Associations of Primary and Secondary Organic Aerosols With Airway and Systemic Inflammation in an Elderly Panel Cohort

Background: Exposure-response information about particulate air-pollution constituents is needed to protect sensitive populations. Particulate matter <2.5 mm (PM2.5) components may induce oxidative stress through reactive-oxygen-species generation, including primary organics from combustion sources and secondary organics from photochemically oxidized volatile organic compounds. We evaluated differences in airway versus systemic inflammatory responses to primary versus secondary organic particle components, particle size fractions, and the potential of particles to induce cellular production of reactive oxygen species. Methods: A total of 60 elderly subjects contributed up to 12 weekly measurements of fractional exhaled nitric oxide (NO; airway inflammation biomarker), and plasma interleukin-6 (IL-6; systemic inflammation biomarker). PM2.5 mass fractions were PM0.25 (<0.25 &mgr;m) and PM0.25–2.5 (0.25–2.5 &mgr;m). Primary organic markers included PM2.5 primary organic carbon, and PM0.25 polycyclic aromatic hydrocarbons and hopanes. Secondary organic markers included PM2.5 secondary organic carbon, and PM0.25 water soluble organic carbon and n-alkanoic acids. Gaseous pollutants included carbon monoxide (CO) and nitrogen oxides (NOx; combustion emissions markers), and ozone (O3; photochemistry marker). To assess PM oxidative potential, we exposed rat alveolar macrophages in vitro to aqueous extracts of PM0.25 filters and measured reactive-oxygen-species production. Biomarker associations with exposures were evaluated with mixed-effects models. Results: Secondary organic markers, PM0.25–2.5, and O3 were positively associated with exhaled NO. Primary organic markers, PM0.25, CO, and NOx were positively associated with IL-6. Reactive oxygen species were associated with both outcomes. Conclusions: Particle effects on airway versus systemic inflammation differ by composition, but overall particle potential to induce generation of cellular reactive oxygen species is related to both outcomes.

[1]  R. Brook,et al.  Particulate Matter Air Pollution and Cardiovascular Disease: An Update to the Scientific Statement From the American Heart Association , 2010, Circulation.

[2]  C. Sioutas,et al.  Traffic-related Air Pollution and Blood Pressure in Elderly Subjects With Coronary Artery Disease , 2010, Epidemiology.

[3]  J. Schauer,et al.  Association of Biomarkers of Systemic Inflammation with Organic Components and Source Tracers in Quasi-Ultrafine Particles , 2010, Environmental health perspectives.

[4]  J. Schauer,et al.  Organic compound characterization and source apportionment of indoor and outdoor quasi-ultrafine particulate matter in retirement homes of the Los Angeles Basin. , 2010, Indoor air.

[5]  J. Schauer,et al.  Organic Compound Characterization and Source Apportionment of Indoor and Outdoor Quasi-ultrafine PM in Retirement Homes of the Los Angeles Basin , 2009 .

[6]  W. Leifert,et al.  Cardiovascular biology of interleukin-6. , 2009, Current pharmaceutical design.

[7]  Seung-Hyun Cho,et al.  Electrophilic and redox properties of diesel exhaust particles. , 2009, Environmental research.

[8]  J. Schauer,et al.  Physicochemical and toxicological profiles of particulate matter in Los Angeles during the October 2007 southern California wildfires. , 2009, Environmental science & technology.

[9]  Shaohua Hu,et al.  Redox activity and chemical speciation of size fractioned PM in the communities of the Los Angeles-Long Beach harbor , 2008 .

[10]  L. Sheppard,et al.  Statistical analysis of air pollution panel studies: an illustration. , 2008, Annals of epidemiology.

[11]  M. Hannigan,et al.  A Macrophage-Based Method for the Assessment of the Reactive Oxygen Species (ROS) Activity of Atmospheric Particulate Matter (PM) and Application to Routine (Daily-24 h) Aerosol Monitoring Studies , 2008 .

[12]  John H Seinfeld,et al.  Apportionment of primary and secondary organic aerosols in southern California during the 2005 study of organic aerosols in riverside (SOAR-1). , 2008, Environmental science & technology.

[13]  C. Sioutas,et al.  Circulating Biomarkers of Inflammation, Antioxidant Activity, and Platelet Activation Are Associated with Primary Combustion Aerosols in Subjects with Coronary Artery Disease , 2008, Environmental health perspectives.

[14]  David G. Anderson,et al.  Exposure to Concentrated Ambient Particles Does Not Affect Vascular Function in Patients with Coronary Heart Disease , 2008, Environmental health perspectives.

