A Comparison of Vascular Effects from Complex and Individual Air Pollutants Indicates a Role for Monoxide Gases and Volatile Hydrocarbons

Abstract

BackgroundEmerging evidence suggests that the systemic vasculature may be a target of inhaled pollutants of vehicular origin. We have identified several murine markers of vascular toxicity that appear sensitive to inhalation exposures to combustion emissions.ObjectiveWe sought to examine the relative impact of various pollutant atmospheres and specific individual components on these markers of altered vascular transcription and lipid peroxidation.MethodsApolipoprotein E knockout (ApoE−/−) mice were exposed to whole combustion emissions (gasoline, diesel, coal, hardwood), biogenically derived secondary organic aerosols (SOAs), or prominent combustion-source gases [nitric oxide (NO), NO2, carbon monoxide (CO)] for 6 hr/day for 7 days. Aortas were assayed for transcriptional alterations of endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-2 (TIMP-2), and heme oxygenase-1 (HO-1), along with measures of vascular lipid peroxides (LPOs) and gelatinase activity.ResultsWe noted transcriptional alterations with exposures to gasoline and diesel emissions. Interestingly, ET-1 and MMP-9 transcriptional effects could be recreated by exposure to CO and NO, but not NO2 or SOAs. Gelatinase activity aligned with levels of volatile hydrocarbons and also monoxide gases. Neither gases nor particles induced vascular LPO despite potent effects from whole vehicular emissions.ConclusionsIn this head-to-head comparison of the effects of several pollutants and pollutant mixtures, we found an important contribution to vascular toxicity from readily bioavailable monoxide gases and possibly from volatile hydrocarbons. These data support a role for traffic-related pollutants in driving cardiopulmonary morbidity and mortality.

Interaction of matrix metalloproteinases with pulmonary pollutants: Table 1–

“…The main results of the study by CAMPEN et al [87] indicate that gasoline and, to a lesser extent, diesel exposure induced MMP-9 mRNA expression and activity in the aorta. Interestingly, whereas gasoline exposure also induced an increased gelatinase activity, such an effect was absent after exposure to diesel combustion.…”

“…In order to better understand the role of the different components of gasoline exhaust on MMP induction and activation, the same group of investigators analysed the comparative effects of various gases representative of gasoline exhaust on vascular toxicity and MMP-9 expression and activity [87]. Exposure atmospheres included gasoline and diesel engine exhaust, hardwood smoke, a simulated ''downwind'' coal combustion atmosphere (SDCCA), biogenically derived secondary organic aerosols (SOAs), and individual combustion source gases (nitric oxide (NO), NO 2 and CO).…”

“…In this study by CAMPEN et al [87], the diesel exhaust, SDCCA, hardwood smoke and SOA exposures were conducted at matching particulate matter concentrations (300 mg?m -3 ). Because gasoline exhaust contains a very low mass of particulate matter, mice were also exposed to the highest concentration used in a previous study (60 mg?m -3 particulate matter).…”

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

“…The SPHERES program was developed to enable the development of irradiation chamber technology that is coupled to inhalation exposure systems and to subsequently carry out toxicological experiments to comprehensively evaluate the potential toxicity of SOA. The results of the SPHERES studies on α-pinene have been reported Campen et al, 2010). This manuscript reports on the design and characterization of the SPHERES inhalation system along with initial findings assessing the cardiopulmonary response in rodents exposed to SOA derived from the oxidation of a single anthropogenic hydrocarbon (i.e.…”

Public health and components of particulate matter: The changing assessment of black carbon

“…Studies beyond laboratory exposure to single pollutants are relatively rare, but there are useful examples (Ayala et al, 2012;Campen et al, 2010;Ljubimova et al, 2013;Mauderly et al, 2010;Seilkop et al, 2012). The linkage between air chemistry and exposure could be exploited with study designs that take advantage of advanced aerosol generation and analytical methods to provide aged mixtures to in vitro or in vivo procedures.…”