Cardiopulmonary response to inhalation of secondary organic aerosol derived from gas-phase oxidation of toluene

Inhal Toxicol. 2012 Sep;24(11):689-97. doi: 10.3109/08958378.2012.712164.


The biological response to inhalation of secondary organic aerosol (SOA) was determined in rodents exposed to SOA derived from the oxidation of toluene, a precursor emitted from anthropogenic sources. SOA atmospheres were produced to yield 300 µg·m(-3) of particulate matter (PM) plus accompanying gases. Whole-body exposures were conducted in mice to assess both pulmonary and cardiovascular effects. ApoE(-/-) mice were exposed for 7 days and measurements of TBARS and gene expression of heme-oxygenase-1 (HO-1), endothelin-1 (ET-1), and matrix metalloproteinase-9 (MMP-9) were made in aorta. Pulmonary inflammatory responses in both species were measured by bronchoalveolar lavage fluid (BALF) cell counts. No pulmonary inflammation was observed. A mild response was observed in mouse aorta for the upregulation of ET-1 and HO-1, with a trend for increased MMP-9 and TBARS, and. Overall, toluene-derived SOA revealed limited biological response compared with previous studies using this exposure protocol with other environmental pollutants.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aerosols / chemistry*
  • Aerosols / toxicity*
  • Air Pollutants / chemistry
  • Air Pollutants / toxicity*
  • Animals
  • Apolipoproteins E / genetics
  • Apolipoproteins E / metabolism
  • Atmosphere Exposure Chambers
  • Gases
  • Gene Expression Regulation
  • Inhalation Exposure
  • Male
  • Mice
  • Mice, Knockout
  • Molecular Structure
  • Oxidation-Reduction
  • Toluene / chemistry*
  • Toluene / toxicity*


  • Aerosols
  • Air Pollutants
  • Apolipoproteins E
  • Gases
  • Toluene