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Background  Inflammation and oxidative stress play critical roles in the pathogenesis of inhaled air pollutant-mediated metabolic disease. Inflammation in the adipose tissues niches are widely believed to exert important effects on organ dysfunction. Recent data from both human and animal models suggest a role for inflammation and oxidative stress in epicardial adipose tissue (EAT) as a risk factor for the development of cardiovascular disease. We hypothesized that inhalational exposure to concentrated ambient fine particulates (CAPs) and ozone (O 3 ) exaggerates inflammation and oxidative stress in EAT and perirenal adipose tissue (PAT).    Methods  Eight- week-old Male Sprague–Dawley rats were fed a normal diet (ND) or high fructose diet (HFr) for 8 weeks, and then exposed to ambient AIR, CAPs at a mean of 356 μg/m 3 , O 3  at 0.485 ppm, or CAPs (441 μg/m 3 ) + O 3  (0.497 ppm) in Dearborn, MI, 8 hours/day, 5 days/week, for 9 days over 2 weeks.    Results  EAT and PAT showed whitish color in gross, and less mitochondria, higher mRNA expression of white adipose specific and lower brown adipose specific genes than in brown adipose tissues. Exposure to CAPs and O 3  resulted in the increase of macrophage infiltration in both EAT and PAT of HFr groups. Proinflammatory genes of  Tnf-α, Mcp-1  and  leptin  were significantly upregulated while  IL-10  and  adiponectin , known as antiinflammatory genes, were reduced after the exposures. CAPs and O 3  exposures also induced an increase in inducible nitric oxide synthase (iNOS) protein expression, and decrease in mitochondrial area in EAT and PAT. We also found significant increases in macrophages of HFr-O 3  rats. The synergetic interaction of HFr and dirty air exposure on the inflammation was found in most of the experiments. Surprisingly, exposure to CAPs or O 3  induced more significant inflammation and oxidative stress than co-exposure of CAPs and O 3  in EAT and PAT.    Conclusion  EAT and PAT are both white adipose tissues. Short-term exposure to CAPs and O 3 , especially with high fructose diet, induced inflammation and oxidative stress in EAT and PAT in rats. These findings may provide a link between air-pollution exposure and accelerated susceptibility to cardiovascular disease and metabolic complications.

Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet