore processing activities. Control measures included environmental remediation, chelation therapy, public health education, and control of mining activities.

KEY WORDS: artisanal gold mining, childhood, environmental health, lead poisoning, nervous system. Environ Health Perspect 120:601-607 (2012). http://dx.doi.org/10.1289/ehp.1103965 [Online 20 December 20111

Childhood lead exposure results in lower intelligence and behavior problems and negatively affects multiple body systems (Bellinger 2004; Canfield et al. 2003; Lanphear et al. 2005; Mendelsohn et al. 1998; Tellez-Rojo et al. 2006). Young children are particularly susceptible to lead exposure because of behavioral factors, such as frequent hand-to-mouth activities, and biological factors including greater gastrointestinal absorption and developing neurological systems (Bellinger 2004; Henretig 2006; Lidsky and Schneider 2003). Encephalopathy typically occurs with blood lead levels (BLLs) [greater than or equal to] 100 tig/dL but can occur with BLLs as low as 70 [micro]g/dL [Centers for Disease Control and Prevention (CDC) 2002; Henretig 2006]. Symptoms of acute lead encephalopathy include vomiting, changes in behavior, ataxia, convulsions, and coma (CDC 2002; Henretig 2006). Currently, childhood lead poisoning resulting in encephalopathy and death in developed countries is rarely reported, and the last documented child fatality from lead poisoning in the United States was in 2006 (Berg et al. 2006). However, hundreds of U.S. pediatric deaths from acute lead encephalopathy were recorded in the first half of the 20th century. For example, 202 deaths from childhood lead poisoning were recorded in U.S. cities from 1931 and 1940, with 25% occurring in Baltimore, Maryland (McDonald and Kaplan 1942). Most lead poisoning in this period occurred in urban settings from deteriorating lead house paint and lead-painted cribs. Lead-poisoned children in this era frequently had high BLLs. One study evaluating lead poisoning in 293 children from 1931 to 1970 found the mean BLL for children with mild, severe, and fatal acute lead encephalopathy to be 328 [micro]g/dL, 336 [micro]g/dL, and 327 [micro]g/dL, respectively (National Research Council 1972). …