Abstract
BackgroundDeleterious consequences of exposure to traffic emissions may derive from interactions between carbonaceous particulate matter (PM) and gaseous components in a manner that is dependent on the surface area or complexity of the particles. To determine the validity of this hypothesis, we examined pulmonary and neurological inflammatory outcomes in C57BL/6 and apolipoprotein E knockout (ApoE−/−) male mice after acute and chronic exposure to vehicle engine-derived particulate matter, generated as ultrafine (UFP) and fine (FP) sizes, with additional exposures using UFP or FP combined with gaseous copollutants derived from fresh gasoline and diesel emissions, labeled as UFP + G and FP + G.ResultsThe UFP and UFP + G exposure groups resulted in the most profound pulmonary and neuroinflammatory effects. Phagocytosis of UFP + G particles via resident alveolar macrophages was substantial in both mouse strains, particularly after chronic exposure, with concurrent increased proinflammatory cytokine expression of CXCL1 and TNFα in the bronchial lavage fluid. In the acute exposure paradigm, only UFP and UFP + G induced significant changes in pulmonary inflammation and only in the ApoE−/− animals. Similarly, acute exposure to UFP and UFP + G increased the expression of several cytokines in the hippocampus of ApoE−/− mice including Il-1β, IL-6, Tgf-β and Tnf-α and in the hippocampus of C57BL/6 mice including Ccl5, Cxcl1, Il-1β, and Tnf-α. Interestingly, Il-6 and Tgf-β expression were decreased in the C57BL/6 hippocampus after acute exposure. Chronic exposure to UFP + G increased expression of Ccl5, Cxcl1, Il-6, and Tgf-β in the ApoE−/− hippocampus, but this effect was minimal in the C57BL/6 mice, suggesting compensatory mechanisms to manage neuroinflammation in this strain.ConclusionsInflammatory responses the lung and brain were most substantial in ApoE−/− animals exposed to UFP + G, suggesting that the surface area-dependent interaction of gases and particles is an important determinant of toxic responses. As such, freshly generated UFP, in the presence of combustion-derived gas phase pollutants, may be a greater health hazard than would be predicted from PM concentration, alone, lending support for epidemiological findings of adverse neurological outcomes associated with roadway proximity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0177-x) contains supplementary material, which is available to authorized users.
Highlights
Deleterious consequences of exposure to traffic emissions may derive from interactions between carbonaceous particulate matter (PM) and gaseous components in a manner that is dependent on the surface area or complexity of the particles
We developed a complex exposure paradigm that allows for the vapor phase of mixed engine emissions to be combined with carbonaceous PM distinctly in ultrafine particle (UFP) or fine particle (FP) modes, which were used for exposures in a sensitive model of vascular disease, the apolipoprotein E-deficient mouse (ApoE−/−)
PM distribution in the ultrafine range is shown in Fig. 1d–g, with UFP atmospheres exhibiting comparable distributions (UFP mmad = 147.1 ± 1.3 nm; UFP + G mmad = 142.1 ± 1.3 nm), while FP atmospheres were largely devoid of detectable PM in the ultrafine range, despite close matching of the overall mass concentrations
Summary
Deleterious consequences of exposure to traffic emissions may derive from interactions between carbonaceous particulate matter (PM) and gaseous components in a manner that is dependent on the surface area or complexity of the particles. Tyler et al Particle and Fibre Toxicology (2016) 13:64 effectively lower PM emissions from vehicles by filtration, but gaseous components may still be as high or higher. These components can interact with background PM or resuspended road dust during operation. Recent in vivo and in vitro studies have reported exposure to particulate matter induces adverse neurological outcomes, including neuroinflammation assessed by oxidative stress and cytokine production, associated with impaired cognitive function and neuropathology reminiscent of neurodegenerative disorders including AD and Parkinson’s disease [11,12,13,14,15]. Chronic systemic inflammation resulting from cardiovascular disease (CVD) may be associated with an increased risk for developing neuroinflammation potentially leading to neurodegenerative disorders [17]
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