Document Detail


Source apportionment of particulate matter in the U.S. and associations with lung inflammatory markers.
MedLine Citation:
PMID:  18464055     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Size-fractionated particulate matter (PM) samples were collected from six U.S. cities and chemically analyzed as part of the Multiple Air Pollutant Study. Particles were administered to cultured lung cells and the production of three different proinflammatory markers was measured to explore the association between the health effect markers and PM. Ultrafine, fine, and coarse PM samples were collected between December 2003 and May 2004 over a 4-wk period in each city. Filters were pooled for each city and the PM samples were extracted then analyzed for trace metals, ions, and elemental carbon. Particle extracts were applied to cultured human primary airway epithelial cells, and the secreted levels of interleukin-8 (IL-8), heme oxygenase-1, and cyclooxygenase-2 were measured 1 and 24 h following exposure. Fine PM sources were quantified by the chemical mass balance (CMB) model. The relationship between toxicological measures, PM sources, and individual species were evaluated using linear regression. Ultrafine and fine PM mass were associated with increases in IL-8 (r(2) = .80 for ultrafine and r(2) = .52 for fine). Sources of fine PM and their relative contributions varied across the sampling sites and a strong linear association was observed between IL-8 and secondary sulfate from coal combustion (r(2) = .79). Ultrafine vanadium, lead, copper, and sulfate were also associated with increases in IL-8. Increases in inflammatory markers were not observed for coarse PM mass and source markers. These findings suggest that certain PM size fractions and sources are associated with markers of lung injury or inflammation.
Authors:
Rachelle M Duvall; Gary A Norris; Lisa A Dailey; Janet M Burke; John K McGee; M Ian Gilmour; Terry Gordon; Robert B Devlin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Inhalation toxicology     Volume:  20     ISSN:  1091-7691     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-05-08     Completed Date:  2008-08-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  671-83     Citation Subset:  IM    
Affiliation:
National Exposure Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. duvall.rachelle@epa.gov
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MeSH Terms
Descriptor/Qualifier:
Air Pollutants / analysis,  toxicity*
Biological Markers / metabolism
Cells, Cultured
Cities
Cyclooxygenase 2 / genetics*
Epithelial Cells / drug effects*,  metabolism
Heme Oxygenase-1 / genetics*
Humans
Inflammation / metabolism
Interleukin-8 / genetics*
Lung / cytology
Metals / analysis,  toxicity
Nitrates / analysis,  toxicity
Particle Size
Particulate Matter / analysis,  toxicity*
RNA, Messenger / metabolism
Sulfates / analysis,  toxicity
United States
Grant Support
ID/Acronym/Agency:
ES000260/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Air Pollutants; 0/Biological Markers; 0/Interleukin-8; 0/Metals; 0/Nitrates; 0/Particulate Matter; 0/RNA, Messenger; 0/Sulfates; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.3/Heme Oxygenase-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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