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

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

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1
Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. jmcdonal@lrri.org

Abstract

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.

PMID:
22954394
DOI:
10.3109/08958378.2012.712164
[Indexed for MEDLINE]
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