Mercury exposure, malaria, and serum antinuclear/antinucleolar antibodies in amazon populations in Brazil: A cross-sectional study

被引：69
作者：
Silva I.A. [1 ,2 ,3 ]
Nyland J.F. [1 ,2 ,3 ]
Gorman A. [1 ,2 ,3 ]
Perisse A. [1 ,2 ,3 ]
Ventura A.M. [1 ,2 ,3 ]
Santos E.C.O. [1 ,2 ,3 ]
De Souza J.M. [1 ,2 ,3 ]
Burek C.L. [1 ,2 ,3 ]
Rose N.R. [1 ,2 ,3 ]
Silbergeld E.K. [1 ,2 ,3 ]
机构：
[1] Johns Hopkins University Bloomberg, School of Public Health, Baltimore, MD 21201
[2] Department of Epidemiology, Univ. of Maryland Medical School, Baltimore, MD
[3] Institute Evandro Chagas (IEC), Fund. Nacional da Saúde
来源：
Environmental Health | / 3卷 / 1期
关键词：
Mercury; Malaria; Fish Consumption; Prevalent Malaria; Mercury Level;
D O I：
10.1186/1476-069X-3-11
中图分类号：
学科分类号：
摘要：
Background: Mercury is an immunotoxic metal that induces autoimmune disease in rodents. Highly susceptible mouse strains such as SJL/N, A.SW, B10.S (H-2s) develop multiple autoimmune manifestations after exposure to inorganic mercury, including lymphoproliferation, elevated levels of autoantibodies, overproduction of IgG and IgE, and circulating immune complexes in kidney and vasculature. A few studies have examined relationships between mercury exposures and adverse immunological reactions in humans, but there is little evidence of mercury-associated autoimmunity in humans. Methods: To test the immunotoxic effects of mercury in humans, we studied communities in Amazonian Brazil with well-characterized exposures to mercury. Information was collected on diet, mercury exposures, demographic data, and medical history. Antinuclear and antinucleolar autoantibodies (ANA and ANoA) were measured by indirect immunofluorescence. Anti-fibrillarin autoantibodies (AFA) were measured by immunoblotting. Results: In a gold mining site, there was a high prevalence of ANA and ANoA: 40.8% with detectable ANoA at ≥1:10 serum dilution, and 54.1% with detectable ANA (of which 15% had also detectable ANoA). In a riverine town, where the population is exposed to methylmercury by fish consumption, both prevalence and levels of autoantibodies were lower: 18% with detectable ANoA and 10.7% with detectable ANA. In a reference site with lower mercury exposures, both prevalence and levels of autoantibodies were much lower: only 2.0% detectable ANoA, and only 7.1% with detectable ANA. In the gold mining population, we also examined serum for AFA in those subjects with detectable ANoA (≥1:10). There was no evidence for mercury induction of this autoantibody. Conclusions: This is the first study to report immunologic changes, indicative of autoimmune dysfunction in persons exposed to mercury, which may also reflect interactions with infectious disease and other factors. © 2004 Silva et al; licensee BioMed Central Ltd.
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