Dataset Information

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

ABSTRACT:

Rationale

Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited.

Objectives

Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation.

Methods

BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample.

Results

Measured median BC was 0.19 µg/m³ (interquartile range, IQR=0.22 µg/m³). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1.

Conclusions

These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.

SUBMITTER: Garshick E

PROVIDER: S-EPMC6007002 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Publications

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

Garshick Eric E Grady Stephanie T ST Hart Jaime E JE Coull Brent A BA Schwartz Joel D JD Laden Francine F Moy Marilyn L ML Koutrakis Petros P

Environmental research 20180518

<h4>Rationale</h4>Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited.<h4>Objectives</h4>Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation.<h4>Methods</h4>BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year ...[more]

PMID: 29783085

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Project description:BackgroundWe hypothesized that particulate matter (PM) gamma activity (gamma radiation associated with PM) is associated with systemic effects.ObjectiveExamine short-term relationships between ambient and indoor exposures to PM gamma activities with systemic inflammation and endothelial activation in chronic obstructive pulmonary disease (COPD) patients.MethodsIn 85 COPD patients from Eastern Massachusetts, USA from 2012 to 2014, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured seasonally up to four times. We used US EPA RadNet data measuring ambient gamma radiation attached to PM adjusted for background radiation, and estimated in-home gamma radiation exposures using the ratio of in-home-to-ambient sulfur in PM2.5. Linear mixed-effects regression models were used to determine associations between moving averages of PM gamma activities through the week before phlebotomy with these biomarkers. We explored ambient and indoor PM2.5, black carbon (BC), and NO2 as confounders.ResultsAmbient and indoor PM gamma activities measured as energy spectra classes 3 through 9 were positively associated with CRP and IL-6. For example, averaged from phlebotomy day through previous 6 days, each IQR increase in indoor PM gamma activity for each spectra class, was associated with an CRP increase ranging from 7.45% (95%CI: 2.77, 12.4) to 13.4% (95%CI: 5.82, 21.4) and for ambient exposures were associated with an increase of 8.75% (95%CI: -0.57, 18.95) to 14.8% (95%CI: 4.5, 26.0). Indoor exposures were associated with IL-6 increase of 3.56% (95%CI: 0.31, 6.91) to 6.46% (95%CI:1.33, 11.85) and ambient exposures were associated with an increase of 0.03% (95%CI: -6.37, 6.87) to 3.50% (95%CI: -3.15, 10.61). There were no positive associations with sVCAM-1. Sensitivity analyses using two-pollutant models showed similar effects.ConclusionsOur results demonstrate that short-term exposures to environmental PM gamma radiation activities were associated with systemic inflammation in COPD patients.

Project description:RationaleLittle is known about personal characteristics and systemic responses to particulate pollution in patients with COPD.ObjectivesAssess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 μm in diameter (PM2.5) on systemic inflammation and endothelial activation.Methods144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates.ResultsMedian (25%ile, 75%ile) indoor BC and PM2.5 were 0.6 (0.5,0.7) μg/m3 and 6.8 (4.8,10.4) μg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6-36.3) than statin users (11.1%; 2.1-20.9). There were also positive associations greater among non-statin users between PM2.5 and CRP. For IL-6, associations with BC and PM2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5-38.5) in persons with diabetes than without diabetes (10.3%; 0.92-20.6) with similar effects of PM2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1.ConclusionsAssociations between indoor BC and PM2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM2.5 in persons with COPD.

Project description:BackgroundParticulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure–response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution.ObjectivesWe aimed to assess associations between pulmonary function and indoor and ambient PM [Formula: see text] ([Formula: see text]) and black carbon (BC).MethodsBetween November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and [Formula: see text] were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure.ResultsThere were 367 study visits; the median (IQR) indoor BC and [Formula: see text] were 0.19 (0.22) [Formula: see text] and 6.67 (5.80) [Formula: see text], respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s [Formula: see text] and forced vital capacity (FVC), and [Formula: see text]. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a [Formula: see text] [95% confidence interval (CI): [Formula: see text], [Formula: see text]] decrease in pre-bronchodilator [Formula: see text]. Increases in indoor [Formula: see text] were associated with decreases in [Formula: see text] and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient [Formula: see text] was only associated with decreases in FVC and increases in [Formula: see text], and neither indoor nor ambient BC or [Formula: see text] were associated with post-bronchodilator pulmonary function.ConclusionsLow-level exposures to indoor BC and [Formula: see text], but not ambient exposures, were consistently associated with decreases in pre-bronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. https://doi.org/10.1289/EHP3668.

