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Genome-wide DNA methylation in peripheral blood, and long-term exposure to source-specific transportation noise and air pollution, the SAPALDIA study

Genome-wide DNA methylation in peripheral blood, and long-term exposure to source-specific transportation noise and air pollution, the SAPALDIA study
Genome-wide DNA methylation in peripheral blood, and long-term exposure to source-specific transportation noise and air pollution, the SAPALDIA study
Background:
Few epigenome-wide association studies (EWAS) on air pollutants exist, and none have been done on transportation noise exposures, which also contribute to environmental burden of disease.

Objective:
We performed mutually independent EWAS on transportation noise and air pollution exposures.

Methods:
We used data from two time points of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) from 1,389 participants contributing 2,542 observations. We applied multiexposure linear mixed-effects regressions with participant-level random intercept to identify significant Cytosine-phosphate-Guanine (CpG) sites and differentially methylated regions (DMRs) in relation to 1-y average aircraft, railway, and road traffic day-evening-night noise (Lden); nitrogen dioxide (NO2); and particulate matter (PM) with aerodynamic diameter <2.5μm (PM2.5). We performed candidate (CpG-based; cross-systemic phenotypes, combined into “allostatic load”) and agnostic (DMR-based) pathway enrichment tests, and replicated previously reported air pollution EWAS signals.

Results:
We found no statistically significant CpGs at false discovery rate <0.05. However, 14, 48, 183, 8, and 71 DMRs independently associated with aircraft, railway, and road traffic Lden; NO2; and PM2.5, respectively, with minimally overlapping signals. Transportation Lden and air pollutants tendentially associated with decreased and increased methylation, respectively. We observed significant enrichment of candidate DNA methylation related to C-reactive protein and body mass index (aircraft, road traffic Lden, and PM2.5), renal function and “allostatic load” (all exposures). Agnostic functional networks related to cellular immunity, gene expression, cell growth/proliferation, cardiovascular, auditory, embryonic, and neurological systems development were enriched. We replicated increased methylation in cg08500171 (NO2) and decreased methylation in cg17629796 (PM2.5).

Conclusions:
Mutually independent DNA methylation was associated with source-specific transportation noise and air pollution exposures, with distinct and shared enrichments for pathways related to inflammation, cellular development, and immune responses. These findings contribute in clarifying the pathways linking these exposures and age-related diseases but need further confirmation in the context of mediation analyses. https://doi.org/10.1289/EHP6174
0091-6765
1-14
Eze, Ikenna C.
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Jeong, Ayoung
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Schaffner, Emmanuel
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Rezwan, Faisal I.
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Ghantous, Akram
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Foraster, Maria
8968447a-d909-49c0-a62a-ac37104b1770
Vienneau, Danielle
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Kronenberg, Florian
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Herceg, Zdenko
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Vineis, Paolo
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Brink, Mark
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Wunderli, Jean-Marc
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Schindler, Christian
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Cajochen, Christian
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Roosli, Martin
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Holloway, John
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Imboden, Medea
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Probst-Hensch, Nicole
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Eze, Ikenna C.
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Jeong, Ayoung
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Schaffner, Emmanuel
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Rezwan, Faisal I.
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Ghantous, Akram
c078d3dc-5baa-4ec3-b157-f200f843a0d1
Foraster, Maria
8968447a-d909-49c0-a62a-ac37104b1770
Vienneau, Danielle
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Kronenberg, Florian
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Herceg, Zdenko
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Vineis, Paolo
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Brink, Mark
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Wunderli, Jean-Marc
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Schindler, Christian
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Cajochen, Christian
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Roosli, Martin
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Holloway, John
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Imboden, Medea
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Probst-Hensch, Nicole
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Eze, Ikenna C., Jeong, Ayoung, Schaffner, Emmanuel, Rezwan, Faisal I., Ghantous, Akram, Foraster, Maria, Vienneau, Danielle, Kronenberg, Florian, Herceg, Zdenko, Vineis, Paolo, Brink, Mark, Wunderli, Jean-Marc, Schindler, Christian, Cajochen, Christian, Roosli, Martin, Holloway, John, Imboden, Medea and Probst-Hensch, Nicole (2020) Genome-wide DNA methylation in peripheral blood, and long-term exposure to source-specific transportation noise and air pollution, the SAPALDIA study. Environmental Health Perspectives, 128 (6), 1-14, [067003]. (doi:10.1289/EHP6174).

Record type: Article

Abstract

Background:
Few epigenome-wide association studies (EWAS) on air pollutants exist, and none have been done on transportation noise exposures, which also contribute to environmental burden of disease.

