Circulating biomarkers of inflammation, antioxidant activity, and platelet activation are associated with primary combustion aerosols in subjects with coronary artery disease.
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Delfino RJ, Staimer N, Tjoa T, Polidori A, Arhami M, Gillen DL, Kleinman MT, Vaziri ND, Longhurst J, Zaldivar F, Sioutas C
Circulating biomarkers of inflammation, antioxidant activity, and platelet activation are associated with primary combustion aerosols in subjects with coronary artery disease.
Environ Health Perspect. 2008 Jul;116(7):898-906. doi: 10.1289/ehp.11189.
- PubMed ID
- 18629312 [ View in PubMed]
- Abstract
BACKGROUND: Biomarkers of systemic inflammation have been associated with risk of cardiovascular morbidity and mortality. OBJECTIVES: We aimed to clarify associations of particulate matter (PM) air pollution with systemic inflammation using models based on size-fractionated PM mass and markers of primary and secondary aerosols. METHODS: We followed a panel of 29 nonsmoking elderly subjects with a history of coronary artery disease (CAD) living in retirement communities in the Los Angeles, California, air basin. Blood plasma biomarkers were measured weekly over 12 weeks and included C-reactive protein (CRP), fibrinogen, tumor necrosis factor-alpha (TNF-alpha) and its soluble receptor-II (sTNF-RII), interleukin-6 (IL-6) and its soluble receptor (IL-6sR), fibrin D-dimer, soluble platelet selectin (sP-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1), intracellular adhesion molecule-1 (sICAM-1), and myeloperoxidase (MPO). To assess changes in antioxidant capacity, we assayed erythrocyte lysates for glutathione peroxidase-1 (GPx-1) and copper-zinc superoxide dismutase (Cu,Zn-SOD) activities. We measured indoor and outdoor home daily size-fractionated PM mass, and hourly pollutant gases, total particle number (PN), fine PM elemental carbon (EC) and organic carbon (OC), estimated secondary organic aerosol (SOA) and primary OC (OCpri) from total OC, and black carbon (BC). We analyzed data with mixed models controlling for temperature and excluding weeks with infections. RESULTS: We found significant positive associations for CRP, IL-6, sTNF-RII, and sP-selectin with outdoor and/or indoor concentrations of quasi-ultrafine PM < or = 0.25 microm in diameter, EC, OCpri, BC, PN, carbon monoxide, and nitrogen dioxide from the current-day and multiday averages. We found consistent positive but largely nonsignificant coefficients for TNF-alpha, sVCAM-1, and sICAM-1, but not fibrinogen, IL-6sR, or D-dimer. We found inverse associations for erythrocyte Cu,Zn-SOD with these pollutants and other PM size fractions (0.25-2.5 and 2.5-10 microm). Inverse associations of GPx-1 and MPO with pollutants were largely nonsignificant. Indoor associations were often stronger for estimated indoor EC, OCpri, and PN of outdoor origin than for uncharacterized indoor measurements. There was no evidence for positive associations with SOA. CONCLUSIONS: Results suggest that traffic emission sources of OCpri and quasi-ultrafine particles lead to increased systemic inflammation and platelet activation and decreased antioxidant enzyme activity in elderly people with CAD.
DrugBank Data that Cites this Article
- Pharmaco-proteomics
Drug Drug Groups Gene Gene ID Change Interaction Chromosome Carbon monoxide Approved Investigational SOD1 6647 decreased Carbon Monoxide results in decreased expression of SOD1 protein 21q22.11 Carbon monoxide Approved Investigational CRP 1401 increased Carbon Monoxide results in increased expression of CRP protein 1q23.2 Carbon monoxide Approved Investigational SELP 6403 increased Carbon Monoxide results in increased expression of SELP protein modified form 1q24.2 Carbon monoxide Approved Investigational TNFRSF1B 7133 increased Carbon Monoxide results in increased expression of TNFRSF1B protein modified form 1p36.22 Carbon monoxide Approved Investigational IL6 3569 increased Carbon Monoxide results in increased expression of IL6 protein 7p15.3