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Environmental Health Perspectives Volume 111, Number 10, August 2003 Open Access
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Low-Dose Exposure to Inorganic Mercury Accelerates Disease and Mortality in Acquired Murine Lupus

Charles S. Via,1,2 Phuong Nguyen,1,2 Florin Niculescu,1,2 John Papadimitriou,3 Dennis Hoover,4 and Ellen K. Silbergeld4

1Research Service, Department of Veteran Affairs Medical Center, Baltimore, Maryland, USA; 2Division of Rheumatology and Clinical Immunology, and 3Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA; 4Bloomberg School of Public Health, Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland, USA

Abstract
Inorganic mercury (iHg) is known to induce autoimmune disease in susceptible rodent strains. Additionally, in inbred strains of mice prone to autoimmune disease, iHg can accelerate and exacerbate disease manifestations. Despite these well-known links between iHg and autoimmunity in animal models, no association between iHg alone and autoimmune disease in humans has been documented. However, it is possible that low-level iHg exposure can interact with disease triggers to enhance disease expression or susceptibility. To address whether exposure to iHg can alter the course of subsequent acquired autoimmune disease, we used a murine model of acquired autoimmunity, lupus-like chronic graft-versus-host disease (GVHD) , in which autoimmunity is induced using normal, nonautoimmune prone donor and F1 recipient mice resistant to Hg-induced autoimmunity. Our results indicate that a 2-week exposure to low-dose iHg (20 or 200 µg/kg every other day) to donor and host mice ending 1 week before GVHD induction can significantly worsen parameters of disease severity, resulting in premature mortality. iHg pretreatment clearly worsened chronic lupus-like disease, rather than GVHD worsening iHg immunotoxicity. These results are consistent with the hypothesis that low-level, nontoxic iHg preexposure may interact with other risk factors, genetic or acquired, to promote subsequent autoimmune disease development. Key words: , , , , , . Environ Health Perspect 111:1273-1277 (2003) . doi:10.1289/ehp.6064 available via http://dx.doi.org/ doi:10.1289/ehp.6064 available via http://dx.doi.org/ [Online 1 April 2003]


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