Impacts of the Mitochondrial Genome on the Relationship of Long-Term Ambient Fine Particle Exposure with Blood DNA Methylation Age

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dc.authoridLaue, Hannah/0000-0002-2578-103X
dc.authoridCAYIR, AKIN/0000-0002-2014-6635
dc.authoridColicino, Elena/0000-0002-1875-8448
dc.authoridJust, Allan/0000-0003-4312-5957
dc.authoridSanchez-Guerra, Marco/0000-0002-8354-1157
dc.authoridDi, Qian/0000-0002-1584-4770
dc.contributor.authorNwanaji-Enwerem, Jamaji C.
dc.contributor.authorColicino, Elena
dc.contributor.authorDai, Lingzhen
dc.contributor.authorCayir, Akin
dc.contributor.authorSanchez-Guerra, Marco
dc.contributor.authorLaue, Hannah E.
dc.contributor.authorNguyen, Vy. T.
dc.date.accessioned2025-01-27T20:49:55Z
dc.date.available2025-01-27T20:49:55Z
dc.date.issued2017
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractThe mitochondrial genome has long been implicated in age-related disease, but no studies have examined its role in the relationship of long-term fine particle (PM2.5) exposure and DNA methylation age (DNAm-age)-a novel measure of biological age. In this analysis based on 940 observations between 2000 and 2011 from 552 Normative Aging Study participants, we determined the roles of mitochondrial DNA haplogroup variation and mitochondrial genome abundance in the relationship of PM2.5 with DNAm-age. We used the GEOS-chem transport model to estimate address-specific, one-year PM2.5 levels for each participant. DNAm-age and mitochondrial DNA markers were measured from participant blood samples. Nine haplogroups (H, I, J, K, T, U, V, W, and X) were present in the population. In fully adjusted linear mixed-effects models, the association of PM2.5 with DNAm-age (in years) was significantly diminished in carriers of haplogroup V (P-interaction = 0.01; beta = 0.18, 95%CI: -0.41, 0.78) compared to noncarriers (beta = 1.25, 95%CI: 0.58, 1.93). Mediation analysis estimated that decreases in mitochondrial DNA copy number, a measure of mitochondrial genome abundance, mediated 12% of the association of PM2.5 with DNAm-age. Our data suggests that the mitochondrial genome plays a role in DNAm-age relationships particularly in the context of long-term PM2.5 exposure.
dc.description.sponsorshipNational Institute of Environmental Health Sciences (NIEHS) [R01ES021733, R01ES025225, ES015172, ES014663, ES020010, P30ES009089, P30ES000002]; Environmental Protection Agency (EPA) [RD832416, RD83587201]; National Heart, Lung, and Blood Institute (NHLBI) [2T32HL007118-41]; Cooperative Studies Program/ERIC, US Department of Veterans Affairs; US Department of Agriculture, Agricultural Research Service [53-K06-510]; The Scientific and Technological Research Council of Turkey [TUBITAK-2219]
dc.description.sponsorshipThis work was supported by grants from the National Institute of Environmental Health Sciences (NIEHS) (R01ES021733 and R01ES025225). Other support comes from NIEHS grants ES015172, ES014663, ES020010, P30ES009089, P30ES000002; Environmental Protection Agency (EPA) grants RD832416 and RD83587201; and National Heart, Lung, and Blood Institute (NHLBI) grant 2T32HL007118-41. The US Department of Veterans Affairs (VA) Normative Aging Study (NAS) is supported by the Cooperative Studies Program/ERIC, US Department of Veterans Affairs, and is a research component of the Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC). The views expressed in this paper are those of the authors and do not necessarily represent the views of the US Department of Veterans Affairs. Additional support was provided by the US Department of Agriculture, Agricultural Research Service (contract 53-K06-510). AC was supported by The Scientific and Technological Research Council of Turkey (TUBITAK-2219). All graphics were created by the authors.
dc.identifier.doi10.1021/acs.est.7b02409
dc.identifier.endpage8195
dc.identifier.issn0013-936X
dc.identifier.issn1520-5851
dc.identifier.issue14
dc.identifier.pmid28636816
dc.identifier.scopus2-s2.0-85025115669
dc.identifier.scopusqualityQ1
dc.identifier.startpage8185
dc.identifier.urihttps://doi.org/10.1021/acs.est.7b02409
dc.identifier.urihttps://hdl.handle.net/20.500.12428/25358
dc.identifier.volume51
dc.identifier.wosWOS:000406086100048
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAmer Chemical Soc
dc.relation.ispartofEnvironmental Science & Technology
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectParticulate Air-Pollution
dc.subjectOxidative Stress
dc.subjectEpigenetic Clock
dc.subjectCopy Number
dc.subjectPm2.5
dc.subjectMatter
dc.subjectHaplogroups
dc.subjectAssociation
dc.subjectCancer
dc.subjectModel
dc.titleImpacts of the Mitochondrial Genome on the Relationship of Long-Term Ambient Fine Particle Exposure with Blood DNA Methylation Age
dc.typeArticle

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