Search

Copyright of Canadian Journal of Respiratory, Critical Care, & Sleep Medicine is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Rationale: Outdoor air pollution is a potential risk factor for lower lung function and chronic obstructive pulmonary disease (COPD). Little is known about how airway abnormalities and lung growth might modify this relationship. Objectives: To evaluate the associations of ambient air pollution exposure with lung function and COPD and examine possible interactions with dysanapsis. Methods: We made use of cross-sectional postbronchodilator spirometry data from 1,452 individuals enrolled in the CanCOLD (Canadian Cohort Obstructive Lung Disease) study with linked ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) air pollution estimates. Dysanapsis, or the ratio of the airway-to-lung volume calculated from thoracic computed tomography images, was used to examine possible interactions. Measurements and Main Results: In adjusted models, 101.7 ml (95% confidence interval [CI], -166.2 to -37.2) and 115.0 ml (95% CI, -196.5 to -33.4) lower FEV1 were demonstrated per increase of 2.4 ug/m3 PM2.5 and 9.2 ppb NO2, respectively. Interaction between air pollution and dysanapsis was not statistically significant when modeling the airway-to-lung ratio as a continuous variable. However, a 109.8 ml (95% CI, -209.0 to -10.5] lower FEV1 and an 87% (95% CI, 12% to 213%) higher odds of COPD were observed among individuals in the lowest, relative to highest, airway-to-lung ratio, per 2.4 μg/m3 increment of PM2.5. Conclusions: Ambient air pollution exposure was associated with lower lung function, even at relatively low concentrations. Individuals with dysanaptic lung growth might be particularly susceptible to inhaled ambient air pollutants, especially those at the extremes of dysanapsis. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease patient care must include confirming a diagnosis with postbronchodilator spirometry. Because of the clinical heterogeneity and the reality that airflow obstruction assessed by spirometry only partially reflects disease severity, a thorough clinical evaluation of the patient should include assessment of symptom burden and risk of exacerbations that permits the implementation of evidence-informed pharmacologic and nonpharmacologic interventions. This guideline provides recommendations from a comprehensive systematic review with a meta-analysis and expert-informed clinical remarks to optimize maintenance pharmacologic therapy for individuals with stable COPD, and a revised and practical treatment pathway based on new evidence since the 2019 update of the Canadian Thoracic Society (CTS) Guideline. The key clinical questions were developed using the Patients/Population (P), Intervention(s) (I), Comparison/Comparator (C), and Outcome (O) model for three questions that focuses on the outcomes of symptoms (dyspnea)/health status, acute exacerbations, and mortality. The evidence from this systematic review and meta-analysis leads to the recommendation that all symptomatic patients with spirometry-confirmed COPD should receive long-acting bronchodilator maintenance therapy. Those with moderate to severe dyspnea (modified Medical Research Council ≥ 2) and/or impaired health status (COPD Assessment Test ≥ 10) and a low risk of exacerbations should receive combination therapy with a long-acting muscarinic antagonist/long-acting ẞ2-agonist (LAMA/LABA). For those with a moderate/severe dyspnea and/or impaired health status and a high risk of exacerbations should be prescribed triple combination therapy (LAMA/LABA/inhaled corticosteroids) azithromycin, roflumilast or N-acetylcysteine is recommended for specific populations; a recommendation against the use of theophylline, maintenance systemic oral corticosteroids such as prednisone and inhaled corticosteroid monotherapy is made for all COPD patients., Competing Interests: Financial/Nonfinancial Disclosures Members of the CTS COPD Guideline Panel declared potential conflicts of interest at the time of appointment, and these were updated throughout the process in accordance with the CTS Conflict of Interest Disclosure Policy. J. B. reports grants from McGill University, the McGill University Health Centre Foundation, the Canadian Institute Health Research, Grifols, Novartis, Sanofi, and the Respiratory Health Network of the Fonds de la recherche en santé du Québec; grants and personal fees from Astra Zeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, and Trudell Canada Ltd; and personal fees from Pfizer Canada Ltd, and COVIS Pharma Canada Ltd, outside the submitted work. M. B. reports personal fees and grants outside the submitted work from AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Novartis, Sanofi-Genzyme, the