Associations between ambient wood smoke and other particulate pollutants and biomarkers of systemic inflammation, coagulation and thrombosis in cardiac patients

Increased particulate air pollution has been associated with both an increased risk of myocardial infarction (MI) and adverse changes in cardiac biomarkers. Up to 30% of ambient wintertime fine particles (PM2.5) in Rochester, NY are from wood burning. Our study examined associations between ambient...

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Bibliographic Details
Published in:Environmental research Vol. 154; pp. 352 - 361
Main Authors: Croft, Daniel P., Cameron, Scott J., Morrell, Craig N., Lowenstein, Charles J., Ling, Frederick, Zareba, Wojciech, Hopke, Philip K., Utell, Mark J., Thurston, Sally W., Thevenet-Morrison, Kelly, Evans, Kristin A., Chalupa, David, Rich, David Q.
Format: Journal Article
Language:English
Published: Netherlands Elsevier Inc 01-04-2017
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Summary:Increased particulate air pollution has been associated with both an increased risk of myocardial infarction (MI) and adverse changes in cardiac biomarkers. Up to 30% of ambient wintertime fine particles (PM2.5) in Rochester, NY are from wood burning. Our study examined associations between ambient levels of a marker of wood smoke (Delta-C) and other particulate air pollutants and biomarkers of inflammation, coagulation and thrombosis. We measured blood concentrations of C-reactive protein (CRP), D-dimer, fibrinogen, P-selectin, platelet factor 4 (PF-4), von Willebrand factor (vWF), and myeloperoxidase (MPO) of 135 patients undergoing cardiac catheterization during the winters of 2011–2013. We coupled these data with hourly ambient concentrations of Delta-C, black carbon (BC; marker of traffic pollution), and ultrafine (10–100nm; UFP), accumulation mode (100–500nm; AMP), and fine particles (<2.5µm; PM2.5). Using linear regression models, we estimated the change in each biomarker associated with increased pollutant concentrations at intervals between 1 and 96h preceding blood collection. Each 0.13µg/m3 increase in Delta-C concentration in the prior 12h was associated with a 0.91% increase in fibrinogen levels (95% CI=0.23%, 1.59%), but unexpectedly in the prior 48h, each 0.17µg/m3 increase in Delta-C concentration was associated with a 2.75% decrease in MPO levels (95% CI=−5.13%,−0.37%). We did not see associations between Delta-C concentrations and any other biomarkers. Interquartile range (IQR) increases in PM2.5, BC, UFP, and AMP concentrations were generally associated with increased CRP and fibrinogen, but not PF4, D-dimer, vWF, or P-selectin. In a population of cardiac patients, we noted adverse changes in fibrinogen associated with increased concentrations of a marker of wood smoke. Increases in PM2.5, BC, AMP, and UFP concentrations in the previous 96h were also associated with adverse changes in markers of systemic inflammation and coagulation, but not with markers of endothelial cell dysfunction or platelet activation. •Biomarkers in 135 cardiac patients were matched to air pollution in prior four days.•Increased particulate pollution and wood smoke associated with increased fibrinogen.•No changes in biomarkers related to endothelial dysfunction or platelet activation.•More research needed for association between wood smoke and inflammation/coagulation.
ISSN:0013-9351
1096-0953
DOI:10.1016/j.envres.2017.01.027