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dc.contributor.authorTinkelman, Naomi E
dc.contributor.authorSpratlen, Miranda Jones
dc.contributor.authorDomingo-Relloso, Arce
dc.contributor.authorTellez-Plaza, Maria 
dc.contributor.authorGrau-Perez, Maria
dc.contributor.authorFrancesconi, Kevin A
dc.contributor.authorGoessler, Walter
dc.contributor.authorHoward, Barbara V
dc.contributor.authorMacCluer, Jean
dc.contributor.authorNorth, Kari E
dc.contributor.authorUmans, Jason G
dc.contributor.authorFactor-Litvak, Pam
dc.contributor.authorCole, Shelley A
dc.contributor.authorNavas-Acien, Ana
dc.identifier.citationEnviron Int. 2020 Feb 11;137:105531.es_ES
dc.description.abstractExperimental and prospective epidemiologic evidence suggest that arsenic exposure has diabetogenic effects. However, little is known about how family exposure to arsenic may affect risk for type 2 diabetes (T2D)-related outcomes in adulthood. We evaluated the association of both maternal and offspring arsenic exposure with fasting glucose and incident T2D in 466 participants of the Strong Heart Family Study. Total arsenic (ΣAs) exposure was calculated as the sum of inorganic arsenic (iAs) and methylated (MMA, DMA) arsenic species in maternal and offspring baseline urine. Median maternal ΣAs at baseline (1989-91) was 7.6 µg/g creatinine, while median offspring ΣAs at baseline (2001-03) was 4.5 µg/g creatinine. Median offspring glucose in 2006-2009 was 94 mg/dL, and 79 participants developed T2D. The fully adjusted mean difference (95% CI) for offspring glucose was 4.40 (-3.46, 12.26) mg/dL per IQR increase in maternal ΣAs vs. 2.72 (-4.91 to 10.34) mg/dL per IQR increase in offspring ΣAs. The fully adjusted odds ratio (95%CI) of incident T2D was 1.35 (1.07, 1.69) for an IQR increase in maternal ΣAs and 1.15 (0.92, 1.43) for offspring ΣAs. The association of maternal ΣAs with T2D outcomes were attenuated with adjustment for offspring adiposity markers. Familial exposure to arsenic, as measured in mothers 15-20 years before offspring follow-up, is associated with increased odds of offspring T2D. More research is needed to confirm findings and better understand the importance of family exposure to arsenic in adult-onset diabetes.es_ES
dc.description.sponsorshipThis study was supported by the National Institute of EnvironmentalHealth Sciences, Unites States (P42ES010349, P30ES009089,R01ES028758, R01ES025216).N.T., P.F.-L., and A.N.-A. contributed to the preparation of researchdata and writing of the manuscript. N.T, M.J.S, A.D.-R., M.T.-P., M.G.-P., and A.N.-A. contributed to the statistical analysis. B.V.H., J.M., K.N.,J.G.U., and S.C. contributed as the primary investigators of the SHS andSHFS, and to the preparation of the research data. K.A.F. and W.G.contributed to the arsenic measurements in the SHS and SHFS partici-pants. A.N.-A. is the guarantor of this work and, as such, had full accessto all the data in the study and takes responsibility for the integrity ofthe data and the accuracy of the data analysis.es_ES
dc.publisherElsevier es_ES
dc.subjectAmerican Indianses_ES
dc.subjectFasting glucosees_ES
dc.subjectIndigenous populationses_ES
dc.subjectInsulin resistancees_ES
dc.subjectPrenatal exposureses_ES
dc.subjectProspective cohort studieses_ES
dc.titleAssociations of maternal arsenic exposure with adult fasting glucose and insulin resistance in the Strong Heart Study and Strong Heart Family Studyes_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.contributor.funderNIH - National Institute of Environmental Health Sciences (NIEHS) (Estados Unidos) 
dc.identifier.journalEnvironment internationales_ES
dc.repisalud.centroISCIII::Centro Nacional de Epidemologíaes_ES
dc.rights.accessRightsopen accesses_ES

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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