Canadian Institute Health Research, CHEST, The Lung Association of Alberta, The University of Alberta Hospital Foundation, Alberta Innovates Health Solutions, Valeo, and Covis. P. H. reports grants from the Canadian Institute Health Research, the Lung Association of Nova Scotia, the Nova Scotia Health Authority Research Fund, Astra Zeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, Cyclomedica, Grifols, Respivant, and Vertex; and personal fees from Astra Zeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Janssen, Merck, Novartis, Sanofi-Aventis, and Trudell, outside the submitted work. S. D. A. receives grants from CIHR. He has received speaking honoraria or has participated on advisory boards for GSK, AZ, Chiesi, and Sanofi. M-F. B. reports grants and personal fees from the Cercle du doyen (Faculté de pharmacie, Université de Montréal) and Astra Zeneca Canada Ltd. A. D. reports receiving research, consulting and lecturing fees from GlaxoSmithkline, Sepracor, Schering Plough, Altana, Methapharma, AstraZeneca, ONO pharma, Merck Canada, Forest Laboratories, Novartis Canada/USA, Boehringer Ingelheim (Canada) Ltd, Pfizer Canada, SkyePharma, and KOS Pharmaceuticals and Almirall, Sanofigenzyme and TEVA Canada, Valeopharma Canada. F. M. reports grants from AstraZeneca and GlaxoSmithKline, Boehringer Ingelheim, GSK, Sanofi, and Novartis, and personal fees for serving on speaker bureaus and consultation panels from GlaxoSmithKline, Grifols, and Novartis. He is financially involved with Oxynov, a company which is developing an oxygen delivery system. S. M. reports grants outside the submitted work from Canadian Institute of Health Research and Canadian Lung Association in partnership with Boehringer Ingelheim Canada Ltd and Astra Zeneca Canada Ltd. E. P. reports personal fees from COVIS Pharma, Sanofi Genzyme, Boehringer Ingelheim Canada Ltd, Astra Zeneca Canada Ltd, GlaxoSmithKline Canada Ltd, and Novartis; and grants from the Canadian Institute Health Research, the Saskatchewan Research Foundation, the Respiratory Research Centre, and Astra Zeneca Canada Ltd, outside the submitted work. D. D. S. reports personal fees from GlaxoSmithKline Canada Ltd, Boehringer Ingelheim, and AstraZeneca outside of the submitted work. J. W. reports personal fees from GlaxoSmithKline Canada Ltd and Astra Zeneca Canada Ltd and a grant from Fisher & Paykel, outside the submitted work. B. L. W. reports personal fees from AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Novartis, Sanofi-Genzyme and Covis Pharma Canada, outside of the submitted work. D. D. M. reports consultancy work with Alberta Health Services, Health Canada, Lung Saskatchewan, Ontario Ministry of Health and Long-Term Care, Saskatchewan Health Authority, Saskatchewan Ministry of Health, Yukon Health and Social Services; reports grants (managed by University of Saskatchewan) from AstraZeneca, Boehringer Ingelheim, Canadian Institute of Health Research, GlaxoSmithKline, Grifols Therapeutics, Lung Saskatchewan, Novartis, Sanofi-Aventis, Saskatchewan Health Research Foundation, Syneos Health, Schering-Plough; employee/roles with University of Saskatchewan, Deputy Editor - CHEST Journal, Board Member - Saskatchewan Health Research Foundation; outside the submitted work. None declared (A. L., A. V. D., S. B. K., J. D. M.)., (Copyright © 2023 Canadian Thoracic Society and American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: Infections are considered as leading causes of acute exacerbations of chronic obstructive pulmonary disease (COPD). Non-infectious risk factors such as short-term air pollution exposure may play a clinically important role. We sought to estimate the relationship between short-term air pollutant exposure and exacerbations in Canadian adults living with mild to moderate COPD., Methods: In this case-crossover study, exacerbations ('symptom based': ≥48 hours of dyspnoea/sputum volume/purulence; 'event based': 'symptom based' plus requiring antibiotics/corticosteroids or healthcare use) were collected prospectively from 449 participants with spirometry-confirmed COPD within the Canadian Cohort Obstructive Lung Disease. Daily nitrogen dioxide (NO 2 ), fine particulate matter (PM 2.5 ), ground-level ozone (O 3 ), composite of NO 2 and O 3 (O x ), mean temperature and relative humidity estimates were obtained from national databases. Time-stratified sampling of hazard and control periods on day '0' (day-of-event) and Lags ('-1' to '-6') were compared by fitting generalised estimating equation models. All data were dichotomised into 'warm' (May-October) and 'cool' (November-April) seasons. ORs and 95% CIs were estimated per IQR increase in pollutant concentrations., Results: Increased warm season ambient concentration