Prolonged, Physiologically Relevant Nicotine Concentrations in the Airways of Smokers
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2023/01/01
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Details
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Personal Author:Alexis NE ; Barjaktarevic I ; Boucher RC ; Bowler RP ; Comellas AP ; Cooper CB ; Curtis JL ; Esther CR Jr. ; Halper-Stromberg E ; Hastie AT ; Koch AL ; O'Neal WK ; Ortega VE ; Peters SP ; Raffield LM ; Rennard SI ; Ronish B ; Wells JM
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Description:Nicotine from cigarette smoke is a biologically active molecule that has pleiotropic effects in the airway, which could play a role in smoking-induced lung disease. However, whether nicotine and its metabolites reach sustained, physiologically relevant concentrations on airway surfaces of smokers is not well defined. To address these issues, concentrations of nicotine, cotinine, and hydroxycotinine were measured by mass spectrometry (MS) in supernatants of induced sputum obtained from participants in the subpopulations and intermediate outcome measures in COPD study (SPIROMICS), an ongoing observational study that included never smokers, former smokers, and current smokers with and without chronic obstructive pulmonary disease (COPD). A total of 980 sputum supernatants were analyzed from 77 healthy never smokers, 494 former smokers (233 with COPD), and 396 active smokers (151 with COPD). Sputum nicotine, cotinine, and hydroxycotinine concentrations corresponded to self-reported smoking status and were strongly correlated to urine measures. A cutoff of approx. 8-10 ng/mL of sputum cotinine distinguished never smokers from active smokers. Accounting for sample dilution during processing, active smokers had airway nicotine concentrations in the 70-850 ng/mL (approx. 0.5-5 µM) range, and concentrations remained elevated even in current smokers who had not smoked within 24 h. This study demonstrates that airway nicotine and its metabolites are readily measured in sputum supernatants and can serve as biological markers of smoke exposure. In current smokers, nicotine is present at physiologically relevant concentrations for prolonged periods, supporting a contribution to cigarette-induced airway disease. [Description provided by NIOSH]
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ISSN:1040-0605
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Place as Subject:Alabama ; Arizona ; California ; Colorado ; Iowa ; Maryland ; Michigan ; Nebraska ; North Carolina ; OSHA Region 10 ; OSHA Region 3 ; OSHA Region 4 ; OSHA Region 5 ; OSHA Region 7 ; OSHA Region 8 ; OSHA Region 9 ; Washington
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Volume:324
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Issue:1
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NIOSHTIC Number:nn:20067127
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Citation:Am J Physiol Lung Cell Mol Physiol 2023 Jan; 324(1):L32-L37
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Contact Point Address:Charles R. Esther Jr., Marsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
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Email:Charles_Esther@med.unc.edu
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CAS Registry Number:
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Federal Fiscal Year:2023
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Performing Organization:University of Washington
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Peer Reviewed:True
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Start Date:20050701
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Source Full Name:American Journal of Physiology: Lung Cellular and Molecular Physiology
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End Date:20250630
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Main Document Checksum:urn:sha-512:38795aaa7f51a721239d8c62ac5984cbb1fc2b0dedb7851d3b991f45acc42ed08a43577abcb1b70b9b9aaded6dc6b7a301bab31b7b4937ea8210aeb9dbe6305a
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