[15]  Gerhard Scheuch,et al.  Deposition, retention, and translocation of ultrafine particles from the central airways and lung periphery. , 2008, American journal of respiratory and critical care medicine.

[16]  R. Poulton,et al.  Association between exhaled nitric oxide and systemic inflammatory markers. , 2007, Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.

[17]  T. Sandström,et al.  Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. , 2007, The New England journal of medicine.

[18]  Thomas Sandström,et al.  Persistent endothelial dysfunction in humans after diesel exhaust inhalation. , 2007, American journal of respiratory and critical care medicine.

[19]  Joost A. de Gouw,et al.  A study of secondary organic aerosol formation in the anthropogenic-influenced southeastern United States , 2007 .

[20]  D. C. Snyder,et al.  Source apportionment of fine organic aerosol in Mexico City during the MILAGRO experiment 2006 , 2007 .

[21]  Allen L Robinson,et al.  Rethinking Organic Aerosols: Semivolatile Emissions and Photochemical Aging , 2007, Science.

[22]  Andrea Polidori,et al.  Indoor/Outdoor Relationships, Trends, and Carbonaceous Content of Fine Particulate Matter in Retirement Homes of the Los Angeles Basin , 2007, Journal of the Air & Waste Management Association.

[23]  Joel Schwartz,et al.  Ambient and Microenvironmental Particles and Exhaled Nitric Oxide Before and After a Group Bus Trip , 2006, Environmental health perspectives.

[24]  D. Dockery,et al.  Health Effects of Fine Particulate Air Pollution: Lines that Connect , 2006, Journal of the Air & Waste Management Association.

[25]  D. Dockery,et al.  Health Effects of Fine Particulate Air Pollution: Lines that Connect , 2006, Journal of the Air & Waste Management Association.

[26]  Joel Schwartz,et al.  Diabetes, Obesity, and Hypertension May Enhance Associations between Air Pollution and Markers of Systemic Inflammation , 2006, Environmental health perspectives.

[27]  Alexandra Schneider,et al.  Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. , 2006, American journal of respiratory and critical care medicine.

[28]  David E Newby,et al.  Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis , 2005, Circulation.

[29]  J. Schwartz,et al.  Association between air pollution exposure and exhaled nitric oxide in an elderly population , 2004, Thorax.

[30]  C. Sioutas,et al.  Development and evaluation of a personal cascade impactor sampler (PCIS) , 2002 .

[31]  R. Barouki,et al.  Organic compounds from diesel exhaust particles elicit a proinflammatory response in human airway epithelial cells and induce cytochrome p450 1A1 expression. , 2001, American journal of respiratory cell and molecular biology.

[32]  A. Dahl,et al.  The rapid alveolar absorption of diesel soot-adsorbed benzo[a]pyrene: bioavailability, metabolism and dosimetry of an inhaled particle-borne carcinogen. , 2001, Carcinogenesis.

[33]  J. Schauer,et al.  Source Apportionment of Wintertime Gas-Phase and Particle-Phase Air Pollutants Using Organic Compounds as Tracers , 2000 .

[34]  J. V. van Amsterdam,et al.  Air pollution is associated with increased level of exhaled nitric oxide in nonsmoking healthy subjects. , 1999, Archives of environmental health.

[35]  R. Abdolrasulnia,et al.  Characterization of a rat alveolar macrophage cell line that expresses a functional mannose receptor , 1998, Journal of leukocyte biology.

[36]  James J. Schauer,et al.  Source apportionment of airborne particulate matter using organic compounds as tracers , 1996 .

[37]  Glen R. Cass,et al.  Quantification of urban organic aerosols at a molecular level: Identification, abundance and seasonal variation , 1993 .

[38]  T. Sandström,et al.  Adverse cardiovascular effects of air pollution , 2009, Nature Clinical Practice Cardiovascular Medicine.

[39]  C. Sioutas,et al.  UC Irvine UC Irvine Previously Published Works Title Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population : Clues to Potential Causal Component mixtures and mechanisms , 2009 .

[40]  R. Harrison,et al.  Evaluating the Toxicity of Airborne Particulate Matter and Nanoparticles by Measuring Oxidative Stress Potential — A Workshop Report and Consensus Statement , 2008 .

[41]  R. Hillamo,et al.  Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe. , 2008, Inhalation toxicology.

[42]  ATS/ERS recommendations for standardized procedures for the online and offline measurement of exhaled lower respiratory nitric oxide and nasal nitric oxide, 2005. , 2005, American journal of respiratory and critical care medicine.