Engine exhaust particulate and gas phase contributions to vascular toxicity

Campen, Matthew J.; Robertson, Stewart A.; Lund, Amie K.; Lucero, JoAnn; McDonald, Jacob D.

doi:10.3109/08958378.2014.897776

Cited by 31 publications

(20 citation statements)

References 30 publications

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“…Specifically, target levels for PM and gases were derived from previous work with this fresh combustion mixture, and more detailed methods and schematics of the system are published elsewhere [3, 23]. DEE was produced from a single-cylinder, 5500-watt, Yanmar diesel-engine generator using a combination of heavy sulfur fuel and Number 2 Diesel Certification Fuel (Phillips Chemical Company) and 40 weight motor oil (Rotella T, Shell) as previously described [25].…”

Section: Methodsmentioning

confidence: 99%

“…UFP atmosphere was generated by passing the MVE from 1-m 3 mixing chamber through a Harvard denuder [23]. This denuder is a parallel plate opposite flow diffusion denuder with gaseous removal efficiency of 80–90%.…”

Section: Methodsmentioning

confidence: 99%

“…Interactions between combustion-source particulate matter and associated gaseous components may potentiate toxicity, resulting in greater systemic inflammation and, potentially, neuroinflammation, thus increasing the risk for development of neurodegenerative disorders, like AD. We have previously demonstrated interactions between gaseous and particulate components in driving cardiovascular effects [3, 23]; however, it was unclear whether such interactions were influenced more by particulate morphology and surface area or chemical composition. In the present study, we hypothesize that smaller PM, with a higher surface area per mass, will have a greater interaction with gaseous co-pollutants and lead to exacerbated pulmonary and systemic toxicity.…”

Section: Introductionmentioning

confidence: 99%

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Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

et al. 2016

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BackgroundDeleterious consequences of exposure to traffic emissions may derive from interactions between carbonaceous particulate matter (PM) and gaseous components in a manner that is dependent on the surface area or complexity of the particles. To determine the validity of this hypothesis, we examined pulmonary and neurological inflammatory outcomes in C57BL/6 and apolipoprotein E knockout (ApoE−/−) male mice after acute and chronic exposure to vehicle engine-derived particulate matter, generated as ultrafine (UFP) and fine (FP) sizes, with additional exposures using UFP or FP combined with gaseous copollutants derived from fresh gasoline and diesel emissions, labeled as UFP + G and FP + G.ResultsThe UFP and UFP + G exposure groups resulted in the most profound pulmonary and neuroinflammatory effects. Phagocytosis of UFP + G particles via resident alveolar macrophages was substantial in both mouse strains, particularly after chronic exposure, with concurrent increased proinflammatory cytokine expression of CXCL1 and TNFα in the bronchial lavage fluid. In the acute exposure paradigm, only UFP and UFP + G induced significant changes in pulmonary inflammation and only in the ApoE−/− animals. Similarly, acute exposure to UFP and UFP + G increased the expression of several cytokines in the hippocampus of ApoE−/− mice including Il-1β, IL-6, Tgf-β and Tnf-α and in the hippocampus of C57BL/6 mice including Ccl5, Cxcl1, Il-1β, and Tnf-α. Interestingly, Il-6 and Tgf-β expression were decreased in the C57BL/6 hippocampus after acute exposure. Chronic exposure to UFP + G increased expression of Ccl5, Cxcl1, Il-6, and Tgf-β in the ApoE−/− hippocampus, but this effect was minimal in the C57BL/6 mice, suggesting compensatory mechanisms to manage neuroinflammation in this strain.ConclusionsInflammatory responses the lung and brain were most substantial in ApoE−/− animals exposed to UFP + G, suggesting that the surface area-dependent interaction of gases and particles is an important determinant of toxic responses. As such, freshly generated UFP, in the presence of combustion-derived gas phase pollutants, may be a greater health hazard than would be predicted from PM concentration, alone, lending support for epidemiological findings of adverse neurological outcomes associated with roadway proximity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0177-x) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

et al. 2016

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“…Inhalation of particles and gases cause systemic pathologies, including inflammation of arteries, adipose, and neural tissues, vasoconstriction and atherosclerotic remodeling (Campen et al, 2014; Sun et al, 2005; Vedal et al, 2013). MVE specifically has been extensively characterized in mouse models and has clear vasculotoxic effects (Aragon et al, 2015; Lund et al, 2011; Vedal et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Metabolomic changes in murine serum following inhalation exposure to gasoline and diesel engine emissions

