ATS 2021 will feature presentations of original research from accepted abstracts. Mini Symposia and Thematic Poster Sessions are abstract based sessions.
Please use the form below to browse scientific abstracts and case reports accepted for ATS 2021. Abstracts presented at the ATS 2021 will be published in the Online Abstract Issue of the American Journal of Respiratory and Critical Care Medicine, Volume 203, May 3, 2021.
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Effect of Diesel Exhaust on Exercise Endurance and Cardiorespiratory Responses to Exercise in Chronic Obstructive Pulmonary Disease and Healthy Controls - A Randomized, Placebo Controlled, Crossover Study
Session Title
A12 - A012 NEW INSIGHTS INTO STRUCTURE AND FUNCTION IN COPD
Abstract
A1054 - Effect of Diesel Exhaust on Exercise Endurance and Cardiorespiratory Responses to Exercise in Chronic Obstructive Pulmonary Disease and Healthy Controls - A Randomized, Placebo Controlled, Crossover Study
Author Block: N. Syed1, M. H. Ryu2, S. S. Dhillon1, M. R. Schaeffer1, C. J. Ryerson2, A. H. Ramsook1, J. Leung2, C. Carlsten2, J. A. Guenette1; 1Physical Therapy, The University of British Columbia & Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada, 2Medicine, The University of British Columbia & Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada.
RATIONALE: Previous studies in humans show an association between chronic exposure to traffic-related air pollution (TRAP) and various indices of morbidity and mortality. Although individuals with chronic obstructive pulmonary disease (COPD) have increased sensitivity to TRAP such as diesel exhaust (DE), little is known about the acute effects of TRAP on cardiorespiratory responses to exercise in COPD. We tested the hypothesis that DE would more negatively impact exercise performance and ventilatory responses to exercise in COPD compared to healthy controls.
METHODS: In this double-blind, randomized, crossover, controlled exposure study, 11 healthy never smokers and 9 ex-smokers with COPD were separately exposed to filtered air (FA) and DE300 (nominal concentration of PM2.5=300 µg/m3) for 2-hrs separated by a minimum of 4 weeks. During exposures, participants performed two 15-min bouts of cycling at 30% of peak work rate to increase ventilation. Participants then performed a constant work rate cycling test until exhaustion at 80% of peak cycle work rate within 2.5 hours of exposure. Linear mixed-effects models were used to evaluate the main effects of DE300 on exercise variables. Wilcoxon signed-rank test was used to compare exercise endurance time between exposures.
RESULTS: Individuals with mild-to-moderate COPD and healthy controls were well-matched for sex, height, mass, and body mass index, although participants with COPD were older than controls (69±5 vs. 55±8 years respectively). There was a significant negative effect of DE300 on exercise endurance time in healthy controls (DE300 vs. FA: 10.2±8.2 vs. 12.9±9.5 min, respectively; p=0.03) but not in COPD (9.8±6.4 vs. 8.4±6.6 min, respectively, p=0.26). Respiratory exchange ratio, inspiratory duty cycle, end-expiratory lung volume, and end-inspiratory lung volume were all higher in DE300 compared to FA in healthy controls (p=0.02, 0.03, <0.01, and 0.01, respectively). In contrast, there were no negative effects of DE300 on any cardiorespiratory variables in COPD.
CONCLUSION: DE300 did not impact exercise endurance time or cardiorespiratory physiology during exercise in individuals with COPD. In contrast, DE300 had an adverse impact on endurance time in healthy participants, which may have been related to alterations in ventilatory timing and operating lung volumes. We speculate that the negative effects of DE300 in healthy individuals compared to COPD may be due to relatively greater deposition of DE300 particles owing to higher absolute ventilation and possible bronchodilation during DE300 exposure. Future work is needed to elucidate the precise mechanisms for the differing effects of DE300 in health versus COPD.
Author Block: N. Syed1, M. H. Ryu2, S. S. Dhillon1, M. R. Schaeffer1, C. J. Ryerson2, A. H. Ramsook1, J. Leung2, C. Carlsten2, J. A. Guenette1; 1Physical Therapy, The University of British Columbia & Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada, 2Medicine, The University of British Columbia & Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada.
RATIONALE: Previous studies in humans show an association between chronic exposure to traffic-related air pollution (TRAP) and various indices of morbidity and mortality. Although individuals with chronic obstructive pulmonary disease (COPD) have increased sensitivity to TRAP such as diesel exhaust (DE), little is known about the acute effects of TRAP on cardiorespiratory responses to exercise in COPD. We tested the hypothesis that DE would more negatively impact exercise performance and ventilatory responses to exercise in COPD compared to healthy controls.
METHODS: In this double-blind, randomized, crossover, controlled exposure study, 11 healthy never smokers and 9 ex-smokers with COPD were separately exposed to filtered air (FA) and DE300 (nominal concentration of PM2.5=300 µg/m3) for 2-hrs separated by a minimum of 4 weeks. During exposures, participants performed two 15-min bouts of cycling at 30% of peak work rate to increase ventilation. Participants then performed a constant work rate cycling test until exhaustion at 80% of peak cycle work rate within 2.5 hours of exposure. Linear mixed-effects models were used to evaluate the main effects of DE300 on exercise variables. Wilcoxon signed-rank test was used to compare exercise endurance time between exposures.
RESULTS: Individuals with mild-to-moderate COPD and healthy controls were well-matched for sex, height, mass, and body mass index, although participants with COPD were older than controls (69±5 vs. 55±8 years respectively). There was a significant negative effect of DE300 on exercise endurance time in healthy controls (DE300 vs. FA: 10.2±8.2 vs. 12.9±9.5 min, respectively; p=0.03) but not in COPD (9.8±6.4 vs. 8.4±6.6 min, respectively, p=0.26). Respiratory exchange ratio, inspiratory duty cycle, end-expiratory lung volume, and end-inspiratory lung volume were all higher in DE300 compared to FA in healthy controls (p=0.02, 0.03, <0.01, and 0.01, respectively). In contrast, there were no negative effects of DE300 on any cardiorespiratory variables in COPD.
CONCLUSION: DE300 did not impact exercise endurance time or cardiorespiratory physiology during exercise in individuals with COPD. In contrast, DE300 had an adverse impact on endurance time in healthy participants, which may have been related to alterations in ventilatory timing and operating lung volumes. We speculate that the negative effects of DE300 in healthy individuals compared to COPD may be due to relatively greater deposition of DE300 particles owing to higher absolute ventilation and possible bronchodilation during DE300 exposure. Future work is needed to elucidate the precise mechanisms for the differing effects of DE300 in health versus COPD.
