Reactive Oxygen Species Generation Linked to Sources of Atmospheric Particulate Matter and Cardiorespiratory Effects.

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Reactive Oxygen Species Generation Linked to Sources of Atmospheric Particulate Matter and Cardiorespiratory Effects.

Environ Sci Technol. 2015 Oct 12;

Authors: Bates JT, Weber RJ, Abrams J, Verma V, Fang T, Klein M, Strickland M, Sarnat SE, Chang HH, Mulholland JA, Tolbert PE, Russell AG

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 modeling was used to relate PM2.5 emissions sources to ROS-generation potential and to estimate historical levels of DTT activity for use in an epidemiologic analysis for the period 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 ?g-1source, 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.biological plausibility to associations of adverse health outcomes with PM2.5 mass, supporting oxidative stress as a mechanism.

PMID: 26457347 [PubMed – as supplied by publisher]

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