STUDY OBJECTIVE: To characterize the pulmonary response of asthmatic and healthy nonsmoking adult men to 0.20 ppm ozone by controlled chamber exposure. DESIGN: A prospective, crossover study of five atopic asthmatic and five normal subjects randomly exposed toozone and filtered purified air (FPA) for 6 h, consisting of 30-min alternating periods of rest and moderate exercise. The two exposures were separated by at least 30 days. SETTING: A controlled exposure in a stainless steel chamber. PATIENTS: Five atopic asthmatic and five normal subjects between 18 and 45 years of age. Treatment with medications was withheld from asthmatics prior to the exposures. All subjects were nonsmokers. INTERVENTIONS: Symptoms were assessed throughout the exposures. Pulmonary function was measured at baseline, hourly throughout an exposure, and after an exposure. Bronchoalveolar lavage (BAL) was performed 18 h after the completion of an exposure. The BAL fluid (BALF) was analyzed for cell count and differential; the cell-free supernatant was analyzed for albumin, tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), and interleukin 8 (IL-8). RESULTS: There were statistically significant increases in IL-8 levels, as well as percent polymorphonuclear neutrophils (PMNs) and PMNs per milliliter of lavage in asthmatics exposed to ozone as compared with the same asthmatics exposed to FPA and the same normal subjects exposed to ozone and FPA. Interleukin 6 was also significantly increased in asthmatics exposed to ozone. The BALF albumin, TNF, and IL-1 levels were not significantly different among the four groups. There were no differences between asthmatics and healthy controls exposed to ozone or FPA in baseline to postexposure FEV1, FVC, FEV1/FVC, and sRaw. CONCLUSIONS: We conclude that asthmatics exposed to ozone develop a significant BALF neutrophilia and increased levels of the cytokines, IL-8 and IL-6. These BALF findings occur even though the level of ozone exposure was not significant enough to reduce pulmonary function.
RCT Entities:
STUDY OBJECTIVE: To characterize the pulmonary response of asthmatic and healthy nonsmoking adult men to 0.20 ppm ozone by controlled chamber exposure. DESIGN: A prospective, crossover study of five atopic asthmatic and five normal subjects randomly exposed to ozone and filtered purified air (FPA) for 6 h, consisting of 30-min alternating periods of rest and moderate exercise. The two exposures were separated by at least 30 days. SETTING: A controlled exposure in a stainless steel chamber. PATIENTS: Five atopic asthmatic and five normal subjects between 18 and 45 years of age. Treatment with medications was withheld from asthmatics prior to the exposures. All subjects were nonsmokers. INTERVENTIONS: Symptoms were assessed throughout the exposures. Pulmonary function was measured at baseline, hourly throughout an exposure, and after an exposure. Bronchoalveolar lavage (BAL) was performed 18 h after the completion of an exposure. The BAL fluid (BALF) was analyzed for cell count and differential; the cell-free supernatant was analyzed for albumin, tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), and interleukin 8 (IL-8). RESULTS: There were statistically significant increases in IL-8 levels, as well as percent polymorphonuclear neutrophils (PMNs) and PMNs per milliliter of lavage in asthmatics exposed to ozone as compared with the same asthmatics exposed to FPA and the same normal subjects exposed to ozone and FPA. Interleukin 6 was also significantly increased in asthmatics exposed to ozone. The BALF albumin, TNF, and IL-1 levels were not significantly different among the four groups. There were no differences between asthmatics and healthy controls exposed to ozone or FPA in baseline to postexposure FEV1, FVC, FEV1/FVC, and sRaw. CONCLUSIONS: We conclude that asthmatics exposed to ozone develop a significant BALF neutrophilia and increased levels of the cytokines, IL-8 and IL-6. These BALF findings occur even though the level of ozone exposure was not significant enough to reduce pulmonary function.
Authors: Mehrdad Arjomandi; Allyson Witten; Emilio Abbritti; Kurt Reintjes; Isabelle Schmidlin; Wenwu Zhai; Colin Solomon; John Balmes Journal: Am J Respir Crit Care Med Date: 2005-06-03 Impact factor: 21.405
Authors: Katherine K Nishimura; Kensho Iwanaga; Sam S Oh; Maria Pino-Yanes; Celeste Eng; Anjeni Keswani; Lindsey A Roth; Elizabeth A Nguyen; Shannon M Thyne; Harold J Farber; Denise Serebrisky; Kelley Meade; Michael A LeNoir; William Rodriguez-Cintron; Luisa N Borrell; Kirsten Bibbins-Domingo; Fred Lurmann; Śaunak Sen; Jose R Rodriguez-Santana; Emerita Brigino-Buenaventura; Pedro C Avila; John R Balmes; Rajesh Kumar; Esteban G Burchard Journal: J Allergy Clin Immunol Date: 2016-06-11 Impact factor: 10.793
Authors: Barbara Vagaggini; Maria Laura E Bartoli; Silvana Cianchetti; Francesco Costa; Elena Bacci; Federico L Dente; Antonella Di Franco; Laura Malagrinò; Pierluigi Paggiaro Journal: Respir Res Date: 2010-01-19