Objective:
We performed mutually independent EWAS on transportation noise and air pollution exposures.

Methods:
We used data from two time points of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) from 1,389 participants contributing 2,542 observations. We applied multiexposure linear mixed-effects regressions with participant-level random intercept to identify significant Cytosine-phosphate-Guanine (CpG) sites and differentially methylated regions (DMRs) in relation to 1-y average aircraft, railway, and road traffic day-evening-night noise (Lden); nitrogen dioxide (NO2); and particulate matter (PM) with aerodynamic diameter <2.5μm (PM2.5). We performed candidate (CpG-based; cross-systemic phenotypes, combined into “allostatic load”) and agnostic (DMR-based) pathway enrichment tests, and replicated previously reported air pollution EWAS signals.

Results:
We found no statistically significant CpGs at false discovery rate <0.05. However, 14, 48, 183, 8, and 71 DMRs independently associated with aircraft, railway, and road traffic Lden; NO2; and PM2.5, respectively, with minimally overlapping signals. Transportation Lden and air pollutants tendentially associated with decreased and increased methylation, respectively. We observed significant enrichment of candidate DNA methylation related to C-reactive protein and body mass index (aircraft, road traffic Lden, and PM2.5), renal function and “allostatic load” (all exposures). Agnostic functional networks related to cellular immunity, gene expression, cell growth/proliferation, cardiovascular, auditory, embryonic, and neurological systems development were enriched. We replicated increased methylation in cg08500171 (NO2) and decreased methylation in cg17629796 (PM2.5).

Conclusions:
Mutually independent DNA methylation was associated with source-specific transportation noise and air pollution exposures, with distinct and shared enrichments for pathways related to inflammation, cellular development, and immune responses. These findings contribute in clarifying the pathways linking these exposures and age-related diseases but need further confirmation in the context of mediation analyses. https://doi.org/10.1289/EHP6174

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More information

Accepted/In Press date: 30 April 2020
e-pub ahead of print date: 1 June 2020
Published date: June 2020
Additional Information: Funding Information: This work was supported by the Swiss National Science Foundation, SNF-SAPALDIA (grant numbers 33CS30-148470/1, 33CSCO-134276/1, 33CSCO-108796, 324730_135673, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099, PMPDP3_129021/1, PMPDP3_141671/1); SNF-SiRENE (grant number CRSII3_147635); the European Commission Horizon 2020 research and innovation programme (ALEC study; grant number 633212); grant FP7 of the European Commission “Enhanced exposure 36 assessment and -omic profiling for high priority environmental exposures in Europe” (EXPOsOMICS study; grant number 308610). Funding Information: SAPALDIA is also supported by the Swiss Federal Office for the Environment; Federal Office of Public Health; the Federal Office of Roads and Transport; the canton’s government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, and Zürich; the Swiss Lung League; the canton’s Lung League of Basel Stadt/Basel Landschaft, Geneva, Ticino, Valais, Graubünden and Zurich, Stiftung ehemals Bündner Heilstätten, SUVA, Freiwillige Akademische Gesellschaft; UBS Wealth Foundation; Talecris Biotherapeutics GmbH; Abbott Diagnostics; European Commission 018996 (GABRIEL); and Wellcome Trust WT 084703MA. MF. has received support of the Beatriu de Pinós postdoctoral programme of the Government of Catalonia’s Secretariat for Universities and Research of the Ministry of Economy and Knowledge. Publisher Copyright: © 2020, Public Health Services, US Dept of Health and Human Services. All rights reserved.

Identifiers

Local EPrints ID: 440771
URI: http://eprints.soton.ac.uk/id/eprint/440771
ISSN: 0091-6765
PURE UUID: 31c0d492-ad0d-4e91-a90f-79baa217b3db
ORCID for Faisal I. Rezwan: ORCID iD orcid.org/0000-0001-9921-222X
ORCID for John Holloway: ORCID iD orcid.org/0000-0001-9998-0464

Catalogue record

Date deposited: 15 May 2020 16:57
Last modified: 17 Mar 2024 05:32

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Contributors

Author: Ikenna C. Eze
Author: Ayoung Jeong
Author: Emmanuel Schaffner
Author: Faisal I. Rezwan ORCID iD
Author: Akram Ghantous
Author: Maria Foraster
Author: Danielle Vienneau
Author: Florian Kronenberg
Author: Zdenko Herceg
Author: Paolo Vineis
Author: Mark Brink
Author: Jean-Marc Wunderli
Author: Christian Schindler
Author: Christian Cajochen
Author: Martin Roosli
Author: John Holloway ORCID iD
Author: Medea Imboden
Author: Nicole Probst-Hensch

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