Effect of Early Particulate Air Pollution Exposure on Obesity in Mice

Abstract

Objective To evaluate the role of early-life exposure to airborne fine particulate matter (diameter, <2.5 µm [PM2.5]) pollution on metabolic parameters, inflammation, and adiposity; and to investigate the involvement of oxidative stress pathways in the development of metabolic abnormalities. Methods and Results PM2.5 inhalation exposure (6 h/d, 5 d/wk) was performed in C57BL/6 mice (wild type) and mice deficient in the cytosolic subunit of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p47phox (p47phox−/−) beginning at the age of 3 weeks for a duration of 10 weeks. Both groups were simultaneously fed a normal diet or a high-fat diet for 10 weeks. PM2.5-exposed C57BL/6 mice fed a normal diet exhibited metabolic abnormalities after exposure to PM2.5 or FA for 10 weeks. Consistent with insulin resistance, these abnormalities included enlarged subcutaneous and visceral fat contents, increased macrophage infiltration in visceral adipose tissue, and vascular dysfunction. Ex vivo–labeled and infused monocytes demonstrated increased adherence in the microcirculation of normal diet– or high-fat diet–fed PM2.5-exposed mice. p47phox−/− mice exhibited an improvement in parameters of insulin resistance, vascular function, and visceral inflammation in response to PM2.5. Conclusion Early-life exposure to high levels of PM2.5 is a risk factor for subsequent development of insulin resistance, adiposity, and inflammation. Reactive oxygen species generation by NADPH oxidase appears to mediate this risk.

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