Air Pollution and Insulin Resistance: Do All Roads Lead to Rome?

The World Health Organization estimates that worldwide in 2012, nearly 7 million deaths occurred prematurely due to air pollution (1). In addition to respiratory and cardiovascular diseases, air pollution exposure is also linked to increased incidence of diabetes (2). Notably, the prevalence of diabetes and dyslipidemia escalated exponentially in the latter half of the 20th century coincident with the manufacture, use, and release of massive amounts of chemicals and pollution. The increase in the prevalence of these chronic conditions also coincides with an increase in sedentary lifestyles, calorie-rich diets, and human stress. Together, these factors contribute to metabolic disease. This complex tapestry suggests that many elements, including air pollution, are likely involved in an interactive manner to increase the risk of certain health conditions. Determining how air pollution might be linked to diabetes is useful not only in understanding how environmental factors contribute to the pathogenesis of this disease but also for identifying molecular targets for potential therapeutic strategies. Improved understanding of this dynamic also provides further rationale for improving air quality standards and public health. Ozone is produced in the air by photochemical reaction of components of anthropogenic emissions, and it contributes substantially to the societal burden of respiratory and cardiovascular disease. The pulmonary effects of ozone have been studied for decades (3), with recent attention turning to the metabolic and cardiovascular effects of this exposure. A number of mechanisms have been proposed for extrapulmonary effects of inhaled pollutants. On the basis of experimental studies examining the metabolic effects of ambient particulate matter (chemically complex mixtures consisting of many components) in mouse models, Rajagopalan and Brook (4) proposed that systemic inflammation, oxidative stress, and neuronal mechanisms might be involved in adipose inflammation and tissue insulin resistance. In this issue of Diabetes , Vella et al. …