The effects of α-pinene versus toluene-derived secondary organic aerosol exposure on the expression of markers associated with vascular disease

Abstract

To investigate the toxicological effects of biogenic- versus anthropogenic-source secondary organic aerosol (SOA) on the cardiovascular system, the Secondary Particulate Health Effects Research program irradiation chamber was used to expose atherosclerotic apolipoprotein E null (Apo E−/−) mice to SOA from the oxidation of either α-pinene or toluene for 7 days. SOA atmospheres were produced to yield 250–300 μg/m3 of particulate matter and ratios of 10:1:1 α-pinene:nitrogen oxide (NO_x):ammonia (NH_3); 10:1:1:1 α-pinene:NO_x:NH_3:sulfur dioxide (SO2) or 10:1:1 toluene:NO_x:NH_3; and 10:1:1:1 toluene:NO_x:NH_3:SO_2. Resulting effects on the cardiovascular system were assessed by measurement of vascular lipid peroxidation (thiobarbituric acid reactive substance (TBARS)), as well as quantification of heme-oxygenase (HO)-1, endothelin (ET)-1, and matrix metalloproteinase (MMP)-9 mRNA expression for comparison to previous program exposure results. Consistent with similar previous studies, vascular TBARS were not increased significantly with any acute SOA exposure. However, vascular HO-1, MMP-9, and ET-1 observed in Apo E−/− mice exposed to α-pinene + NOx + NH_3 + SO_2 increased statistically, while α-pinene + NO_x + NH3 exposure to either toluene + NO_x + NH_3 or toluene +NO_x + NH_3 + SO_2 resulted in a decreased expression of these vascular factors. Such findings suggest that the specific chemistry created by the presence or absence of acidic components may be important in SOA-mediated toxicity in the cardiovascular system and/or progression of cardiovascular disease.

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