Brower

Doyle-Eisele

Moeller

et al. 2016

Inhalation Toxicology

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The adverse health effects of environmental exposure to gaseous and particulate components of vehicular emissions are a major concern among urban populations. A link has been established between respiratory exposure to vehicular emissions and the development of cardiovascular disease (CVD), but the mechanisms driving this interaction remain unknown. Chronic inhalation exposure to mixed vehicle emissions has been linked to CVD in animal models. This study evaluated the temporal effects of acute exposure to mixed vehicle emissions (MVE; mixed gasoline and diesel emissions) on potentially active metabolites in the serum of exposed mice. C57Bl/6 mice were exposed to a single 6 hour exposure to filtered air (FA) or MVE (100 or 300 µg/m3) by whole body inhalation. Immediately after and 18 hours after the end of the exposure period, animals were sacrificed for serum and tissue collection. Serum was analyzed for metabolites that were differentially present between treatment groups and time points. Changes in metabolite levels suggestive of increased oxidative stress (oxidized glutathione, cysteine disulfide, taurine), lipid peroxidation (13-HODE, 9-HODE), energy metabolism (lactate, glycerate, branched chain amino acid catabolites, butrylcarnitine, fatty acids), and inflammation (DiHOME, palmitoyl ethanolamide) were observed immediately after the end of exposure in the serum of animals exposed to MVE relative to those exposed to FA. By 18 hours post exposure, serum metabolite differences between animals exposed to MVE versus those exposed to FA were less pronounced. These findings highlight complex metabolomics alterations in the circulation following inhalation exposure to a common source of combustion emissions.

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“…Following exposure to diesel exhaust or a major component thereof, nitrogen dioxide, healthy humans exhibited changes in the plasma bioactivity that led to increased expression of inflammatory adhesion molecules and chemokines in cultured endothelial cells (Channell, Paffett et al 2012). Furthermore, serum from mice exposed to ozone (O 3 ) or fresh engine emissions (combined diesel and gasoline) was capable of inhibiting endothelial-dependent vasodilation in vessels from unexposed mice (Robertson, Colombo et al 2013, Campen, Robertson et al 2014). The observed mechanistic role for CD36, a multi-ligand scavenger receptor, suggests that more than a single factor in the serum or plasma may be responsible for pathophysiological effects on systemic endothelial cells (Robertson, Colombo et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Endothelial inflammatory transcriptional responses to an altered plasma exposome following inhalation of diesel emissions

Schisler

Ronnebaum

Madden

et al. 2015

Inhalation Toxicology

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Background Air pollution, especially emissions derived from traffic sources, is associated with adverse cardiovascular outcomes. However, it remains unclear how inhaled factors drive extrapulmonary pathology. Objectives Previously, we found that canonical inflammatory response transcripts were elevated in cultured endothelial cells treated with plasma obtained after exposure compared with pre-exposure samples or filtered air (sham) exposures. While the findings confirmed the presence of bioactive factor(s) in the plasma after diesel inhalation, we wanted to better examine the complete genomic response to investigate 1) major responsive transcripts and 2) collected response pathways and ontogeny that may help to refine this method and inform the pathogenesis. Methods We assayed endothelial RNA with gene expression microarrays, examining the responses of cultured endothelial cells to plasma obtained from 6 healthy human subjects exposed to 100 μg/m3 diesel exhaust or filtered air for 2 h on separate occasions. In addition to pre-exposure baseline samples, we investigated samples obtained immediately-post and 24h-post exposure. Results Microarray analysis of the coronary artery endothelial cells challenged with plasma identified 855 probes that changed over time following diesel exhaust exposure. Over-representation analysis identified inflammatory cytokine pathways were upregulated both at the 2 and 24 h condition. Novel pathways related to FOX transcription factors and secreted extracellular factors were also identified in the microarray analysis. Conclusions These outcomes are consistent with our recent findings that plasma contains bioactive and inflammatory factors following pollutant inhalation. The specific study design implicates a novel pathway related to inflammatory blood borne components that may drive the extrapulmonary toxicity of ambient air pollutants.

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Engine exhaust particulate and gas phase contributions to vascular toxicity

Cited by 31 publications

References 30 publications

Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

Metabolomic changes in murine serum following inhalation exposure to gasoline and diesel engine emissions

Endothelial inflammatory transcriptional responses to an altered plasma exposome following inhalation of diesel emissions

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