title: Reactive Oxygen Species Generation Linked to Sources of Atmospheric Particulate Matter and Cardiorespiratory Effects.
abstract: Exposure to atmospheric fine particulate matter (PM2.5) is associated with cardiorespiratory morbidity and mortality, but the mechanisms are not well understood. We assess the hypothesis that PM2.5 induces oxidative stress in the body via catalytic generation of reactive oxygen species (ROS). A dithiothreitol (DTT) assay was used to measure the ROS-generation potential of water-soluble PM2.5. Source apportionment on ambient (Atlanta, GA) PM2.5 was performed using the chemical mass balance method with ensemble-averaged source impact profiles. Linear regression analysis was used to relate PM2.5 emission sources to ROS-generation potential and to estimate historical levels of DTT activity for use in an epidemiologic analysis for the period of 1998-2009. Light-duty gasoline vehicles (LDGV) exhibited the highest intrinsic DTT activity, followed by biomass burning (BURN) and heavy-duty diesel vehicles (HDDV) (0.11 ± 0.02, 0.069 ± 0.02, and 0.052 ± 0.01 nmol min(-1) μg(-1)source, respectively). BURN contributed the largest fraction to total DTT activity over the study period, followed by LDGV and HDDV (45, 20, and 14%, respectively). DTT activity was more strongly associated with emergency department visits for asthma/wheezing and congestive heart failure than PM2.5. This work provides further epidemiologic evidence of a biologically plausible mechanism, that of oxidative stress, for associations of adverse health outcomes with PM2.5 mass and supports continued assessment of the utility of the DTT activity assay as a measure of ROS-generating potential of particles.
authors.forename: Josephine T
authors.initials: JT
authors.lastname: Bates
authors.forename: Rodney J
authors.initials: RJ
authors.lastname: Weber
authors.forename: Joseph
authors.initials: J
authors.lastname: Abrams
authors.affiliation: Department of Civil and Environmental Engineering, University of Illinois at Urbana-Champaign , Champaign, Illinois 61801, United States.
authors.forename: Vishal
authors.initials: V
authors.lastname: Verma
authors.forename: Ting
authors.initials: T
authors.lastname: Fang
authors.forename: Mitchel
authors.initials: M
authors.lastname: Klein
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Strickland
authors.forename: Stefanie Ebelt
authors.initials: SE
authors.lastname: Sarnat
authors.forename: Howard H
authors.initials: HH
authors.lastname: Chang
authors.forename: James A
authors.initials: JA
authors.lastname: Mulholland
authors.forename: Paige E
authors.initials: PE
authors.lastname: Tolbert
authors.forename: Armistead G
authors.initials: AG
authors.lastname: Russell
mesh_terms: D000393:Air Pollutants / Q000032:analysis; D000397:Air Pollution / Q000009:adverse effects; D001249:Asthma / Q000453:epidemiology / Q000209:etiology*; D002947:Cities; D004229:Dithiothreitol; D005742:Gasoline / Q000032:analysis; D005845:Georgia / Q000453:epidemiology; D006333:Heart Failure / Q000453:epidemiology / Q000209:etiology*; D006801:Humans; D008962:Models, Theoretical; D018986:Motor Vehicles; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000032:analysis / Q000633:toxicity*; D012044:Regression Analysis; D014116:Toxicology / Q000379:methods
chemical_list: D000393:Air Pollutants; D005742:Gasoline; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D004229:Dithiothreitol