HFE H63D polymorphism as a modifier of the effect of cumulative lead exposure on pulse pressure: the normative aging study
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HFE H63D polymorphism as a modifier of the effect of cumulative lead exposure on pulse pressure: the normative aging study
| Title: | HFE H63D polymorphism as a modifier of the effect of cumulative lead exposure on pulse pressure: the normative aging study |
| Author: |
Zhang, Aimin; Mukherjee, Bhramar; Nie, Huiling; Hu, Howard; Park, Sung Kyun; Wright, Robert O.; Weisskopf, Marc G.; Sparrow, David
Note: Order does not necessarily reflect citation order of authors. |
| Citation: | Zhang, Aimin, Sung Kyun Park, Robert O. Wright, Marc G. Weisskopf, Bhramar Mukherjee, Huiling Nie, David Sparrow, and Howard Hu. 2010. HFE H63D polymorphism as a modifier of the effect of cumulative lead exposure on pulse pressure: the normative aging study. Environmental Health Perspectives 118(9): 1261-1266. |
| Full Text & Related Files: |
2944087.pdf (560.8Kb; PDF) 
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| Abstract: | Background: Cumulative lead exposure is associated with a widened pulse pressure (PP; the difference between systolic and diastolic blood pressure), a marker of arterial stiffness and a predictor of cardiovascular disease. Polymorphisms in the hemochromatosis gene (HFE) have been shown to modify the impact of cumulative lead exposure on measures of adult cognition and cardiac function. Objectives: We examined whether the HFE mutations modify the impact of lead on PP in community-dwelling older men. Methods: We examined 619 participants with a total of 1,148 observations of PP from a substudy of bone lead levels (a measure of cumulative exposure, measured by in vivo K-shell X-ray fluorescence) and health in the Normative Aging Study between 1991 and 2001. Linear mixed-effects regression models with random intercepts were constructed. Results: Of the 619 subjects, 138 and 72 carried the HFE H63D and C282Y variants, respectively. After adjusting for age; education; alcohol intake; smoking; daily intakes of calcium, sodium, and potassium; total calories; family history of hypertension; diabetes; height; heart rate; high-density lipoprotein (HDL); total cholesterol:HDL ratio; and waist circumference, baseline bone lead levels were associated with steeper increases in PP in men with at least one H63D allele (p-interaction = 0.03 for tibia and 0.02 for patella) compared with men with only the wild types or C282Y variant. Conclusions: The HFE H63D polymorphism, but not the C282Y mutation, appears to enhance susceptibility to the deleterious impact of cumulative lead on PP, possibly via prooxidative or pro-inflammatory mechanisms. |
| Published Version: | doi:10.1289/ehp.1002251 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944087/pdf/ |
| Terms of Use: | This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA |
| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:4885968 |
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