Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

dc.contributor.author

Ward-Caviness, Cavin K

dc.contributor.author

Russell, Armistead G

dc.contributor.author

Weaver, Anne M

dc.contributor.author

Slawsky, Erik

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Dhingra, Radhika

dc.contributor.author

Kwee, Lydia Coulter

dc.contributor.author

Jiang, Rong

dc.contributor.author

Neas, Lucas M

dc.contributor.author

Diaz-Sanchez, David

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Devlin, Robert B

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Cascio, Wayne E

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Olden, Kenneth

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Hauser, Elizabeth R

dc.contributor.author

Shah, Svati H

dc.contributor.author

Kraus, William E

dc.date.accessioned

2023-08-01T14:05:13Z

dc.date.available

2023-08-01T14:05:13Z

dc.date.issued

2020-12

dc.date.updated

2023-08-01T14:05:11Z

dc.description.abstract

Background

Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures.

Methods

Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status.

Results

We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5.

Conclusion

Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.
dc.identifier

202341

dc.identifier.issn

1945-4589

dc.identifier.issn

1945-4589

dc.identifier.uri

https://hdl.handle.net/10161/28583

dc.language

eng

dc.publisher

Impact Journals, LLC

dc.relation.ispartof

Aging

dc.relation.isversionof

10.18632/aging.202341

dc.subject

Humans

dc.subject

Genetic Markers

dc.subject

Risk Assessment

dc.subject

Vehicle Emissions

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Environmental Exposure

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Environmental Monitoring

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Age Factors

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Residence Characteristics

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DNA Methylation

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Epigenesis, Genetic

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Aging

dc.subject

Blood Pressure

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Aged

dc.subject

Middle Aged

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Urban Health

dc.subject

North Carolina

dc.subject

Female

dc.subject

Male

dc.subject

Peripheral Arterial Disease

dc.subject

Traffic-Related Pollution

dc.subject

Heart Disease Risk Factors

dc.title

Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

dc.type

Journal article

duke.contributor.orcid

Kwee, Lydia Coulter|0000-0002-6997-8571

duke.contributor.orcid

Hauser, Elizabeth R|0000-0003-0367-9189

duke.contributor.orcid

Shah, Svati H|0000-0002-3495-2830

duke.contributor.orcid

Kraus, William E|0000-0003-1930-9684

pubs.begin-page

24141

pubs.end-page

24155

pubs.issue

23

pubs.organisational-group

Duke

pubs.organisational-group

School of Medicine

pubs.organisational-group

School of Nursing

pubs.organisational-group

Staff

pubs.organisational-group

Nursing

pubs.organisational-group

Basic Science Departments

pubs.organisational-group

Clinical Science Departments

pubs.organisational-group

Institutes and Centers

pubs.organisational-group

Biostatistics & Bioinformatics

pubs.organisational-group

Medicine

pubs.organisational-group

Psychiatry & Behavioral Sciences

pubs.organisational-group

Medicine, Cardiology

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Duke Cancer Institute

pubs.organisational-group

Duke Clinical Research Institute

pubs.organisational-group

Duke Molecular Physiology Institute

pubs.organisational-group

Psychiatry & Behavioral Sciences, Behavioral Medicine & Neurosciences

pubs.publication-status

Published

pubs.volume

12

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