Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.
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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.
SUBMITTER: Ward-Caviness CK
PROVIDER: S-EPMC7762491 | biostudies-literature | 2020 Dec
REPOSITORIES: biostudies-literature
Publications
Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.
Ward-Caviness Cavin K CK Russell Armistead G AG Weaver Anne M AM Slawsky Erik E Dhingra Radhika R Kwee Lydia Coulter LC Jiang Rong R Neas Lucas M LM Diaz-Sanchez David D Devlin Robert B RB Cascio Wayne E WE Olden Kenneth K Hauser Elizabeth R ER Shah Svati H SH Kraus William E WE
Aging 20201207 23
<h4>Background</h4>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.<h4>Methods</h4>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 apporti ...[more]
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Project description:BackgroundWe conducted a meta-analysis to evaluate the association between traffic-related air pollution and lung cancer in order to provide evidence for control of traffic-related air pollution.MethodsSeveral databases were searched for relevant studies up to December 2013. The quality of articles obtained was evaluated by the Strengthening the Reporting of Observational Studies in Epidemiology checklist. Statistical analysis, including pooling effective sizes and confidential intervals, was performed.ResultsA total of 1106 records were obtained through the database and 36 studies were included in our analysis. Among the studies included, 14 evaluated the association between ambient exposure to traffic-related air pollution and lung cancer and 22 studies involved occupational exposure to air pollution among professional drivers. Twenty-two studies were marked A level regarding quality, 13 were B level, and one was C level. Exposure to nitrogen dioxide (meta-odds ratio [OR]: 1.06, 95% confidence interval [CI]: 0.99-1.13), nitrogen oxide (meta-OR: 1.04, 95% CI: 1.01-1.07), sulfur dioxide (meta-OR: 1.03, 95% CI: 1.02-1.05), and fine particulate matter (meta-OR: 1.11, 95% CI: 1.00-1.22) were positively associated with a risk of lung cancer. Occupational exposure to air pollution among professional drivers significantly increased the incidence (meta-OR: 1.27, 95% CI: 1.19-1.36) and mortality of lung cancer (meta-OR: 1.14, 95% CI: 1.04-1.26).ConclusionExposure to traffic-related air pollution significantly increased the risk of lung cancer.
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Project description:BackgroundExposure to traffic-related air pollution (TRAP) has been linked to childhood anxiety symptoms. Neuroimaging in patients with anxiety disorders indicate altered neurochemistry.ObjectivesEvaluate the impact of TRAP on brain metabolism and its relation to childhood anxiety symptoms in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS).MethodsAdolescents (n = 145) underwent magnetic resonance spectroscopy. Brain metabolites, including myo-inositol, N-acetylaspartate, creatine, choline, glutamate, glutamate plus glutamine, and glutathione were measured in the anterior cingulate cortex. Anxiety symptoms were assessed using the Spence Children's Anxiety Scale. TRAP exposure in early-life, averaged over childhood, and during the 12 months prior to imaging was estimated using a validated land use regression model. Associations between TRAP exposure, brain metabolism, and anxiety symptoms were estimated using linear regression and a bootstrapping approach for testing mediation by brain metabolite levels.ResultsRecent exposure to high levels of TRAP was associated with significant increases in myo-inositol (β = 0.26; 95%CI 0.01, 0.51) compared to low TRAP exposure. Recent elevated TRAP exposure (β = 4.71; 95% CI 0.95, 8.45) and increased myo-inositol levels (β = 2.98; 95% CI 0.43, 5.52) were also significantly associated with increased generalized anxiety symptoms with 12% of the total effect between TRAP and generalized anxiety symptoms being mediated by myo-inositol levels.ConclusionsThis is the first study of children to utilize neuroimaging to link TRAP exposure, metabolite dysregulation in the brain, and generalized anxiety symptoms among otherwise healthy children. TRAP may elicit atypical excitatory neurotransmission and glial inflammatory responses leading to increased metabolite levels and subsequent anxiety symptoms.
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Project description:BackgroundWhile air pollution has been associated with depression and anxiety in adults, its impact on childhood mental health is understudied.ObjectiveWe examined lifetime exposure to traffic-related air pollution (TRAP) and symptoms of depression and anxiety at age 12 years in the Cincinnati Childhood Allergy and Air Pollution Study cohort.MethodsWe estimated exposure to elemental carbon attributable to traffic (ECAT), a surrogate of diesel exhaust, at birth, age 12 years, and average exposure throughout childhood, using a validated land use regression model. We assessed depression and anxiety at age 12 years by parent report with the Behavior Assessment System for Children-2, and by child report with the Child Depression Inventory-2 (CDI-2) and the Spence Children's Anxiety Scale (SCAS). Associations between TRAP at birth, age 12 years, and childhood average and mental health outcomes were estimated using linear regression models adjusting for covariates including parent depression, secondhand smoke exposure, race, household income, and others.ResultsExposure to ECAT was not significantly associated with parent-reported depression or anxiety. However, exposure to ECAT at birth was associated with increased child-reported depression and anxiety. Each 0.25 µg/m3 increase in ECAT was associated with a 3.5 point increase (95% CI 1.6-5.5) in CDI-2 scores and 2.3 point increase (95% CI 0.8-3.9) in SCAS total anxiety scores. We observed similar associations between average childhood ECAT exposures but not for concurrent exposures at age 12.ConclusionsTRAP exposure during early life and across childhood was significantly associated with self-reported depression and anxiety symptoms in children. The negative impact of air pollution on mental health previously reported among adults may also be present during childhood.
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