Findings. Results of this investigation demonstrated widespread childhood lead poisoning and lead contamination among villages in Anka, Bukkuyum, and Maru LGAs in Zamfara State. The majority of villages surveyed had at least one child < 5 years of age with a BLL ≥ 10 µg/dL, regardless of ore-processing status, and children < 5 years with convulsions and death following convulsions also were reported in both ore-processing and non-ore-processing villages. However, childhood convulsions and deaths and high soil/dust-lead levels were significantly more likely to be found in villages reporting recent gold ore processing than in other villages. Our data support the hypothesis that processing lead-rich gold ore resulted in lead-contaminated villages and homes, lead poisoning among young children, and possibly convulsions and death from severe lead poisoning. Urgent interventions are required to reduce lead exposure, morbidity, and mortality in affected communities.
Gold mining and lead exposure.
Gold production has increased worldwide concomitant with global demand. The price of gold has increased approximately 360% from 2001 to 2010 (Swenson et al. 2011
). Among developing countries, small-scale gold ore processing and production have increasingly been adopted by rural communities. The environmental and health impacts of small-scale gold production are often overlooked. Gold mining and processing are known to cause air and water pollution from arsenic, mercury, and cyanide. Gold processing can also cause mercury poisoning in workers because of direct exposure to liquid or vaporized mercury during ore processing (Swenson et al. 2011
). Although lead pollution is not commonly associated with gold mining, studies of small-scale gold mining sites in the Migori gold belt (Kenya) have demonstrated lead, mercury, and arsenic pollution of multiple gold processing sites; recorded soil lead levels ranged from 16 to 14,999 ppm (Odumo et al. 2010
; Ogala et al. 2002
). A study in Ecuador demonstrated lead, manganese, and mercury pollution of river water near the surveyed small-scale gold-mining sites; approximately 40% of adults from the affected communities had BLLs > 20 µg/dL (Betancourt et al. 2005
). The widespread childhood lead poisoning and lead contamination identified during our investigation illustrates the urgent need to monitor and prevent lead pollution from gold ore–processing activities, particularly among small-scale gold mining communities globally.
In Zamfara State, gold mining began in the early 1900s (Nigeria Ministry of Mines and Steel Development 2010a
), but our prior investigation in two affected villages showed that most families did not begin gold ore processing until 2009–2010 (Dooyema et al. 2012
). Lead was not previously known to be present in this part of the country until high lead levels in gold ore from locations in Zamfara State were identified through recent exploration activities intended to identify new mining sites (Nigeria Ministry of Mines and Steel Development 2010a
). A substantial number of geographically dispersed locations in Zamfara State and its neighboring states were reported as sources of ore; lead content in ore from these locations remains unknown. Geologic studies are needed to systematically investigate the lead content of gold ore in this region and identify sources of ore that may increase the risk of lead poisoning among miners and their families.
Processing lead-rich ore inside villages leads to lead contamination. Contaminated soil and household dust are likely to be the main sources of lead exposure for children living in ore-processing villages. During this investigation we applied U.S. EPA standards established to protect children from typical soil-lead exposures in the United States to categorize lead levels in the soil and household dust samples (U.S. EPA 2003). However, because of bare soil flooring, unpaved roads, and lack of vegetative cover, children in the surveyed villages are likely to interact with the soil in their environment more closely and frequently than do children in the United States, which may result in increased exposures at soil-lead levels below U.S. EPA thresholds (U.S. EPA 2003). Therefore, further investigation to determine appropriate standards for health-protective soil-lead levels in such communities is warranted. Furthermore, although BLLs ≥ 45 µg/dL and soil-lead levels > 400 ppm were reported exclusively in ore-processing villages, children with BLLs ≥ 10 µg/dL were present in half of the non-ore-processing villages. Leaded gasoline was phased out in Nigeria during 2003 (United Nations Environmental Program 2010
), but other potential sources of lead exposure, such as water supplies or traditional medicine, should be investigated in future studies.
Recommendations. Villages with high soil-lead levels identified during this investigation should be prioritized for public health messaging and environmental interventions to reduce childhood lead exposure. Because gold ore processing has become an important source of income, banning villagers from conducting any gold ore–processing activity would be impractical and may damage their economic viability. Instead, gold ore–processing activities should be prohibited inside villages and moved to secured locations that are inaccessible to children. Miners and persons who process ore should be educated regarding occupational precautions and protective measures to reduce the risk of harmful lead exposure for themselves and their families. Miners should change their clothes and shoes when entering and leaving worksites to reduce the likelihood of carrying lead-contaminated dust home. Gold ore–processing activities within villages should be monitored and prohibited to prevent further contamination. Radio programs, dramas, and community gatherings are being used to educate villagers about the health effects of lead, sources of lead, and ways to reduce lead exposure in their homes, villages, and worksites. Both ore-processing villages and non-ore-processing villages should receive these messages given the rapid proliferation of gold ore processing in this region.
Villages with high soil lead levels should also be prioritized for environmental interventions. Assessments should include measurement of lead exposure in all public areas and all households in the village, and environmental remediation efforts should include removal of lead-contaminated ore-processing materials, surface soil, and household dust, and replacing removed surface soil with clean soil. During June 2010–March 2011, such environmental remediation was successfully conducted in seven villages (Blacksmith Institute 2011
Case identification and treatment for lead poisoning should first be extended to villages in which a child with a BLL ≥ 45 µg/dL was identified, followed by villages with childhood lead poisoning, lead contamination, or both. Children with frank lead poisoning will require long-term follow-up and support. Health care providers in this region need to be trained to diagnose and treat lead poisoning, and medical treatment should be coordinated with environmental interventions because chelation therapy alone will be ineffective if children remain in contaminated homes.
Even with remediation efforts and medical treatment, recontamination and recurrent lead poisoning can occur if the source of lead exposure (e.g., ore processing) continues to be present or is reintroduced in villages. State and local authorities should develop and sustain the capacity to institute blood and environmental lead surveillance to identify new cases and affected villages, and monitor BLLs and environmental lead contamination during and after implementation of control measures.
Limitations. Villages of interest were identified through a chain-referral sampling process that might not have captured all villages involved with gold ore processing in Zamfara State, and hard-to-reach or inaccessible villages of interest were not investigated. Therefore, we did not fully determine the geographic extent of childhood lead poisoning in Zamfara State. Second, we could only sample approximately five children in each village. Although we oversampled children from homes with gold ore processing and sick children to increase the likelihood of detecting elevated BLLs, the number of villages with childhood lead poisoning might have been underestimated. Third, we used convulsions and deaths as clinical indicators for lead poisoning because symptoms of lead poisoning are generally nonspecific, and blood lead testing was unavailable at the beginning of the outbreak when the majority of affected children died. However, convulsions and deaths are not sensitive as markers of lead poisoning because they typically occur at BLLs that are higher than the levels detected in most blood samples collected from these villages, and convulsions and death are not specific for lead poisoning because they can result from other locally endemic diseases, including malaria and bacterial meningitis. Finally, we did not assess lead poisoning among children ≥ 5 years of age, adults, or livestock. Older children and adults are also at risk for harmful lead exposure and its adverse health effects, and children may be exposed in utero or through breast-feeding if their mothers have elevated BLLs. In addition, villagers may be exposed through consumption of lead-contaminated food or dairy products. Therefore, characterizing the depth and extent of lead poisoning in older children, adults, and livestock is an important topic for further investigation.