Ambient Air Pollution and Type 2 Diabetes: Do the Metabolic Effects of Air Pollution Start Early in Life?

Abstract

The adverse health effects of ambient (outdoor) air pollution have been recognized since increased mortality due to smog was reported in London in 1952 (1). Suspended particles (particulate matters) from soot were associated with increased mortality and morbidity related to both respiratory and cardiovascular disorders (1). Since then, great efforts have been made to control ambient air pollution on a national level. For example, the Clean Air Act in the U.S. resulted in improvements in ambient air quality. Between 1990 and 2015, annual concentrations of particulate matter <10 µm in aerodynamic diameter (PM10) dropped by 39% in the U.S. (2). Nonetheless, ambient air pollution is still one of the leading causes of global disease burden (3,4). In fact, the World Health Organization has estimated that ambient air pollution is responsible for more than 3 million deaths, representing 5.4% of total deaths in 2012 (5). Recently, scientific communities have suggested that ambient air pollution may increase the risk of type 2 diabetes. Animal models have provided convincing evidence and suggested potential mechanisms including particle-mediated alterations in glucose homeostasis, inflammation in visceral adipose tissue, endoplasmic reticulum stress in liver and lung, mitochondrial dysfunction and brown adipose tissue dysfunction, inflammation mediated through Toll-like receptors and nucleotide-binding oligomerization domain-like receptors, and inflammatory signaling in key regions of the hypothalamus (6). Although the evidence is still limited, epidemiological studies have also supported the hypothesis that ambient air pollution exposure is associated with elevated risk for type …