Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 Jun;30(6):2115-22.
doi: 10.1096/fj.201500142. Epub 2016 Feb 18.

Chronic Exposure to Air Pollution Particles Increases the Risk of Obesity and Metabolic Syndrome: Findings From a Natural Experiment in Beijing

Affiliations
Free PMC article

Chronic Exposure to Air Pollution Particles Increases the Risk of Obesity and Metabolic Syndrome: Findings From a Natural Experiment in Beijing

Yongjie Wei et al. FASEB J. .
Free PMC article

Abstract

Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early-life exposure to ambient particles either increases susceptibility to diet-induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non-diet-induced weight increases. In a rodent model, we found that breathing Beijing's highly polluted air resulted in weight gain and cardiorespiratory and metabolic dysfunction. Compared to those exposed to filtered air, pregnant rats exposed to unfiltered Beijing air were significantly heavier at the end of pregnancy. At 8 wk old, the offspring prenatally and postnatally exposed to unfiltered air were significantly heavier than those exposed to filtered air. In both rat dams and their offspring, after continuous exposure to unfiltered air we observed pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissue and systemic oxidative stress, dyslipidemia, and an enhanced proinflammatory status of epididymal fat. Results suggest that TLR2/4-dependent inflammatory activation and lipid oxidation in the lung can spill over systemically, leading to metabolic dysfunction and weight gain.-Wei, Y., Zhang, J., Li, Z., Gow, A., Chung, K. F., Hu, M., Sun, Z., Zeng, L., Zhu, T., Jia, G., Li, X., Duarte, M., Tang, X. Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

Keywords: chronic inflammation; metabolic dysfunction; particulate matter.

Conflict of interest statement

This work was supported in part by grants from the National Natural Science Foundation of China (21190051, 21477119), the Open Fund of the State Key Joint Laboratory of Environment Simulation and Pollution Control (13K03ESPCP), and the China Postdoctoral Science Foundation (201003010).

Figures

Figure 1.
Figure 1.
Pregnant rats exposed to unfiltered Beijing air vs. those exposed to filtered Beijing air. A) Body mass measured from d 0, when rats went into chambers, to d 14 (in first set of experiments) and measured at d 19 (in second set of experiments). Error bars represent ±sd. B) Lung histology (hematoxylin and eosin stain) showing inflammation in alveoli of rat after 19 d exposure to unfiltered air (a), but no apparent inflammation in alveolus of rat after 19 d filtered air exposure (b). Similar histologic evidence for inflammation in bronchus of unfiltered air exposed rat (c) in reference to that of filtered air exposed rat (d). Higher-magnification micrograph indicates that inflammatory cells are mainly mononuclear cells (e). C) Blood biomarkers measured in pregnant rats after 19 d exposure protocol. Significant differences between groups are indicated. *P < 0.05, **P < 0.01.
Figure 2.
Figure 2.
Rats exposed prenatally and continuously for 8 wk to unfiltered Beijing air vs. those exposed to filtered Beijing air. A) Biomarkers of oxidative stress, MDA, and 8-isoprostane, in tissues of lung, liver, spleen, and brain of 8-wk-old male pups. *P < 0.05. B) GeneMania network of up-regulated genes involved in cytokine signaling from lung tissue. Black circles indicate query genes identified as up-regulated between groups by RNA-Seq; gray circles, those connected via prediction or expression network analysis. C) Cytokine/chemokine concentrations in epididymal fat tissue of male rats. *P < 0.05, **P < 0.01, ***P < 0.001.
Figure 3.
Figure 3.
Lung histology (hematoxylin and eosin stain) of 8-wk-old rats, showing inflammation in alveoli of rat exposed to unfiltered air (A) compared to alveoli of rat exposed to filtered air exposure (B). Similar histologic evidence of inflammation in bronchus of unfiltered air exposed rats (C) in reference to that of filtered air exposed rats (D). Higher-magnification micrograph indicates that inflammatory cells are mainly mononuclear cells (E).
Figure 4.
Figure 4.
Mechanistic framework explaining how inhaled air pollutants disrupt metabolic state. Inhalation of air pollutants (especially particulate matter) can lead to direct activation of alveolar macrophages through TLR2/4-dependent mechanisms and generation of oxidized lipids within lung lining. These oxidized lipids can further activate inflammatory processes through TLR2/4 binding or be released to vasculature, where they will initiate systemic inflammation and oxidative stress responses. TLR2/4-dependent inflammatory activation, through activity of MyD88, will lead to release of proinflammatory cytokines, such as CCL-2 and IL-6, from lung, also generating systemic inflammation. These systemic inflammatory activation processes, along with loss of anti-inflammatory functions from incretins such as GLP-1, will lead to increased recruitment of activated inflammatory cells to tissues and in particular adipose. Recruitment of such cells to adipose will worsen metabolic profile, leading to weight gain and metabolic disease state. Prenatal exposure may enhance cellular and functional responses shown here.

Similar articles

See all similar articles

Cited by 34 articles

See all "Cited by" articles

Publication types

LinkOut - more resources

Feedback