Cheng Chen1, Pengcheng Xun1, Leslie A McClure2, John Brockman3, Leslie MacDonald4, Mary Cushman5, Jianwen Cai6, Lisa Kamendulis7, Jason Mackey8, Ka He9. 1. Department of Epidemiology and Biostatistics, School of Public Health - Bloomington, Indiana University, Bloomington, IN 47405, USA. 2. Department of Epidemiology and Biostatistics, Dornsife School of Public Health, Drexel University, Philadelphia, PA 19104, USA. 3. Columbia Research Reactor, University of Missouri, Columbia, MO 65211, USA. 4. National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, OH 45226, USA. 5. Department of Medicine, Larner College of Medicine at the University of Vermont, Burlington, VT 05401, USA. 6. Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. 7. Department of Environmental Health, School of Public Health - Bloomington, Indiana University, Bloomington, IN 47405, USA. 8. Department of Neurology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA. 9. Department of Epidemiology and Biostatistics, School of Public Health - Bloomington, Indiana University, Bloomington, IN 47405, USA. Electronic address: kahe@indiana.edu.
Abstract
BACKGROUND: Although biologically plausible, epidemiological evidence linking exposure to methylmercury with increased risk of ischemic stroke is limited. The effects of methylmercury may be modified by selenium, which is an anti-oxidant that often co-exists with mercury in fish. OBJECTIVES: To examine the association between serum mercury levels with the incidence of ischemic stroke and to explore the possible effect modifications by serum selenium levels and demographic and geographic factors. METHODS: A case-cohort study was designed nested in the REasons for Geographic and Racial Differences in Stroke cohort, including 662 adjudicated incident cases of ischemic stroke and 2494 participants in a randomly selected sub-cohort. Serum mercury was measured using samples collected at recruitment. Multivariable-adjusted hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs) were estimated using the Barlow-weighting method for the Cox proportional hazards regression model. RESULTS: No statistically significant association was observed between serum mercury concentration and the incidence of ischemic stroke (the highest vs. lowest quintile of mercury levels: HR = 0.82; 95% CI = 0.55-1.22; P for linear trend = 0.42). Sex (P for interaction = 0.06), but not serum selenium levels, modified the association; a more evident trend toward lower incidence of ischemic stroke with higher mercury levels was observed among women. CONCLUSION: This study does not support an association between mercury and the incidence of ischemic stroke within a population with low-to-moderate level of exposure. Further studies are needed to explore the possibility of mercury-induced ischemic stroke toxicity in other populations at higher exposure levels.
BACKGROUND: Although biologically plausible, epidemiological evidence linking exposure to methylmercury with increased risk of ischemic stroke is limited. The effects of methylmercury may be modified by selenium, which is an anti-oxidant that often co-exists with mercury in fish. OBJECTIVES: To examine the association between serum mercury levels with the incidence of ischemic stroke and to explore the possible effect modifications by serum selenium levels and demographic and geographic factors. METHODS: A case-cohort study was designed nested in the REasons for Geographic and Racial Differences in Stroke cohort, including 662 adjudicated incident cases of ischemic stroke and 2494 participants in a randomly selected sub-cohort. Serum mercury was measured using samples collected at recruitment. Multivariable-adjusted hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs) were estimated using the Barlow-weighting method for the Cox proportional hazards regression model. RESULTS: No statistically significant association was observed between serum mercury concentration and the incidence of ischemic stroke (the highest vs. lowest quintile of mercury levels: HR = 0.82; 95% CI = 0.55-1.22; P for linear trend = 0.42). Sex (P for interaction = 0.06), but not serum selenium levels, modified the association; a more evident trend toward lower incidence of ischemic stroke with higher mercury levels was observed among women. CONCLUSION: This study does not support an association between mercury and the incidence of ischemic stroke within a population with low-to-moderate level of exposure. Further studies are needed to explore the possibility of mercury-induced ischemic stroke toxicity in other populations at higher exposure levels.
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