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Inhalation Toxicology
International Forum for Respiratory Research
Volume 22, 2010 - Issue 3
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Review Article

Cardiopulmonary response to inhalation of biogenic secondary organic aerosol

, , , , , , , , & show all
Pages 253-265 | Received 28 Apr 2009, Accepted 26 Jun 2009, Published online: 12 Feb 2010
 

Abstract

An irradiation chamber designed for reproducible generation of inhalation test atmospheres of secondary organic aerosol (SOA) was used to evaluate cardiopulmonary responses in rodents exposed to SOA derived from the oxidation of α-pinene. SOA atmospheres were produced with 10:1 ratios of α-pinene:nitrogen oxides (NOx) and 10:1:1 ratios of α-pinene:nitrogen oxides:sulfur dioxide (SO2). SOA atmospheres were produced to yield 200 μg m−3 of particulate matter (PM). Exposures were conducted downstream of honeycomb denuders employed to remove the gas-phase precursors and reaction products. Nose-only exposures were conducted with both rats (pulmonary effects) and mice (pulmonary and cardiovascular effects). Composition of the atmospheres was optimized to ensure that the SOA generated resembled SOA observed in previous irradiation studies, and contained specific SOA compounds of interest (e.g., organosulfates) identified in ambient air. Pulmonary and cardiovascular toxicity were measured in two different rodent species. In situ chemiluminescence and thiobarbituric acid– reactive substances (TBARS) were used to evaluate oxidative reactions in the F344 rats. ApoE−/− mice were exposed for 7 days and measurements of TBARS and gene expression of heme oxygenase-1 (HO-1), endothelin-1 (ET-1), 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 in either species. A mild response was observed in mouse aorta for the upregulation of HO-1 and MMP-9, but was not seen for ET-1. Overall, α-pinene–derived SOA, including SOA that included organosulfate compounds, revealed limited biological response after short-term inhalation exposures

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