The influence of chemical composition, aerosol acidity, and metal dissolution on the oxidative potential of fine particulate matter and redox potential of the lung lining fluid.

Air pollution is a major risk factor for human health. Chemical reactions in the epithelial lining fluid (ELF) of the human respiratory tract result in the formation of reactive oxygen species (ROS), which can lead to oxidative stress and adverse health effects. We use kinetic modeling to quantify the effects of fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) on ROS formation, interconversion, and reactivity, and discuss different chemical metrics for oxidative stress, such as cumulative production of ROS and hydrogen peroxide (H2O2) to hydroxyl radical (OH) conversion. All three air pollutants produce ROS that accumulate in the ELF as H2O2, which serves as reservoir for radical species. At low PM2.5 concentrations ( 10 μg m-3), however, Fenton chemistry overwhelms the ROS buffering effect and leads to a tipping point in H2O2 fate, causing a strong nonlinear increase in OH production. This shift in ROS chemistry and the enhanced OH production provide a tentative mechanistic explanation for how the inhalation of PM2.5 induces oxidative stress and adverse health effects.

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Hydroxyl Radical Production by Air Pollutants in Epithelial Lining Fluid Governed by Interconversion and Scavenging of Reactive Oxygen Species.

Chemical composition and oxidative potential of atmospheric particles heavily impacted by residential wood burning in the alpine region of northern Italy

Environmental inhalation exposures are inherently mixed (gases and particles), yet regulations are still based on single toxicant exposures. While the impacts of individual components of environmental pollution have received substantial attention, the impact of inhalation co-exposures is poorly understood. Here, we mechanistically investigated pulmonary inflammation and lung function decline after inhalation co-exposure and individual exposures to ozone (O3) and ultrafine carbon black (CB). Environmentally/occupationally relevant lung deposition levels in mice were achieved after inhalation of stable aerosols with similar aerodynamic and mass median distributions. X-ray photoemission spectroscopy detected increased surface oxygen contents on particles in co-exposure aerosols. Compared with individual exposures, co-exposure aerosols produced greater acellular and cellular oxidants detected by electron paramagnetic resonance (EPR) spectroscopy, and in vivo immune-spin trapping (IST), as well as synergistically increased lavage neutrophils, lavage proteins and inflammation related gene/protein expression. Co-exposure induced a significantly greater respiratory function decline compared to individual exposure. A synthetic catalase-superoxide dismutase mimetic (EUK-134) significantly blunted lung inflammation and respiratory function decline confirming the role of oxidant imbalance. We identified a significant induction of epithelial alarmin (thymic stromal lymphopoietin-TSLP)-dependent interleukin-13 pathway after co-exposure, associated with increased mucin and interferon gene expression. We provided evidence of interactive outcomes after air pollution constituent co-exposure and identified a key mechanistic pathway that can potentially explain epidemiological observation of lung function decline after an acute peak of air pollution. Developing and studying the co-exposure scenario in a standardized and controlled fashion will enable a better mechanistic understanding of how environmental exposures result in adverse outcomes.

Oxidant-induced epithelial alarmin pathway mediates lung inflammation and functional decline following ultrafine carbon and ozone inhalation co-exposure.

Solvent extraction of PM25 samples collected on the filter is a preliminary step for assessing the PM25 oxidative potential (OP) using cell-free assays, as the dithiothreitol (DTT) and the ascorbic acid (AA) assays In this study, we evaluated the effect of the solvent choice by extracting ambient PM25 samples with different solvents: methanol, as organic solvent, and two aqueous buffers, ie, phosphate buffer (PB) and Gamble’s solution (G), as a lung fluid surrogate solution Both the measured volume-based OPVDTT and OPVAA responses varied for the different extraction methods, since methanol extraction generated the lowest values and phosphate buffer the highest Although all the tested solvents produced intercorrelated OPVDTT values, the phosphate buffer resulted the most useful for OPDTT assessment, as it provided the most sensible measure (nearly double values) compared with other extractions The association of the measured OPV values with PM chemical composition suggested that oxidative properties of the investigated PM25 samples depend on both transition metals and quinones, as also supported by additional experimental measurements on standard solutions of redox-active species

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Effect of filter extraction solvents on the measurement of the oxidative potential of airborne PM2.5

Regulations on ambient particulate matter (PM) are becoming more stringent because of adverse health effects arising from PM exposure. PM-induced oxidant production is a key mechanism behind the observed health effects and is heavily dependent on PM composition. Measurement of the intrinsic oxidative potential (OP) of PM could provide an integrated indicator of PM bioreactivity and could serve as a better metric of PM hazard exposure than PM mass concentration. The OP of two chemically contrasted PM2.5 samples was compared through four acellular assays, and OP predictive capability was evaluated in different cellular assays on two in vitro lung cell models. PM2.5 collected in Paris at a site close to the traffic exhibited a systematically higher OP in all assays compared to PM2.5 enriched in particles from domestic wood burning. Similar results were obtained for oxidative stress, expression of antioxidant enzymes, and pro-inflammatory chemokine in human bronchial epithelial and endothelial cells. The strongest correlations between OP assays and cellular responses were observed with the antioxidant (ascorbic acid and glutathione) depletion (OPAO) assay. Multivariate regression analysis from OP daily measurements suggested that OPAO was strongly correlated with polycyclic aromatic hydrocarbons at the traffic site while it was correlated with potassium for the domestic wood burning sample.

Linh Chi Bui

Papers

Lung Antioxidant Depletion: A Predictive Indicator of Cellular Stress Induced by Ambient Fine Particles