| Lung function and inflammatory responses in healthy young adults exposed to 0.06 ppm ozone for 6.6 hours. | |
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MedLine Citation:
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PMID: 21216881 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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RATIONALE: Exposure to ozone causes a decrease in spirometric lung function and an increase in airway inflammation in healthy young adults at concentrations as low as 0.08 ppm, close to the National Ambient Air Quality Standard for ground level ozone. OBJECTIVES: To test whether airway effects occur below the current ozone standard and if they are more pronounced in potentially susceptible individuals, such as those deficient in the antioxidant gene glutathione S-transferase mu 1 (GSTM1). METHODS: Pulmonary function and subjective symptoms were measured in 59 healthy young adults (19-35 yr) immediately before and after exposure to 0.0 (clean air, CA) and 0.06 ppm ozone for 6.6 hours in a chamber while undergoing intermittent moderate exercise. The polymorphonuclear neutrophil (PMN) influx was measured in 24 subjects 16 to 18 hours postexposure. MEASUREMENTS AND MAIN RESULTS: Subjects experienced a significantly greater (P = 0.008) change in FEV(1) (± SE) immediately after exposure to 0.06 ppm ozone compared with CA (-1.71 ± 0.50% vs. -0.002 ± 0.46%). The decrement in FVC was also greater (P = 0.02) after ozone versus CA (-2.32 ± 0.41% vs. -1.13 ± 0.34%). Similarly, changes in %PMN were greater after ozone (54.0 ± 4.6%) than CA (38.3 ± 3.7%) exposure (P < 0.001). Symptom scores were not different between ozone versus CA. There were no significant differences in changes in FEV(1), FVC, and %PMN between subjects with GSTM1-positive and GSTM1-null genotypes. CONCLUSIONS: Exposure of healthy young adults to 0.06 ppm ozone for 6.6 hours causes a significant decrement of FEV(1) and an increase in neutrophilic inflammation in the airways. GSTM1 genotype alone appears to have no significant role in modifying the effects. |
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Authors:
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Chong S Kim; Neil E Alexis; Ana G Rappold; Howard Kehrl; Milan J Hazucha; John C Lay; Mike T Schmitt; Martin Case; Robert B Devlin; David B Peden; David Diaz-Sanchez |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-01-07 |
Journal Detail:
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Title: American journal of respiratory and critical care medicine Volume: 183 ISSN: 1535-4970 ISO Abbreviation: Am. J. Respir. Crit. Care Med. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-02 Completed Date: 2011-07-11 Revised Date: 2012-05-01 |
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: 1215-21 Citation Subset: AIM; IM |
Affiliation:
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Environmental Public Health Division (MD-58B), National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. kim.chong@epa.gov |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Air Pollutants / toxicity* Exercise Female Forced Expiratory Volume / drug effects Glutathione Transferase / drug effects Humans Inflammation / physiopathology* Inhalation Exposure* Lung / drug effects*, physiopathology* Male Neutrophils / drug effects Ozone / toxicity* Reference Values Respiratory Function Tests / methods Reverse Transcriptase Polymerase Chain Reaction Spirometry Time Factors Vital Capacity / drug effects Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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R01 ES012706-05/ES/NIEHS NIH HHS; R01ES012706/ES/NIEHS NIH HHS; RC1 ES018417-02/ES/NIEHS NIH HHS; RC1ES018417/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Air Pollutants; 10028-15-6/Ozone; EC 2.5.1.18/Glutathione Transferase; EC 2.5.1.18/glutathione S-transferase M1 |
| Comments/Corrections | |
Comment In:
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Am J Respir Crit Care Med. 2011 Dec 15;184(12):1421-2
[PMID:
22174117
]
Am J Respir Crit Care Med. 2011 Jul 15;184(2):150-1 [PMID: 21765027 ] |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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