Experimental setup and analytical methods for the non-invasive determination of volatile organic compounds, formaldehyde and NOx in exhaled human breath

2010 ◽  
Vol 669 (1-2) ◽  
pp. 53-62 ◽  
Author(s):  
Ulrich Riess ◽  
Uwe Tegtbur ◽  
Christian Fauck ◽  
Frank Fuhrmann ◽  
Doreen Markewitz ◽  
...  
2011 ◽  
Vol 25 (3) ◽  
pp. 391-397 ◽  
Author(s):  
Agnieszka Ulanowska ◽  
Tomasz Kowalkowski ◽  
Katarzyna Hrynkiewicz ◽  
Marek Jackowski ◽  
Bogusław Buszewski

1992 ◽  
Vol 26 (10) ◽  
pp. 1932-1938 ◽  
Author(s):  
Alan D. Hewitt ◽  
Paul H. Miyares ◽  
Daniel C. Leggett ◽  
Thomas F. Jenkins

2022 ◽  
Author(s):  
Dapeng Chen ◽  
Noella A. Bryden ◽  
Wayne A. Bryden ◽  
Michael McLoughlin ◽  
Dexter Smith ◽  
...  

Abstract Human breath contains trace amounts of non-volatile organic compounds (NOCs) which might inform non-invasive methods for evaluation of individual health. In previous work, we demonstrated that lipids detected in exhaled breath aerosol (EBA) could be used as markers of active tuberculosis (TB). Here, we advanced our analytical platform in characterizing small metabolites and lipids in EBA samples collected from participants enrolled in clinical trials designed to identify molecular signatures of active TB. EBA samples from 26 participants with active TB and 73 healthy participants were processed using a dual-phase extraction method, and metabolites and lipids were identified via mass spectrometry (MS) database matching. In total, 13 metabolite and 9 lipid markers were identified with optimized relative standard deviation values that were statistically different between individuals diagnosed with active TB and the healthy controls. A feature ranking algorithm reduced this number to 10 molecules, with the membrane glycerophospholipid, phosphatidylinositol 24:4, emerging as top driver of segregation between the two groups. These results support the utility of this approach to identify consistent NOC signatures from EBA samples in active TB cases and suggest the potential to apply this method to other human diseases which alter respiratory NOC release.


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