Dataset Information

Oxidative stress, inflammatory biomarkers, and toxicity in mouse lung and liver after inhalation exposure to 100% biodiesel or petroleum diesel emissions.

ABSTRACT: Over the past decade, soy biodiesel (BD) has become a first alternative energy source that is economically viable and meets requirements of the Clean Air Act. Due to lower mass emissions and reduced hazardous compounds compared to diesel combustion emissions (CE), BD exposure is proposed to produce fewer adverse health effects. However, considering the broad use of BD and its blends in different industries, this assertion needs to be supported and validated by mechanistic and toxicological data. Here, adverse effects were compared in lungs and liver of BALB/cJ mice after inhalation exposure (0, 50, 150, or 500 ?g/m3; 4 h/d, 5 d/wk, for 4 wk) to CE from 100% biodiesel (B100) and diesel (D100). Compared to D100, B100 CE produced a significant accumulation of oxidatively modified proteins (carbonyls), an increase in 4-hydroxynonenal (4-HNE), a reduction of protein thiols, a depletion of antioxidant gluthatione (GSH), a dose-related rise in the levels of biomarkers of tissue damage (lactate dehydrogenase, LDH) in lungs, and inflammation (myeloperoxidase, MPO) in both lungs and liver. Significant differences in the levels of inflammatory cytokines interleukin (IL)-6, IL-10, IL-12p70, monocyte chemoattractant protein (MCP)-1, interferon (IFN) ?, and tumor necrosis factor (TNF)-? were detected in lungs and liver upon B100 and D100 CE exposures. Overall, the tissue damage, oxidative stress, inflammation, and cytokine response were more pronounced in mice exposed to BD CE. Further studies are required to understand what combustion products in BD CE accelerate oxidative and inflammatory responses.

SUBMITTER: Shvedova AA

PROVIDER: S-EPMC4671493 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Oxidative stress, inflammatory biomarkers, and toxicity in mouse lung and liver after inhalation exposure to 100% biodiesel or petroleum diesel emissions.

Shvedova Anna A AA Yanamala Naveena N Murray Ashley R AR Kisin Elena R ER Khaliullin Timur T Hatfield Meghan K MK Tkach Alexey V AV Krantz Q T QT Nash David D King Charly C Ian Gilmour M M Gavett Stephen H SH

Journal of toxicology and environmental health. Part A 20130101 15

Over the past decade, soy biodiesel (BD) has become a first alternative energy source that is economically viable and meets requirements of the Clean Air Act. Due to lower mass emissions and reduced hazardous compounds compared to diesel combustion emissions (CE), BD exposure is proposed to produce fewer adverse health effects. However, considering the broad use of BD and its blends in different industries, this assertion needs to be supported and validated by mechanistic and toxicological data. ...[more]

PMID: 24156694

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Project description:Air pollution, especially emissions derived from traffic sources, is associated with adverse cardiovascular outcomes. However, it remains unclear how inhaled factors drive an extrapulmonary pathology, as the lung is an effective barrier for solid particulates and many gases. Previously, using plasma from healthy human subjects exposed to diesel exhaust under controlled conditions, we found that canonical inflammatory response transcripts of interleukin-8 (IL-8), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were elevated in endothelial cells treated wih 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. Thus, we assayed previousy collected RNA with microarray chips, 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. Primary human coronary artery endothelial cells were grown to confluence and treated with 10% plasma for 24 h, followed by isolation of RNA for microarrays. Microarray analysis of the coronary artery endothelial cells challenged with plasma identified 855 probes that change over time following diesel exhaust exposure. Over-representation analysis identified inflammatory cytokine pathways were upregulated both at the 2 and 24 h condition. These outcomes are consistent with our recent findings that plasma contains bioactive and inflammatory factors following pollutant inhalation and provide a novel pathway to explain the well-reported extrapulmonary toxicity of ambient air pollutants.

Project description:Diesel exhaust emissions have been reported for a number of engine operating strategies, after-treatment technologies, and fuels. However, information is limited regarding emissions of many pollutants during idling and when biodiesel fuels are used. This study investigates regulated and unregulated emissions from both light-duty passenger car (1.7 L) and medium-duty (6.4 L) diesel engines at idle and load and compares a biodiesel blend (B20) to conventional ultralow sulfur diesel (ULSD) fuel. Exhaust aftertreatment devices included a diesel oxidation catalyst (DOC) and a diesel particle filter (DPF). For the 1.7 L engine under load without a DOC, B20 reduced brake-specific emissions of particulate matter (PM), elemental carbon (EC), nonmethane hydrocarbons (NMHCs), and most volatile organic compounds (VOCs) compared to ULSD; however, formaldehyde brake-specific emissions increased. With a DOC and high load, B20 increased brake-specific emissions of NMHC, nitrogen oxides (NOx), formaldehyde, naphthalene, and several other VOCs. For the 6.4 L engine under load, B20 reduced brake-specific emissions of PM2.5, EC, formaldehyde, and most VOCs; however, NOx brake-specific emissions increased. When idling, the effects of fuel type were different: B20 increased NMHC, PM2.5, EC, formaldehyde, benzene, and other VOC emission rates from both engines, and changes were sometimes large, e.g., PM2.5 increased by 60% for the 6.4 L/2004 calibration engine, and benzene by 40% for the 1.7 L engine with the DOC, possibly reflecting incomplete combustion and unburned fuel. Diesel exhaust emissions depended on the fuel type and engine load (idle versus loaded). The higher emissions found when using B20 are especially important given the recent attention to exposures from idling vehicles and the health significance of PM2.5. The emission profiles demonstrate the effects of fuel type, engine calibration, and emission control system, and they can be used as source profiles for apportionment, inventory, and exposure purposes.

Dataset Information

Oxidative stress, inflammatory biomarkers, and toxicity in mouse lung and liver after inhalation exposure to 100% biodiesel or petroleum diesel emissions.

Publications

Oxidative stress, inflammatory biomarkers, and toxicity in mouse lung and liver after inhalation exposure to 100% biodiesel or petroleum diesel emissions.

Similar Datasets

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