Dataset Information

Engine exhaust particulate and gas phase contributions to vascular toxicity.

ABSTRACT: Cardiovascular health effects of near-roadway pollution appear more substantial than other sources of air pollution. The underlying cause of this phenomenon may simply be concentration-related, but the possibility remains that gases and particulate matter (PM) may physically interact and further enhance systemic vascular toxicity. To test this, we utilized a common hypercholesterolemic mouse model (Apolipoprotein E-null) exposed to mixed vehicle emission (MVE; combined gasoline and diesel exhausts) for 6?h/d?×?50?d, with additional permutations of removing PM by filtration and also removing gaseous species from PM by denudation. Several vascular bioassays, including matrix metalloproteinase-9 protein, 3-nitrotyrosine and plasma-induced vasodilatory impairments, highlighted that the whole emissions, containing both particulate and gaseous components, was collectively more potent than MVE-derived PM or gas mixtures, alone. Thus, we conclude that inhalation of fresh whole emissions induce greater systemic vascular toxicity than either the particulate or gas phase alone. These findings lend credence to the hypothesis that the near-roadway environment may have a more focused public health impact due to gas-particle interactions.

SUBMITTER: Campen M

PROVIDER: S-EPMC4137573 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature

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Engine exhaust particulate and gas phase contributions to vascular toxicity.

Campen Matthew M Robertson Sarah S Lund Amie A Lucero Joann J McDonald Jacob J

Inhalation toxicology 20140501 6

Cardiovascular health effects of near-roadway pollution appear more substantial than other sources of air pollution. The underlying cause of this phenomenon may simply be concentration-related, but the possibility remains that gases and particulate matter (PM) may physically interact and further enhance systemic vascular toxicity. To test this, we utilized a common hypercholesterolemic mouse model (Apolipoprotein E-null) exposed to mixed vehicle emission (MVE; combined gasoline and diesel exhaus ...[more]

PMID: 24730681

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Project description:BackgroundDiesel engine exhaust (DEE) exposure causes lung cancer, but the molecular mechanisms by which this occurs are not well understood.ObjectivesTo assess transcriptomic alterations in nasal epithelium of DEE-exposed factory workers to better understand the cellular and molecular effects of DEE.MethodsNasal epithelial brushings were obtained from 41 diesel engine factory workers exposed to relatively high levels of DEE (17.2-105.4 μg/m3), and 38 unexposed workers from factories without DEE exposure. mRNA was profiled for gene expression using Affymetrix microarrays. Linear modeling was used to identify differentially expressed genes associated with DEE exposure and interaction effects with current smoking status. Pathway enrichment among differentially expressed genes was assessed using EnrichR. Gene Set Enrichment Analysis (GSEA) was used to compare gene expression patterns between datasets.Results225 genes had expression associated with DEE exposure after adjusting for smoking status (FDR q < 0.25) and were enriched for genes in pathways related to oxidative stress response, cell cycle pathways such as MAPK/ERK, protein modification, and transmembrane transport. Genes up-regulated in DEE-exposed individuals were enriched among the genes most up-regulated by cigarette smoking in a previously reported bronchial airway smoking dataset. We also found that the DEE signature was enriched among the genes most altered in two previous studies of the effects of acute DEE on PBMC gene expression. An exposure-response relationship was demonstrated between air levels of elemental carbon and the first principal component of the DEE signature.ConclusionsA gene expression signature was identified for workers occupationally exposed to DEE that was altered in an exposure-dependent manner and had some overlap with the effects of smoking and the effects of acute DEE exposure. This is the first study of gene expression in nasal epithelial cells of workers heavily exposed to DEE and provides new insights into the molecular alterations that occur with DEE exposure.

Dataset Information

Engine exhaust particulate and gas phase contributions to vascular toxicity.

Publications

Engine exhaust particulate and gas phase contributions to vascular toxicity.

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