Dataset Information

Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

ABSTRACT:

Background

Epidemiologic studies of fine particulate matter [aerodynamic diameter ? 2.5 ?m (PM(2.5))] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in residential infiltration efficiencies (F(inf)) will affect epidemiologic study results.

Objective

We aimed to develop models to predict F(inf) for > 6,000 homes in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study of PM(2.5) exposure, subclinical cardiovascular disease, and clinical outcomes.

Methods

We collected 526 two-week, paired indoor-outdoor PM(2.5) filter samples from a subset of study homes. PM(2.5) elemental composition was measured by X-ray fluorescence, and F(inf) was estimated as the indoor/outdoor sulfur ratio. We regressed F(inf) on meteorologic variables and questionnaire-based predictors in season-specific models. Models were evaluated using the R² and root mean square error (RMSE) from a 10-fold cross-validation.

Results

The mean ± SD F(inf) across all communities and seasons was 0.62 ± 0.21, and community-specific means ranged from 0.47 ± 0.15 in Winston-Salem, North Carolina, to 0.82 ± 0.14 in New York, New York. F(inf) was generally greater during the warm (> 18°C) season. Central air conditioning (AC) use, frequency of AC use, and window opening frequency were the most important predictors during the warm season; outdoor temperature and forced-air heat were the best cold-season predictors. The models predicted 60% of the variance in 2-week F(inf), with an RMSE of 0.13.

Conclusions

We developed intuitive models that can predict F(inf) using easily obtained variables. Using these models, MESA Air will be the first large epidemiologic study to incorporate variation in residential F(inf) into an exposure assessment.

SUBMITTER: Allen RW

PROVIDER: S-EPMC3385439 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature

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Publications

Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

Allen Ryan W RW Adar Sara D SD Avol Ed E Cohen Martin M Curl Cynthia L CL Larson Timothy T Liu L-J Sally LJ Sheppard Lianne L Kaufman Joel D JD

Environmental health perspectives 20120222 6

<h4>Background</h4>Epidemiologic studies of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM(2.5))] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in residential infiltration efficiencies (F(inf)) will affect epidemiologic study results.<h4>Objective</h4>We aimed to develop models to predict F(inf) for > 6,000 homes in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study of PM(2.5) exposure, su ...[more]

PMID: 22534026

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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

Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

Background

Objective

Methods

Results

Conclusions

Publications

Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

Similar Datasets

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