Project description:The identification and validation of biomarkers to support the assessment of novel therapeutics for COPD continues to be an important area of research. The aim of the current study was to identify systemic protein biomarkers correlated with measures of COPD severity, as well as specific protein signatures associated with comorbidities such as metabolic syndrome. 142 protein analytes were measured in serum of 140 patients with stable COPD, 15 smokers without COPD and 30 non-smoking controls. Seven analytes (sRAGE, EN-RAGE, NGAL, Fibrinogen, MPO, TGF-? and HB-EGF) showed significant differences between severe/very severe COPD, mild/moderate COPD, smoking and non-smoking control groups. Within the COPD subjects, univariate and multivariate analyses identified analytes significantly associated with FEV(1), FEV(1)/FVC and DLCO. Most notably, a set of 5 analytes (HB-EGF, Fibrinogen, MCP-4, sRAGE and Sortilin) predicted 21% of the variability in DLCO values. To determine common functions/pathways, analytes were clustered in a correlation network by similarity of expression profile. While analytes related to neutrophil function (EN-RAGE, NGAL, MPO) grouped together to form a cluster associated with FEV(1) related parameters, analytes related to the EGFR pathway (HB-EGF, TGF-?) formed another cluster associated with both DLCO and FEV(1) related parameters. Associations of Fibrinogen with DLCO and MPO with FEV(1)/FVC were stronger in patients without metabolic syndrome (r ?=? -0.52, p ?=? 0.005 and r ?=? -0.61, p =? 0.023, respectively) compared to patients with coexisting metabolic syndrome (r ?=? -0.25, p ?= ?0.47 and r ?=? -0.15, p ?= ?0.96, respectively), and may be driving overall associations in the general cohort. In summary, our study has identified known and novel serum protein biomarkers and has demonstrated specific associations with COPD disease severity, FEV(1), FEV(1)/FVC and DLCO. These data highlight systemic inflammatory pathways, neutrophil activation and epithelial tissue injury/repair processes as key pathways associated with COPD.

Project description:Black carbon (BC) is a descriptive term that refers to light-absorbing particulate matter (PM) produced by incomplete combustion and is often used as a surrogate for traffic-related air pollution. Exposure to BC has been linked to adverse health effects. Penetration of ambient BC is typically the primary source of indoor BC in the developed world. Other sources of indoor BC include biomass and kerosene stoves, lit candles, and charring food during cooking. Home characteristics can influence the levels of indoor BC. As people spend most of their time indoors, human exposure to BC can be associated to a large extent with indoor environments. At the same time, due to the cost of environmental monitoring, it is often not feasible to directly measure BC inside multiple individual homes in large-scale population-based studies. Thus, a predictive model for indoor BC is needed to support risk assessment in public health. In this study, home characteristics and occupant activities that potentially modify indoor levels of BC were documented in 23 homes, and indoor and outdoor BC concentrations were measured twice. The homes were located in the Cincinnati-Kentucky-Indiana tristate region and measurements occurred from September 2015 through August 2017. A linear mixed-effect model was developed to predict BC concentration in residential environments. The measured outdoor BC concentrations and the documented home characteristics were utilized as predictors of indoor BC concentrations. After the model was developed, a leave-one-out cross-validation algorithm was deployed to assess the predictive accuracy of the output. The following home characteristics and occupant activities significantly modified the concentration of indoor BC: outdoor BC, lit candles and electrostatic or high efficiency particulate air (HEPA) filters in heating, ventilation and air conditioning (HVAC) systems. Predicted indoor BC concentrations explained 78% of the variability in the measured indoor BC concentrations. The data show that outdoor BC combined with home characteristics can be used to predict indoor BC levels with reasonable accuracy.

Dataset Information

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

Rationale

Objectives

Methods

Results

Conclusions

Publications

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

Similar Datasets

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