Dataset Information

Long-term exposure to ambient air pollution and cognitive function in older US adults: The Multi-Ethnic Study of Atherosclerosis.

ABSTRACT: Air pollution effects on cognitive function have been increasingly recognized. Little is known about the impact of different sources of fine particulate (PM_2.5). We aim to evaluate the associations between long-term air pollution exposure, including source-specific components in PM_2.5, and cognition in older adults.

Methods

Cognitive assessment, including the Cognitive Abilities Screening Instrument (CASI), Digit Symbol Coding (DSC), and Digit Span (DS), was completed in 4392 older participants in the United States during 2010-2012. Residence-specific air pollution exposures (i.e., oxides of nitrogen [NO₂/NOx], PM_2.5 and its components: elemental carbon [EC], organic carbon [OC], sulfur [S], and silicon [Si]) were estimated by geo-statistical models. Linear and logistic regression models were used to estimate the associations between each air pollutants metric and cognitive function.

Results

An interquartile range (IQR) increase in EC (0.8 μg/m³) and Si (23.1 ng/m³) was associated with -1.27 (95% confidence interval [CI]: -0.09, -2.45) and -0.88 (95% CI: -0.21, -1.54) lower CASI scores in global cognitive function. For each IQR increase in Si, the odds of low cognitive function (LCF) across domains was 1.29 times higher (95% CI: 1.04, 1.60). For other tests, NO _X was associated with slower processing speed (DSC: -2.01, 95% CI: -3.50, -0.52) and worse working memory (total DS: -0.4, 95% CI: -0.78, -0.01). No associations were found for PM_2.5 and two PM_2.5 components (OC and S) with any cognitive function outcomes.

Conclusion

Higher exposure to traffic-related air pollutants including both tailpipe (EC and NO _x ) and non-tailpipe (Si) species were associated with lower cognitive function in older adults.

SUBMITTER: Wang M

PROVIDER: S-EPMC9916093 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Long-term exposure to ambient air pollution and cognitive function in older US adults: The Multi-Ethnic Study of Atherosclerosis.

Wang Meng M Zhou Xiao-Hua Andrew XA Curl Cynthia C Fitzpatrick Annette A Vedal Sverre S Kaufman Joel J

Environmental epidemiology (Philadelphia, Pa.) 20230207 1

Air pollution effects on cognitive function have been increasingly recognized. Little is known about the impact of different sources of fine particulate (PM<sub>2.5</sub>). We aim to evaluate the associations between long-term air pollution exposure, including source-specific components in PM<sub>2.5</sub>, and cognition in older adults.<h4>Methods</h4>Cognitive assessment, including the Cognitive Abilities Screening Instrument (CASI), Digit Symbol Coding (DSC), and Digit Span (DS), was complete ...[more]

PMID: 36777527

Similar Datasets

Project description:BackgroundLong-term ozone ([Formula: see text]) exposure is associated with cardiovascular mortality, but little is known about the associations between [Formula: see text] and subclinical arterial disease.ObjectivesWe studied the longitudinal association of exposure to [Formula: see text] and progression of key subclinical arterial markers in adults: intima-media thickness of common carotid artery ([Formula: see text]), carotid plaque (CP) burden, and coronary artery calcification (CAC).MethodsCAC was measured one to four times at baseline and at follow-up exams (1999–2012) by computed tomography (CT) in 6,619 healthy adults, recruited at age 45-84 y without cardiovascular disease (CVD), over a mean of 6.5 y (standard deviation: 3.5 y). [Formula: see text] and CP burden were quantified in 3,392 participants using carotid artery ultrasound imaging acquired over a mean of 9 y (1.7 y). Over 91% and 89% participants had at least one follow-up [Formula: see text] and CAC measurement, respectively. Residence-specific [Formula: see text] concentrations were estimated by a validated spatiotemporal model spanning from 1999 to 2012. This model relied on comprehensive monitoring data and geographical variables to predict individualized long-term average concentrations since baseline. Linear mixed models and logistic regression model were used to evaluate relationships of long-term average exposure to [Formula: see text] with longitudinal change in [Formula: see text], CAC, and CP formation, respectively.ResultsMean progression rates of [Formula: see text] and CAC were [Formula: see text] and [Formula: see text]. CP formation was identified in 55% of the subjects. A [Formula: see text] increase in long-term average [Formula: see text] exposure was associated with a [Formula: see text] [95% confidence interval (CI): 1.4, 9.7] greater increase in [Formula: see text] over 10 y. A [Formula: see text] increase in [Formula: see text] was also associated with new CP formation [odds ratio (OR): 1.2 (95% CI: 1.1, 1.4)] but not CAC progression [[Formula: see text] (95% CI: [Formula: see text], 2)]. Associations were robust in the analysis with extended covariate adjustment, including copollutants, i.e., nitrogen oxides ([Formula: see text]) and particulate matter with diameter [Formula: see text] ([Formula: see text]).ConclusionOver almost a decade of follow-up, outdoor [Formula: see text] concentrations were associated with increased rate of carotid wall thickness progression and risk of new plaque formation, suggesting arterial injury in this cohort. https://doi.org/10.1289/EHP3325.

