Dataset Information

Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the multi-ethnic study of atherosclerosis.

ABSTRACT:

Background

Toxicological research suggests that coarse particles (PM10-2.5) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with PM10-2.5 and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis.

Methods

Participants included 3,295 adults (45-84 years of age) from three metropolitan areas. Site-specific spatial models were used to estimate 5-year concentrations of PM10-2.5 mass and copper, zinc, phosphorus, silicon, and endotoxin found in PM10-2.5. Outcomes included interleukin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagulation scores. We used multivariable regression with multiply imputed data to estimate associations while controlling for potential confounders, including co-pollutants such as fine particulate matter.

Results

Some limited evidence was found of relationships between inflammation and coagulation and PM10-2.5. Endotoxin was the PM10-2.5 component most strongly associated with inflammation, with an interquartile range (IQR) increase (0.08 EU/m3) associated with 0.15 (95% CI: 0.01, 0.28; p = 0.03) and 0.08 (95% CI: -0.07, 0.23; p = 0.28) higher inflammation scores before and after control for city, respectively. Copper was the component with the strongest association with coagulation, with a 4-ng/m3 increase associated with 0.19 (95% CI: 0.08, 0.30; p = 0.0008) and 0.12 (95% CI: -0.05, 0.30; p = 0.16) unit higher coagulation scores before and after city adjustment, respectively.

Conclusions

Our cross-sectional analysis provided some evidence that long-term PM10-2.5 exposure was associated with inflammation and coagulation, but associations were modest and depended on particle composition.

SUBMITTER: Adar SD

PROVIDER: S-EPMC4455582 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Publications

Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the multi-ethnic study of atherosclerosis.

Adar Sara D SD D'Souza Jennifer J Mendelsohn-Victor Kari K Jacobs David R DR Cushman Mary M Sheppard Lianne L Thorne Peter S PS Burke Gregory L GL Daviglus Martha L ML Szpiro Adam A AA Diez Roux Ana V AV Kaufman Joel D JD Larson Timothy V TV

Environmental health perspectives 20150120 6

<h4>Background</h4>Toxicological research suggests that coarse particles (PM10-2.5) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with PM10-2.5 and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis.<h4>Methods</h4>Participants included 3,295 adults (45-84 years of age) fro ...[more]

PMID: 25616153

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Project description:BackgroundParticulate matter (PM) exposure may directly affect the pulmonary vasculature. Although the pulmonary vasculature is not easily measurable, differential associations for right ventricular (RV) and left ventricular (LV) mass may provide an indirect assessment of pulmonary vascular damage.ObjectivesWe tested whether long-term exposure to PM < 2.5 ?m (PM2.5) is associated with greater RV mass and RV mass/end-diastolic volume ratio relative to the LV.MethodsThe Multi-Ethnic Study of Atherosclerosis performed cardiac magnetic resonance (CMR) imaging among participants 45-84 years old without clinical cardiovascular disease in 2000-2002 in six U.S. cities. A fine-scale spatiotemporal model estimated ambient PM2.5 exposure in the year before CMR; individually weighted estimates accounted for indoor exposure to ambient PM2.5. Linear regression models were adjusted for demographics, anthropometrics, smoking status, cardiac risk factors, and LV parameters, with additional adjustment for city.ResultsThe 4,041 included participants had a mean age of 61.5 years, and 47% were never smokers. The mean ambient PM2.5 was 16.4 ?g/m3 and individually weighted PM2.5 was 11.0 ?g/m3. PM2.5 exposure was associated with greater RV mass [ambient: 0.11 g per 5 ?g/m3 (95% CI: -0.05, 0.27); individually weighted: 0.20 g per 5 ?g/m3 (95% CI: 0.04, 0.36)] and a greater RV mass/end-diastolic volume ratio conditional on LV parameters. City-adjusted results for RV mass were of greater magnitude and were statistically significant for both measures of PM2.5, whereas those for RV mass/end-diastolic volume ratio were attenuated.ConclusionsLong-term PM2.5 exposures were associated with greater RV mass and RV mass/end-diastolic volume ratio conditional on the LV; however, additional adjustment for city attenuated the RV mass/end-diastolic volume findings. These findings suggest that PM2.5 exposure may be associated with subclinical cardiopulmonary differences in this general population sample.CitationAaron CP, Chervona Y, Kawut SM, Diez Roux AV, Shen M, Bluemke DA, Van Hee VC, Kaufman JD, Barr RG. 2016. Particulate matter exposure and cardiopulmonary differences in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 124:1166-1173;?http://dx.doi.org/10.1289/ehp.1409451.

Project description:Inflammation and the coagulation cascade are considered to be the potential mechanisms of ambient particulate matter (PM) exposure-induced adverse cardiovascular events. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and fibrinogen are arguably the four most commonly assayed markers to reflect the relationships of PM with inflammation and blood coagulation. This review summarized and quantitatively analyzed the existing studies reporting short- and long-term associations of PM2.5(PM with an aerodynamic diameter ≤2.5 μm)/PM10 (PM with an aerodynamic diameter≤10 μm) with important inflammation and blood coagulation markers (TNF-α, IL-6, IL-8, fibrinogen). We reviewed relevant studies published up to July 2020, using three English databases (PubMed, Web of Science, Embase) and two Chinese databases (Wang-Fang, China National Knowledge Infrastructure). The OHAT tool, with some modification, was applied to evaluate risk of bias. Meta-analyses were conducted with random-effects models for calculating the pooled estimate of markers. To assess the potential effect modifiers and the source of heterogeneity, we conducted subgroup analyses and meta-regression analyses where appropriate. The assessment and correction of publication bias were based on Begg's and Egger's test and "trim-and-fill" analysis. We identified 44 eligible studies. For short-term PM exposure, the percent change of a 10 μg/m3 PM2.5 increase on TNF-α and fibrinogen was 3.51% (95% confidence interval (CI): 1.21%, 5.81%) and 0.54% (95% confidence interval (CI): 0.21%, 0.86%) respectively. We also found a significant short-term association between PM10 and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM2.5 and PM10 were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM2.5 and PM10 were significant only found in studies conducted in Asia. Our findings support significant short-term associations of PM with TNF-α and fibrinogen. Future epidemiological studies should address the role long-term PM exposure plays in inflammation and blood coagulation markers level change.

Dataset Information

Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the multi-ethnic study of atherosclerosis.

Background

Methods

Results

Conclusions

Publications

Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the multi-ethnic study of atherosclerosis.

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