of NO 2 was associated with symptom-based exacerbations on Lag-3 (1.14 (1.01 to 1.29), per IQR), and increased cool season ambient PM 2.5 was associated with symptom-based exacerbations on Lag-1 (1.11 (1.03 to 1.20), per IQR). There was a negative association between warm season ambient O 3 and symptom-based events on Lag-3 (0.73 (0.52 to 1.00), per IQR)., Conclusions: Short-term ambient NO 2 and PM 2.5 exposure were associated with increased odds of exacerbations in Canadians with mild to moderate COPD, further heightening the awareness of non-infectious triggers of COPD exacerbations., Competing Interests: Competing interests: BAR reports grants/contracts from the Canadian Institutes of Health Research (CIHR), Réseau de Recherche en Santé Respiratoire du Québec (RSRQ), Research Institute of the MUHC (RI MUHC), Ministère de l'Économie et de l'Innovation (MEI) Québec, McGill University Health Centre (MUHC) Foundation Grant, Fonds de Recherche Santé Québec (FRSQ), and CHEST Foundation Grant; and payments/honoraria from the Canadian Thoracic Society (CTS), CHEST/ACCP, Respiplus (non-profit), Alberta Kinesiology Association (AKA), and McGill University Continuing Professional Development (CPD). SDA reports payments/honoraria from AstraZeneca, GSK; and participation on Data Safety Monitoring/Advisory Board for AstraZeneca, GSK, and Sanofi. PH reports grants/contracts from Boehringer Ingelheim, Cyclomedica, Grifols, Vertex; consulting fees from Acceleron, AstraZeneca, Boehringer Ingelheim, Covis, GlaxoSmithKline, Janssen, Novartis, Sanofi, Teva, Takeda, Valeo; and leadership/fiduciary role in the Canadian Thoracic Society. FM reports grants/contracts from GlaxoSmithKline, AstraZeneca, Sanofi, Novartis, Boehringer Ingelheim, Grifols; consulting fees from AstraZeneca; payment/honoraria from GlaxoSmithKline, Boehringer Ingelheim, Grifols, Novartis; and stock/stock options from Oxynov. DM reports grants/contracts from AstraZeneca, Boehringer Ingelheim, Canadian Institute of Health Research, GlaxoSmithKline, Grifols, Lung Association—Saskatchewan, Novartis, Sanofi, Saskatchewan Health Research Foundation, Schering-Plough; consulting fees from Alberta Health Services, Canadian Foundation for Healthcare Improvement, Health Canada, Lung Association—Saskatchewan, Ontario Ministry of Health and Long-Term Care, Saskatchewan Health Authority, Yukon Health and Social Services; payment/honoraria from the Lung Association—Saskatchewan, American College of Chest Physicians; leadership/fiduciary role in the CHEST journal, Canadian Thoracic Society, American Thoracic Society and AARC; and is an employee of the University of Saskatchewan. DE O’D reports grants/contracts from AstraZeneca, Lung Health Foundation and Boehringer Ingelheim Canada; and payment/honoraria from GSK and Viajes Pacifico. BLW reports payment/honoraria from AstraZeneca, GSK, Sanofi; and Data Safety Monitoring/Advisory Board participation for AstraZeneca, GSK, and Sanofi. JB reports grants/contracts from the Canadian Institute of Health Research (CIHR), Réseau en santé respiratoire du FRQS, McGill University, McGill University Health Centre Foundation, AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GSK, Grifols, Novartis, Sanofil, Trudell Canada Ltd; and payment/honoraria from AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GSK, Pfizer Canada Ltd, and Trudell Canada Ltd., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Individuals with COPD and preserved ratio impaired spirometry (PRISm) findings in clinical settings have an increased risk of cardiovascular disease (CVD)., Research Question: Do individuals with mild to moderate or worse COPD and PRISm findings in community settings have a higher prevalence and incidence of CVD compared with individuals with normal spirometry findings? Can CVD risk scores be improved when impaired spirometry is added?, Study Design and Methods: The analysis was embedded in the Canadian Cohort Obstructive Lung Disease (CanCOLD). Prevalence of CVD (ischemic heart disease [IHD] and heart failure [HF]) and their incidence over 6.3 years were compared between groups with impaired and normal spirometry findings using logistic regression and Cox models, respectively, adjusting for covariables. Discrimination of the pooled cohort equations (PCE) and Framingham risk score (FRS) in predicting CVD were assessed with and without impaired spirometry., Results: Participants (n = 1,561) included 726 people with normal spirometry findings and 835 people with impaired spirometry findings (COPD Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage 1 disease, n = 408; GOLD stage ≥ 2, n = 331; PRISm findings, n = 96). Rates of undiagnosed COPD were 84% in GOLD stage 1 and 58% in GOLD stage ≥ 2 groups. Prevalence of CVD (IHD