Background— There is a strong link between urbanization and type 2 diabetes mellitus. Although a multitude of mechanisms have been proposed, there are no studies evaluating the impact of ambient air pollutants and the propensity to develop type 2 diabetes mellitus. We hypothesized that exposure to ambient fine particulate matter (<2.5 μm; PM _2.5 ) exaggerates diet-induced insulin resistance, adipose inflammation, and visceral adiposity. Methods and Results— Male C57BL/6 mice were fed high-fat chow for 10 weeks and randomly assigned to concentrated ambient PM _2.5 or filtered air (n=14 per group) for 24 weeks. PM _2.5 -exposed C57BL/6 mice exhibited marked whole-body insulin resistance, systemic inflammation, and an increase in visceral adiposity. PM _2.5 exposure induced signaling abnormalities characteristic of insulin resistance, including decreased Akt and endothelial nitric oxide synthase phosphorylation in the endothelium and increased protein kinase C expression. These abnormalilties were associated with abnormalities in vascular relaxation to insulin and acetylcholine. PM _2.5 increased adipose tissue macrophages (F4/80 ⁺ cells) in visceral fat expressing higher levels of tumor necrosis factor-α/interleukin-6 and lower interleukin-10/ N -acetyl-galactosamine specific lectin 1. To test the impact of PM _2.5 in eliciting direct monocyte infiltration into fat, we rendered FVBN mice expressing yellow fluorescent protein (YFP) under control of a monocyte-specific promoter (c- fms , c- fms ^YFP ) diabetic over 10 weeks and then exposed these mice to PM _2.5 or saline intratracheally. PM _2.5 induced YFP cell accumulation in visceral fat and potentiated YFP cell adhesion in the microcirculation. Conclusion— PM _2.5 exposure exaggerates insulin resistance and visceral inflammation/adiposity. These findings provide a new link between air pollution and type 2 diabetes mellitus.

T2-Weighted (T2W) magnetic resonance imaging (MRI) pulse sequences have been used to detect edema in patients with acute myocardial infarction and differentiate acute from chronic infarction. T2W sequences have suffered from several problems including (i) signal intensity variability caused by phased array coils, (ii) high signal from slow moving ventricular chamber blood that can mimic and mask elevated T2 in sub-endocardial myocardium, (iii) motion artifacts, and (iv) the subjective nature of T2W image interpretation. In this work we demonstrate the advantages of a quantitative T2 mapping technique to accurately and reliably detect regions of edematous myocardial tissue without the limitations of qualitative T2W imaging.

Ambient air pollution is a leading environmental cause of morbidity and mortality globally with most of the outcomes of cardiovascular origin. While numerous mechanisms are proposed to explain the link between air pollutants and cardiovascular events, the evidence supports a role for oxidative stress as a critical intermediary pathway in the transduction of systemic responses in the cardiovascular system. Indeed, alterations in vascular function are a critical step in the development of cardiometabolic disorders such as hypertension, diabetes, and atherosclerosis. This review will provide an overview of the impact of particulate and gaseous pollutants on oxidative stress from human and animal studies published in the last five years. We discuss current gaps in knowledge and evidence to date implicating the role of oxidative stress with an emphasis on inhalational exposures. We conclude with the identification of gaps, and an exhortation for further studies to elucidate the impact of oxidative stress in air pollution mediated effects.