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dc.contributor.authorZhang, Aimin
dc.contributor.authorPark, Sung Kyun
dc.contributor.authorWright, Robert O.
dc.contributor.authorWeisskopf, Marc G.
dc.contributor.authorMukherjee, Bhramar
dc.contributor.authorNie, Huiling
dc.contributor.authorSparrow, David
dc.contributor.authorHu, Howard
dc.date.accessioned2011-05-10T01:28:27Z
dc.date.issued2010
dc.identifier.citationZhang, 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.en_US
dc.identifier.issn0091-6765en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:4885968
dc.description.abstractBackground: 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.en_US
dc.language.isoen_USen_US
dc.publisherNational Institute of Environmental Health Sciencesen_US
dc.relation.isversionofdoi:10.1289/ehp.1002251en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944087/pdf/en_US
dash.licenseLAA
dc.subjectgene–environment interactionen_US
dc.subjecthemochromatosis geneen_US
dc.subjectH63D mutationen_US
dc.subjectlead exposureen_US
dc.subjectpulse pressureen_US
dc.titleHFE H63D polymorphism as a modifier of the effect of cumulative lead exposure on pulse pressure: the normative aging studyen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalEnvironmental Health Perspectivesen_US
dash.depositing.authorWright, Robert O.
dc.date.available2011-05-10T01:28:27Z
dash.affiliation.otherHMS^Medicine-Brigham and Women's Hospitalen_US
dash.affiliation.otherSPH^Environmental+Occupational Medicine+Epien_US
dash.affiliation.otherHMS^Pediatrics-Children's Hospitalen_US
dash.affiliation.otherSPH^Environmental+Occupational Medicine+Epien_US
dash.affiliation.otherSPH^Student Stipendsen_US
dc.identifier.doi10.1289/ehp.1002251*
dash.contributor.affiliatedWeisskopf, Marc
dash.contributor.affiliatedWright, Robert
dash.contributor.affiliatedSparrow, David


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