or HF) was significantly higher among individuals with impaired spirometry findings and COPD compared with those with normal spirometry findings, with ORs of 1.66 (95% CI, 1.13-2.43; P = .01∗) (∗ indicates statistical significane with P < .05) and 1.55 (95% CI, 1.04-2.31; P = .033∗), respectively. Prevalence of CVD was significantly higher in participants having PRISm findings and COPD GOLD stage ≥ 2, but not GOLD stage 1. CVD incidence was significantly higher, with hazard ratios of 2.07 (95% CI, 1.10-3.91; P = .024∗) for the impaired spirometry group and 2.09 (95% CI, 1.10-3.98; P = .024∗) for the COPD group compared to individuals with normal spirometry findings. The difference was significantly higher among individuals with COPD GOLD stage ≥ 2, but not GOLD stage 1. The discrimination for predicting CVD was low and limited when impaired spirometry findings were added to either risk score., Interpretation: Individuals with impaired spirometry findings, especially those with moderate or worse COPD and PRISm findings, have increased comorbid CVD compared with their peers with normal spirometry findings, and having COPD increases the risk of CVD developing., (Copyright © 2023 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Objectives: To develop a consensus statement on the use of lung ultrasound (LUS) in the assessment of symptomatic general medical inpatients with known or suspected coronavirus disease 2019 (COVID-19)., Methods: Our LUS expert panel consisted of 14 multidisciplinary international experts. Experts voted in 3 rounds on the strength of 26 recommendations as "strong," "weak," or "do not recommend." For recommendations that reached consensus for do not recommend, a fourth round was conducted to determine the strength of those recommendations, with 2 additional recommendations considered., Results: Of the 26 recommendations, experts reached consensus on 6 in the first round, 13 in the second, and 7 in the third. Four recommendations were removed because of redundancy. In the fourth round, experts considered 4 recommendations that reached consensus for do not recommend and 2 additional scenarios; consensus was reached for 4 of these. Our final recommendations consist of 24 consensus statements; for 2 of these, the strength of the recommendations did not reach consensus., Conclusions: In symptomatic medical inpatients with known or suspected COVID-19, we recommend the use of LUS to: (1) support the diagnosis of pneumonitis but not diagnose COVID-19, (2) rule out concerning ultrasound features, (3) monitor patients with a change in the clinical status, and (4) avoid unnecessary additional imaging for patients whose pretest probability of an alternative or superimposed diagnosis is low. We do not recommend the use of LUS to guide admission and discharge decisions. We do not recommend routine serial LUS in patients without a change in their clinical condition., (© 2020 The Authors. Journal of Ultrasound in Medicine published by Wiley Periodicals LLC on behalf of American Institute of Ultrasound in Medicine.)

Background: Previous studies have associated marijuana exposure with increased respiratory symptoms and chronic bronchitis among long-term cannabis smokers. The long-term effects of smoked marijuana on lung function remain unclear., Methods: We determined the association of marijuana smoking with the risk of spirometrically defined chronic obstructive pulmonary disease (COPD) (post-bronchodilator forced expiratory volume in 1 s (FEV 1 )/forced vital capacity ratio <0.7) in 5291 population-based individuals and the rate of decline in FEV 1 in a subset of 1285 males and females, aged ≥40 years, who self-reported use (or non-use) of marijuana and tobacco cigarettes and performed spirometry before and after inhaled bronchodilator on multiple occasions. Analysis for the decline in FEV 1 was performed using random mixed effects regression models adjusted for age, sex and body mass index. Heavy tobacco smoking and marijunana smoking was defined as >20 pack-years and >20 joint-years, respectively., Results: ∼20% of participants had been or were current marijuana smokers with most having smoked tobacco cigarettes in addition (83%). Among heavy marijuana users, the risk of COPD was significantly increased (adjusted OR 2.45, 95% CI 1.55-3.88). Compared to never-smokers of marijuana and tobacco, heavy marijuana smokers and heavy tobacco smokers experienced a faster decline in FEV 1 by 29.5 mL·year -1 (p=0.0007) and 21.1 mL·year -1 (p<0.0001), respectively. Those who smoked both substances experienced a decline of 32.31 mL·year -1 (p<0.0001)., Interpretation: Heavy marijuana smoking increases the risk of COPD and accelerates FEV 1 decline in concomitant tobacco smokers beyond that observed with