Acute Ozone (O3) Exposure Enhances Aortic Contraction in Healthy Rats while Exacerbating Pulmonary Injury in Diabetics

Air pollution exposure affects health adversely in individuals with type 2 diabetes (T2D) and diet induced obesity (DIO). We hypothesized that T2D and DIO would exacerbate O3 induced pulmonary responses and alter arterial reactivity. Male Wistar and Goto Kakizaki (GK) rats, a lean T2D Wistar derived model, were fed a normal or high cholesterol diet (HCD) for 12 wks starting at 4 wks of age. After the 12 wk diet, rats were exposed to filtered air or 1 ppm O3, 6h/d for 1 or 2 days. Wistars had greater body weights with lower body fat percentages than GKs. HCD induced DIO in both strains as evidenced by increased body weight and body fat percentages. Biomarkers of lung injury including protein, albumin, lactate dehydrogenase and N-acetyl glucosaminidase increased after O3 exposure in both strains. These levels were not altered by DIO but were exacerbated in GKs despite a smaller exposure due to a lower minute volume. Aortic segments were isolated for myographic assessment of vascular reactivity in response to pharmacological intervention after the 2 day O3 exposure. Phenylephrine and KCl increased aortic contractile force in the O3 exposed Wistars, but this response was not found in the T2D or DIO models. Aortas isolated from Wistars had decreased vasorelaxation in response to acetylcholine (ACh) regardless of diet or exposure. L-NAME did not fully block ACh induced vasorelaxation in the GKs, suggesting nitric oxide independent pathways may be involved in vasorelaxation responses. These data indicate that O3 exposure may induce arterial dysfunction in healthy individuals and augment lung injury in diabetics. (This abstract does not reflect US EPA Policy; Research supported by ORISE)