Ultrafine particulate matter combined with ozone exacerbates lung injury in mature adult rats with cardiovascular disease
- Author(s): Wong, EM
- Walby, WF
- Wilson, DW
- Tablin, F
- Schelegle, ES
- et al.
Published Web Locationhttps://doi.org/10.1093/toxsci/kfy018
© The Author(s) 2018. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (~ 250 lg/m3); O3(1.0 ppm); or UFPM+O3 (~ 250 lg/m3+1.0 ppm) combined for 6 h, followed by an 8h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.
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