| Greater ozone-induced inflammatory responses in subjects with asthma. | |
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MedLine Citation:
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PMID: 8680687 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In order to test the hypothesis that ozone (O3)-induced changes in lung function and respiratory tract injury/inflammation are greater in subjects with asthma than in normal subjects, we exposed 18 asthmatic subjects, on separate days, to O3 (0.2 ppm) and filtered air for 4 h during exercise. Symptom questionnaires were administered before and after exposure, and pulmonary function tests (FEV1, FVC, and specific airway resistance [SRaw]) were performed before, during, and immediately after each exposure. Fiberoptic bronchoscopy, with proximal airway lavage (PAL) of the isolated left main bronchus and bronchoalveolar lavage (BAL; bronchial fraction, the first 10 ml of fluid recovered) of the right middle lobe, was performed 18 h after each exposure. The PAL, bronchial fraction, and BAL fluids were analyzed for the following endpoints: total and differential cell counts; total protein, lactate dehydrogenase (LDH), fibronectin, interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), myeloperoxidase (MPO), and transforming growth factor-beta (TGF beta 2) concentrations. We found a significant O3 effect on FEV1, FVC, SRaw (p < 0.04) and lower respiratory symptoms (p < 0.001) for the asthmatic subjects. Ozone exposure also significantly increased the percent neutrophils in PAL (p < 0.01); percent neutrophils, total protein, and IL-8 in the bronchial fraction (p < 0.001, p < 0.05, and p < 0.01, respectively); and the percent neutrophils, total protein, LDH, fibronectin, IL-8, GM-CSF, and MPO in BAL (p < 0.001, p < 0.01, p < 0.01, p < 0.001, p < 0.05, p < 0.01, and p < 0.001, respectively) for the asthmatic subjects. There were no significant differences in the lung function responses of the asthmatic subjects in comparison with a group of normal subjects (n = 81) previously studied using an identical protocol, although there was a trend toward a greater O3-induced increase in SRaw in the asthmatic subjects (p < 0.13). In contrast, the asthmatic subjects showed significantly greater (p < 0.05) O3-induced increases in several inflammatory endpoints (percent neutrophils and total protein concentration) in BAL as compared with normal subjects who underwent bronchoscopy (n = 20). Our results indicate that asthmatic persons may be at risk of developing more severe O3-induced respiratory tract injury/inflammation than normal persons, and may help explain the increased asthma morbidity associated with O3 pollution episodes observed in epidemiologic studies. |
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Authors:
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C Scannell; L Chen; R M Aris; I Tager; D Christian; R Ferrando; B Welch; T Kelly; J R Balmes |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: American journal of respiratory and critical care medicine Volume: 154 ISSN: 1073-449X ISO Abbreviation: Am. J. Respir. Crit. Care Med. Publication Date: 1996 Jul |
Date Detail:
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Created Date: 1996-08-19 Completed Date: 1996-08-19 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9421642 Medline TA: Am J Respir Crit Care Med Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 24-9 Citation Subset: AIM; IM |
Affiliation:
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Lung Biology Center, San Francisco General Hospital, University of California 94143-0854, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Air Pollutants / adverse effects* Airway Resistance / drug effects Asthma / pathology*, physiopathology Biopsy, Needle Bronchoalveolar Lavage Fluid / chemistry, cytology Bronchoscopy Cell Count Female Forced Expiratory Volume / drug effects Humans Inflammation / chemically induced, pathology Lung / pathology Male Ozone / adverse effects* Vital Capacity / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Air Pollutants; 10028-15-6/Ozone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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