Document Detail

Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles.
MedLine Citation:
PMID:  15204794     Owner:  NLM     Status:  MEDLINE    
Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 microm in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis. We hypothesized that ultrafine particle exposure would induce airway inflammation in susceptible humans. This hypothesis was tested in a series of randomized, double-blind studies by exposing healthy subjects and mild asthmatic subjects to carbon ultrafine particles versus filtered air. Both exposures were delivered via a mouthpiece system during rest and moderate exercise. Healthy subjects were exposed to particle concentrations of 10, 25, and 50 microg/m(3), while asthmatics were exposed to 10 microg/m(3). Lung function and airway inflammation were assessed by symptom scores, pulmonary function tests, and airway nitric oxide parameters. Airway inflammatory cells were measured via induced sputum analysis in several of the protocols. There were no differences in any of these measurements in normal or asthmatic subjects when exposed to ultrafine particles at concentrations of 10 or 25 microg/m(3). However, exposing 16 normal subjects to the higher concentration of 50 microg/m(3) caused a reduction in maximal midexpiratory flow rate (-4.34 +/- 1.78% [ultrafine particles] vs. +1.08 +/- 1.86% [air], p =.042) and carbon monoxide diffusing capacity (-1.76 +/- 0.66 ml/min/mm Hg [ultrafine particles] vs. -0.18 +/- 0.41 ml/min/mm Hg [air], p =.040) at 21 h after exposure. There were no consistent differences in symptoms, induced sputum, or exhaled nitric oxide parameters in any of these studies. These results suggest that exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation. Additional studies are required to confirm these findings in normal subjects, compare them with additional susceptible patient populations, and determine their pathophysiologic mechanisms.
Anthony P Pietropaoli; Mark W Frampton; Richard W Hyde; Paul E Morrow; Günter Oberdörster; Christopher Cox; Donna M Speers; Lauren M Frasier; David C Chalupa; Li-Shan Huang; Mark J Utell
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Inhalation toxicology     Volume:  16 Suppl 1     ISSN:  0895-8378     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2004  
Date Detail:
Created Date:  2004-06-18     Completed Date:  2004-10-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  59-72     Citation Subset:  IM    
Department of Medicine, University of Rochester School of Medicine and Dentistry, New York 14642, USA.
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MeSH Terms
Asthma / etiology*,  immunology*
Breath Tests
Carbon / toxicity*
Case-Control Studies
Inhalation Exposure*
Leukocyte Count
Nitric Oxide / analysis,  biosynthesis
Particle Size
Pulmonary Diffusing Capacity
Respiratory Function Tests
Respiratory System / immunology,  pathology
Sputum / cytology,  immunology
Grant Support
Reg. No./Substance:
10102-43-9/Nitric Oxide; 7440-44-0/Carbon

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