tobacco alone., Competing Interests: Conflict of interest: W.C. Tan reports grants from Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program Operating Grants-93326) with industry partners AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, Novartis Pharma Canada Inc., Nycomed Canada Inc., Pfizer Canada Ltd, during the conduct of the study. Conflict of interest: J. Bourbeau reports grants from Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program Operating Grants-93326) with industry partners AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, Novartis Pharma Canada Inc., Nycomed Canada Inc., Pfizer Canada Ltd, during the conduct of the study. Conflict of interest: S.D. Aaron has nothing to disclose. Conflict of interest: J.C. Hogg has nothing to disclose. Conflict of interest: F. Maltais has nothing to disclose. Conflict of interest: P. Hernandez reports grants from Canadian Institute Health Research, during the conduct of the study; grants and personal fees from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis and Takeda, personal fees from Merck, Grifols, Pfizer and Almirall, grants from CSL Behring, outside the submitted work. Conflict of interest: D.D. Marciniuk has nothing to disclose. Conflict of interest: K.R. Chapman reports grants from Novartis, Almirall, Boehringer Ingelheim, Forest, GSK, AstraZeneca, Amgen, Roche, CSL Behring, Grifols, Genentech and Kamada, during the conduct of the study; UHN administered personal support from CIHR (GSK Research Chair in Respiratory Health Care Delivery), outside the submitted work. Conflict of interest: T. To has nothing to disclose. Conflict of interest: J.M. FitzGerald has nothing to disclose. Conflict of interest: B.L. Walker reports grants from Canadian Institute of Health Research, AstraZeneca Canada Ltd, Boehringer Ingelheim Canada, GlaxoSmithKline Canada and Novartis, during the conduct of the study; grants from Respiratory Health Strategic Clinical Network Alberta, personal fees from AstraZeneca, GlaxoSmithKline and Novartis, outside the submitted work. Conflict of interest: J. Road has nothing to disclose. Conflict of interest: L. Zheng has nothing to disclose. Conflict of interest: G. Zhou has nothing to disclose. Conflict of interest: T. Yau has nothing to disclose. Conflict of interest: A. Benedetti has nothing to disclose. Conflict of interest: D. O'Donnell has nothing to disclose. Conflict of interest: D.D. Sin reports grants from Merck, personal fees for advisory board work from Sanofi-Aventis and Regeneron, grants and personal fees from Boehringer Ingelheim, grants and personal fees for lectures and advisory board work from AstraZeneca, personal fees for lectures and advisory board work from Novartis, outside the submitted work., (Copyright ©ERS 2019.)

Background: Patients with psychiatric disorders (depression, anxiety) are more likely to have poor health behaviours, including higher smoking and lower physical activity (PA) levels. Smoking is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD), and PA is critical for COPD management. However, no studies have assessed associations between psychological distress and these behaviours among patients with vs without COPD. This is a sub-analysis of the CanCOLD study that assessed the relationships between psychological disorders (depression, anxiety) and poor health behaviours (smoking, PA)., Methods: 717 COPD and 797 matched non-COPD individuals from the CanCOLD study, completed the Hospital Anxiety Depression Scale (HADS) to assess anxiety and depression. Smoking behaviour was self-reported pack-years smoking. The CHAMPS PA questionnaire determined calorific expenditure as a PA measure. Regressions determined relationships between anxiety/depression and health behaviours, adjusting for age, sex, BMI, GOLD stage and COPD status., Results: Across the whole sample, we observed relationships between depression (β = 1.107 ± 0.197; 95%CI = 0.691-1.462; p < .001) and anxiety (β = 0.780 ± 0.170; 95%CI = 0.446-1.114; p < .001) and pack years. Higher depression (β = -0.220 ± 0.028; 95%CI = -0.275 to -0.165; p < .001) and anxiety (β = -0.091 ± 0.025; 95%CI = -0.139 to -0.043; p < .001) scores were related to lower PA. These associations were comparable across COPD and non-COPD patients., Conclusions: Results showed that higher levels of anxiety and depression were related to higher cumulative smoking and lower levels of PA in patients with and without COPD, suggesting symptoms of psychological distress is similarly associated with poorer health behaviours in COPD and non-COPD individuals. Future studies need to determine if treating symptoms of psychological distress can improve health behaviours and outcomes in this population., (Copyright © 2018. Published by Elsevier Ltd.)