Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Differential responses upon inhalation exposure to biodiesel versus diesel exhaust on oxidative stress, inflammatory, and immune outcomes.

Authors
Shvedova-AA; Yanamala-NV; Tkach-AV; Kisin-EK; Murray-AR; Khaliullin-T; Hatfield-M; Gavett-SH; Gilmour-I
Source
Toxicologist 2013 Mar; 132(1):504
NIOSHTIC No.
20042448
Abstract
Biodiesel (BD) exhaust may have reduced adverse health effects due to lower mass emissions and reduced production of hazardous compounds compared to diesel exhaust. To investigate this possibility, we compared adverse effects in lungs and liver of BALB/cJ mice after inhalation exposure (0, 50, 150 and 500 ug/m3; 4 hr/day, 5 d/wk, for 4 wk) to combustion exhaust from 100% biodiesel (B100) and diesel (D100). Compared to D100, B100 exhaust caused a significant accumulation of oxidatively modified proteins (carbonyls), increase in 4-hydroxynonenal (4-HNE), reduction of protein thiols, depletion of antioxidant - gluthatione (GSH), a dose-dependent increase in the levels of biomarkers of tissue damage (LDH) in lungs, and inflammation (myeloperoxidase, MPO) in both lungs and liver. B100 exposure also significantly enhanced expression of cytokines IL-6, and IL-12p70 (in a dose-dependent manner), along with IL-10, TNF-a and MCP-1 (increased compared to control) in both lung and liver tissues. Overall, the cytokine profiles in the lung and liver suggest that B100 and D100 exhaust elicit similar innate immune responses, predominantly involving T-cell independent pathways; however, the magnitude of inflammation was greater following B100 exhaust exposure. Interestingly, exposure to D100, but not B100 exhaust, induced a significant increase in the levels of IFN-g in the lungs, suggesting a broader engagement of Th1 component by D100 exhaust. Based on this, we hypothesize that the distinctive organic compounds and/or oxidative products formed as a result of increased oxidative stress upon B100 exposure, are capable of targeting biological/molecular pathways that are distinct from D100 exposure. (This abstract does not represent US EPA policy).
Keywords
Toxicology; Nanotechnology; Laboratory-animals; Laboratory-testing; Exposure-assessment; Exposure-levels; Inhalation-studies; Biohazards; Biological-material; Diesel-emissions; Diesel-exhausts; Hazardous-materials; Liver; Liver-cells; Lung; Lung-cells; Immune-system; Immune-reaction; Oxidative-processes; Cellular-reactions; Antioxidants; Myeloid-tissue; Peroxidases; Carbonyls; Thiols; Proteins; Lung-tissue; Cellular-function; Fuels; Biomarkers; Hydroxy-compounds; Cytotoxic-effects; Liver-damage; Liver-tissue; Lung-tissue; Molecular-biology
CAS No.
70-18-8
Publication Date
20130301
Document Type
Abstract
Fiscal Year
2013
NTIS Accession No.
NTIS Price
Identifying No.
B20130502
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Priority Area
Mining
Source Name
The Toxicologist. Society of Toxicology 52nd Annual Meeting and ToxExpo, March 10-14, 2013, San Antonio, Texas
State
WV; NC; TX
TOP