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

Details

• Personal Author:
  Gavett SH ; Gilmour I ; Hatfield M ; Khaliullin T ; Kisin EK ; Murray AR ; Shvedova AA ; Tkach AV ; Yanamala NV
• Description:
  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). [Description provided by NIOSH]
• Subjects:
  Antioxidants Biological Products Biomarkers Cytotoxins Digestive System Digestive System Diseases Environmental Monitoring Fuel Oils Hazardous Substances Immune System Laboratories Liver Lung Occupational Health Respiratory System Safety Sulfhydryl Compounds Toxicology Vehicle Emissions

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• Keywords:
  Biohazards Biological-material Carbonyls Cellular-function Cellular-reactions Cytotoxic-effects Diesel-emissions Diesel-exhausts Exposure-assessment Exposure-levels Fuels Hazardous-materials Hydroxy-compounds Immune-reaction Immune-system Inhalation-studies Laboratory-animals Laboratory-testing Liver-cells Liver-damage Liver-tissue Lung-cells Lung-tissue Molecular-biology Myeloid-tissue Nanotechnology Oxidative-processes Peroxidases Proteins Thiols

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• ISSN:
  1096-6080
• Document Type:
  Text
• Genre:
  Abstract or Summary
• Place as Subject:
  North Carolina ; OSHA Region 3 ; OSHA Region 4 ; OSHA Region 6 ; Texas ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  132
• Issue:
  1
• NIOSHTIC Number:
  nn:20042448
• Citation:
  Toxicologist 2013 Mar; 132(1):504
• CAS Registry Number:
  Glutathione (CAS RN 70-18-8)
• Federal Fiscal Year:
  2013
• NORA Priority Area:
  Mining
• Peer Reviewed:
  False
• Source Full Name:
  The Toxicologist. Society of Toxicology 52nd Annual Meeting and ToxExpo, March 10-14, 2013, San Antonio, Texas
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:4806f8b03cac0439dbc72479f0e4de06f14943e4f03be9efedcc7600418503b8d9b022fe85a4b14bfb771f95928f066f44a01f7ee9f78ae163cfe6f459d6b880
• Download URL:
  https://stacks.cdc.gov/view/cdc/194671/cdc_194671_DS1.pdf
• File Type:
  [PDF - 572.53 KB ]