INTRODUCTION: Chronic smoking related changes in pulmonary function are reflected as accelerated decrease in FEV1 although histologic changes occur in the peripheral bronchi earlier. More sensitive pulmonary function parameters might mirror those early changes and might show a dose response. METHODS: In a randomized three-period cross-over design 57 male adult conventional cigarette (CC)-smokers (age: 45.1+/-7.1 years) smoked eitherCC (tar:11 mg, nicotine:0.8 mg, carbon monoxide:11 mg [Federal Trade Commission (FTC)]), or used as a potential reduced-exposure product the electrically heated smoking system (EHCSS) (tar:5 mg, nicotine:0.3 mg, carbon monoxide:0.45 mg (FTC)) or did not smoke (NS). After each 3-day exposure period, hematology and exposure parameters were determined preceding body plethysmography. RESULTS:Cigarette smoke exposure was significantly (p<0.0001) higher in CC than in EHCSS and in NS: (carboxyhemoglobin: CC: 6.4+/-1.9%; EHCSS: 1.3+/-0.6%; NS: 0.5+/-0.3%; serum nicotine: CC: 18.9+/-7.4 ng/ml; EHCSS: 8.4+/-4.3 ng/ml; NS: 1.2+/-1.6 ng/ml). Significantly lower in CC than in EHCSS and NS were specific airway conductance (0.22+/-0.09; 0.25+/-0.12; 0.25+/-0.1 1/cmH(2)O x s; CC vs EHCSS: p<0.05; CC vs NS: p<0.01), forced expiratory flow 25% (7.6+/-1.7; 7.8+/-1.7; 7.9+/-1.7 L/s; CC vs EHCSS or NS: p<0.01). Thoracic gas volume (5.1+/-1; 5+/-1.1; 5+/-1.1L/min) changed insignificantly. CONCLUSION: The data indicate acute and reversible effects of cigarette smoke exposures and no-smoking on mid to small size pulmonary airways in a dose dependent manner. Copyright 2010 Elsevier Inc. All rights reserved.
RCT Entities:
INTRODUCTION: Chronic smoking related changes in pulmonary function are reflected as accelerated decrease in FEV1 although histologic changes occur in the peripheral bronchi earlier. More sensitive pulmonary function parameters might mirror those early changes and might show a dose response. METHODS: In a randomized three-period cross-over design 57 male adult conventional cigarette (CC)-smokers (age: 45.1+/-7.1 years) smoked either CC (tar:11 mg, nicotine:0.8 mg, carbon monoxide:11 mg [Federal Trade Commission (FTC)]), or used as a potential reduced-exposure product the electrically heated smoking system (EHCSS) (tar:5 mg, nicotine:0.3 mg, carbon monoxide:0.45 mg (FTC)) or did not smoke (NS). After each 3-day exposure period, hematology and exposure parameters were determined preceding body plethysmography. RESULTS: Cigarette smoke exposure was significantly (p<0.0001) higher in CC than in EHCSS and in NS: (carboxyhemoglobin: CC: 6.4+/-1.9%; EHCSS: 1.3+/-0.6%; NS: 0.5+/-0.3%; serum nicotine: CC: 18.9+/-7.4 ng/ml; EHCSS: 8.4+/-4.3 ng/ml; NS: 1.2+/-1.6 ng/ml). Significantly lower in CC than in EHCSS and NS were specific airway conductance (0.22+/-0.09; 0.25+/-0.12; 0.25+/-0.1 1/cmH(2)O x s; CC vs EHCSS: p<0.05; CC vs NS: p<0.01), forced expiratory flow 25% (7.6+/-1.7; 7.8+/-1.7; 7.9+/-1.7 L/s; CC vs EHCSS or NS: p<0.01). Thoracic gas volume (5.1+/-1; 5+/-1.1; 5+/-1.1L/min) changed insignificantly. CONCLUSION: The data indicate acute and reversible effects of cigarette smoke exposures and no-smoking on mid to small size pulmonary airways in a dose dependent manner. Copyright 2010 Elsevier Inc. All rights reserved.
Authors: Christelle Haziza; Guillaume de La Bourdonnaye; Andrea Donelli; Dimitra Skiada; Valerie Poux; Rolf Weitkunat; Gizelle Baker; Patrick Picavet; Frank Lüdicke Journal: Nicotine Tob Res Date: 2020-04-17 Impact factor: 4.244
Authors: Marco Ferrari; Alessandro Zanasi; Elena Nardi; Antonio Maria Morselli Labate; Piero Ceriana; Antonella Balestrino; Lara Pisani; Nadia Corcione; Stefano Nava Journal: BMC Pulm Med Date: 2015-10-12 Impact factor: 3.317