Project description:Air pollution might affect atherosclerosis through DNA methylation changes in cells crucial to atherosclerosis, such as monocytes. We conducted an epigenome-wide study of DNA methylation in CD14+ monocytes and long-term ambient air pollution exposure in adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). We also assessed the association between differentially methylated signals and cis-gene expression. Using spatiotemporal models, one-year average concentrations of outdoor fine particulate matter (PM2.5) and oxides of nitrogen (NOX) were estimated at participants' homes. We assessed DNA methylation and gene expression using Illumina 450k and HumanHT-12 v4 Expression BeadChips, respectively (n = 1,207). We used bump hunting and site-specific approaches to identify differentially methylated signals (false discovery rate of 0.05) and used linear models to assess associations between differentially methylated signals and cis-gene expression. Four differentially methylated regions (DMRs) located on chromosomes 5, 6, 7, and 16 (within or near SDHAP3, ZFP57, HOXA5, and PRM1, respectively) were associated with PM2.5. The DMRs on chromosomes 5 and 6 also associated with NOX. The DMR on chromosome 5 had the smallest p-value for both PM2.5 (p = 1.4×10-6) and NOX (p = 7.7×10-6). Three differentially methylated CpGs were identified for PM2.5, and cg05926640 (near TOMM20) had the smallest p-value (p = 5.6×10-8). NOX significantly associated with cg11756214 within ZNF347 (p = 5.6×10-8). Several differentially methylated signals were also associated with cis-gene expression. The DMR located on chromosome 7 was associated with the expression of HOXA5, HOXA9, and HOXA10. The DMRs located on chromosomes 5 and 16 were associated with expression of MRPL36 and DEXI, respectively. The CpG cg05926640 was associated with expression of ARID4B, IRF2BP2, and TOMM20. We identified differential DNA methylation in monocytes associated with long-term air pollution exposure. Methylation signals associated with gene expression might help explain how air pollution contributes to cardiovascular disease.

Project description:DNA methylation may mediate effects of air pollution on cardiovascular disease. The association between long-term air pollution exposure and DNA methylation in monocytes, which are central to atherosclerosis, has not been studied. We investigated the association between long-term ambient air pollution exposure and DNA methylation (candidate sites and global) in monocytes of adults (aged ?55).One-year average ambient fine particulate matter (PM2.5) and oxides of nitrogen (NOX) concentrations were predicted at participants' (n?=?1,207) addresses using spatiotemporal models. We assessed DNA methylation in circulating monocytes at 1) 2,713 CpG sites associated with mRNA expression of nearby genes and 2) probes mapping to Alu and LINE-1 repetitive elements (surrogates for global DNA methylation) using Illumina's Infinium HumanMethylation450 BeadChip. We used linear regression models adjusted for demographics, smoking, physical activity, socioeconomic status, methyl-nutrients, and technical variables. For significant air pollution-associated methylation sites, we also assessed the association between expression of gene transcripts previously associated with these CpG sites and air pollution.At a false discovery rate of 0.05, five candidate CpGs (cg20455854, cg07855639, cg07598385, cg17360854, and cg23599683) had methylation significantly associated with PM2.5 and none were associated with NOX. Cg20455854 had the smallest p-value for the association with PM2.5 (p?=?2.77?×?10-5). mRNA expression profiles of genes near three of the PM2.5-associated CpGs (ANKHD1, LGALS2, and ANKRD11) were also significantly associated with PM2.5 exposure. Alu and LINE-1 methylation were not associated with long-term air pollution exposure.We observed novel associations between long-term ambient air pollution exposure and site-specific DNA methylation, but not global DNA methylation, in purified monocytes of a multi-ethnic adult population. Epigenetic markers may provide insights into mechanisms underlying environmental factors in complex diseases like atherosclerosis.

Dataset Information

Long-term exposure to ambient air pollution and cognitive function in older US adults: The Multi-Ethnic Study of Atherosclerosis.

Methods

Results

Conclusion

Publications

Long-term exposure to ambient air pollution and cognitive function in older US adults: The Multi-Ethnic Study of Atherosclerosis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets