Chronic obstructive pulmonary disease#Subtypes

File:Symptoms of COPD.svg of stages of COPD]]

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A cardinal symptom of COPD is the chronic and progressive shortness of breath which is most characteristic of the condition. Shortness of breath (breathlessness) is often the most distressing symptom responsible for the associated anxiety and level of disability experienced.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} Symptoms of wheezing and chest tightness associated with breathlessness can be variable over the course of a day or between days and are not always present. Chest tightness often follows exertion.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} Many people with more advanced COPD breathe through pursed lips, which can improve shortness of breath.{{cite journal |vauthors=Mayer AF, Karloh M, Dos Santos K, de Araujo CL, Gulart AA |title=Effects of acute use of pursed-lips breathing during exercise in patients with COPD: a systematic review and meta-analysis |journal=Physiotherapy |volume=104 |issue=1 |pages=9–17 |date=March 2018 |pmid=28969859 |doi=10.1016/j.physio.2017.08.007 |url=}} Shortness of breath is often responsible for reduced physical activity and low levels of physical activity are associated with worse outcomes.{{sfn|Gold Report 2021|pp=90–96|loc=Chapter 4: Management of stable COPD}}{{cite journal | vauthors = O'Donnell DE, Milne KM, James MD, de Torres JP, Neder JA | title = Dyspnea in COPD: New Mechanistic Insights and Management Implications | journal = Advances in Therapy | volume = 37 | issue = 1 | pages = 41–60 | date = January 2020 | pmid = 31673990 | pmc = 6979461 | doi = 10.1007/s12325-019-01128-9 | doi-access = free }} In severe and very severe cases there may be constant tiredness, weight loss, muscle loss and anorexia. People with COPD often have increased breathlessness and frequent colds before seeking treatment.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}

The most often first symptom of COPD is a chronic cough, which may or may not be productive of mucus as phlegm. Phlegm coughed up as sputum can be intermittent and may be swallowed or spat out depending on social or cultural factors and is therefore not always easy to evaluate. However, an accompanying productive cough is only seen in up to 30% of cases. Sometimes limited airflow may develop in the absence of a cough.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} Symptoms are usually worse in the morning.{{cite journal |vauthors=Szalontai K, Gémes N, Furák J |display-authors=et al. |title=Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer |journal=J Clin Med |volume=10 |issue=13 |date=June 2021 |page=2889 |pmid=34209651 |doi=10.3390/jcm10132889 |url=|pmc=8268950 |doi-access=free }}

A chronic productive cough is the result of mucus hypersecretion and when it persists for more than three months each year for at least two years, it is defined as chronic bronchitis.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Chronic bronchitis can occur before the restricted airflow diagnostic of COPD.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Some people with COPD attribute the symptoms to the consequences of smoking. In severe COPD, vigorous coughing may lead to rib fractures or to a brief loss of consciousness.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}

An acute exacerbation is a sudden worsening of signs and symptoms that lasts for several days. The key symptom is increased breathlessness, other more pronounced symptoms are of excessive mucus, increased cough and wheeze. A commonly found sign is air trapping giving a difficulty in complete exhalation.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

The usual cause of an exacerbation is a viral infection, most often the common cold.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} The common cold is usually associated with the winter months but can occur at any time.{{cite web |title=Common Colds |url=https://www.cdc.gov/features/rhinoviruses/ |website=Centers for Disease Control and Prevention |access-date=20 August 2021 |language=en-us |date=7 October 2020 |archive-date=June 18, 2023| archive-url=https://web.archive.org/web/20230618024517/https://www.cdc.gov/features/rhinoviruses/}} Other respiratory infections may be bacterial or in combination sometimes secondary to a viral infection.{{cite journal |vauthors=Guo-Parke H, Linden D, Weldon S, Kidney JC, Taggart CC |title=Mechanisms of Virus-Induced Airway Immunity Dysfunction in the Pathogenesis of COPD Disease, Progression, and Exacerbation |journal=Frontiers in Immunology |volume=11 |issue= |pages=1205 |date=2020 |pmid=32655557 |pmc=7325903 |doi=10.3389/fimmu.2020.01205 |url=|doi-access=free }} The most common bacterial infection is caused by Haemophilus influenzae.{{cite journal |vauthors=Short B, Carson S, Devlin AC |display-authors=etal |title=Non-typeable Haemophilus influenzae chronic colonization in chronic obstructive pulmonary disease (COPD) |journal=Critical Reviews in Microbiology |volume=47 |issue=2 |pages=192–205 |date=March 2021 |pmid=33455514 |doi=10.1080/1040841X.2020.1863330 |s2cid=230608674 |url=|doi-access=free }} Other risks include exposure to tobacco smoke (active and passive) and environmental pollutants{{Snd}}both indoor and outdoor.{{cite web |last1=US EPA |first1=OAR |title=Particulate Matter (PM) Basics |url=https://www.epa.gov/pm-pollution/particulate-matter-pm-basics#effects |website=www.epa.gov |access-date=21 July 2021 |language=en |date=19 April 2016}} During the COVID-19 pandemic, hospital admissions for COPD exacerbations sharply decreased which may be attributable to reduction of emissions and cleaner air. There has also been a marked decrease in the number of cold and flu infections during this time.{{cite journal | vauthors = Iacobucci G | title = Covid lockdown: England sees fewer cases of colds, flu, and bronchitis | journal = BMJ | volume = 370 | pages = m3182 | date = August 2020 | pmid = 32784206 | doi = 10.1136/bmj.m3182 | s2cid = 221097739 | doi-access = free }}

Smoke from wildfires is proving an increasing risk in many parts of the world and government agencies have published protective advice on their websites. In the US the EPA advises that the use of dust masks do not give protection from the fine particles in wildfires and instead advise the use of well-fitting particulate masks.{{cite web |last1=US EPA |first1=OAR |title=Health Effects Attributed to Wildfire Smoke |url=https://www.epa.gov/wildfire-smoke-course/health-effects-attributed-wildfire-smoke |website=www.epa.gov |access-date=21 July 2021 |language=en |date=13 August 2019}} This same advice is offered in Canada and Australia to the effects of their forest fires.{{cite web |title=Forest Fires and Lung Health |url=https://www.lung.ca/lung-health/air-quality/outdoor-air-quality/forest-fires-and-lung-health |website=the lung association |access-date=21 July 2021 |language=en |date=25 August 2014}}{{cite web |title=Bushfire smoke |url=https://farmerhealth.org.au/2014/03/19/bushfire-smoke |website=National Centre for Farmer Health |access-date=21 July 2021 |language=en-AU |date=19 March 2014}}

The number of exacerbations is not seen to relate to any stage of the disease; those with two or more a year are classed as frequent exacerbators and these lead to a worsening in the disease progression.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}} Frailty in ageing increases exacerbations and hospitalization.{{cite journal |vauthors=Luo J, Zhang D, Tang W, Dou LY, Sun Y |title=Impact of Frailty on the Risk of Exacerbations and All-Cause Mortality in Elderly Patients with Stable Chronic Obstructive Pulmonary Disease |journal=Clin Interv Aging |volume=16 |issue= |pages=593–601 |date=2021 |pmid=33880018 |pmc=8053481 |doi=10.2147/CIA.S303852 |url= |doi-access=free }}

Acute exacerbations in COPD are often unexplained and thought to have many causes other than infections. A study has emphasized the possibility of a pulmonary embolism as sometimes being responsible in these cases. Signs can include pleuritic chest pain and heart failure without signs of infection. Such emboli could respond to anticoagulants.{{cite journal | vauthors = Aleva FE, Voets LW, Simons SO, de Mast Q, van der Ven AJ, Heijdra YF | title = Prevalence and Localization of Pulmonary Embolism in Unexplained Acute Exacerbations of COPD: A Systematic Review and Meta-analysis | journal = Chest | volume = 151 | issue = 3 | pages = 544–554 | date = March 2017 | pmid = 27522956 | doi = 10.1016/j.chest.2016.07.034 | s2cid = 7181799 }}

COPD often occurs along with a number of other conditions (comorbidities) due in part to shared risk factors. Common comorbidities include cardiovascular disease, skeletal muscle dysfunction, metabolic syndrome, osteoporosis, depression, anxiety, asthma and lung cancer.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}} Alpha-1 antitrypsin deficiency (A1AD) is an important risk factor for COPD.{{cite journal |vauthors=Edgar RG, Patel M, Bayliss S, Crossley D, Sapey E, Turner AM |title=Treatment of lung disease in alpha-1 antitrypsin deficiency: a systematic review |journal=Int J Chron Obstruct Pulmon Dis |volume=12 |issue= |pages=1295–1308 |date=2017 |pmid=28496314 |pmc=5422329 |doi=10.2147/COPD.S130440 |doi-access=free }} It is advised that everybody with COPD be screened for A1AD.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}} Metabolic syndrome has been seen to affect up to fifty percent of those with COPD and significantly affects the outcomes.{{cite journal |vauthors=Clementi EA, Talusan A, Vaidyanathan S, Veerappan A, Mikhail M, Ostrofsky D, etal |title=Metabolic Syndrome and Air Pollution: A Narrative Review of Their Cardiopulmonary Effects |journal=Toxics |volume=7 |issue=1 |date=January 2019 |page=6 |pmid=30704059 |pmc=6468691 |doi=10.3390/toxics7010006 |doi-access=free |bibcode=2019Toxic...7....6C }} When comorbid with COPD there is more systemic inflammation. It is not known if it co-exists with COPD or develops as a consequence of the pathology. Metabolic syndrome on its own has a high rate of morbidity and mortality and this rate is amplified when comorbid with COPD. Tuberculosis is a risk factor for the development of COPD, and is also a potential comorbidity.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Most people with COPD die from comorbidities and not from respiratory problems.{{cite journal |vauthors=Chan SH, Selemidis S, Bozinovski S, Vlahos R |title=Pathobiological mechanisms underlying metabolic syndrome (MetS) in chronic obstructive pulmonary disease (COPD): clinical significance and therapeutic strategies |journal=Pharmacol Ther |volume=198 |issue= |pages=160–188 |date=June 2019 |pmid=30822464 |pmc=7112632 |doi=10.1016/j.pharmthera.2019.02.013 }}

Anxiety and depression are often complications of COPD.{{cite web |title=Chronic obstructive pulmonary disease (COPD) — Complications |work=BMJ Best Practice |url=https://bestpractice.bmj.com/topics/en-gb/7/complications |access-date=11 July 2021}} Other complications include reduced quality of life and increased disability, cor pulmonale, frequent chest infections including pneumonia, secondary polycythemia, respiratory failure, pneumothorax, lung cancer, and cachexia (muscle wasting).{{cite journal |vauthors=Forfia PR, Vaidya A, Wiegers SE |title=Pulmonary heart disease: The heart-lung interaction and its impact on patient phenotypes |journal=Pulm Circ |volume=3 |issue=1 |pages=5–19 |date=January 2013 |pmid=23662171 |pmc=3641739 |doi=10.4103/2045-8932.109910 |doi-access=free }}

Along with these complications, there is an associated risk of developing pulmonary hypertension. The estimated prevalence of pulmonary hypertension complicating COPD was reported at 39% in a meta-analysis. Of the people with COPD listed for lung transplantation, 82% were documented as having pulmonary hypertension via right heart catheterization, noting a mean pulmonary arterial pressure greater than 20mm Hg. Despite pulmonary hypertension being relatively rare in people with COPD, mild elevations of pulmonary arterial pressure can lead to worse outcomes, including risk of death.{{cite journal |vauthors=Olsson KM, Corte TJ, Kamp JC, Montani D, Nathan SD, Neubert L, Price LC, Kiely DG |title=Pulmonary hypertension associated with lung disease: new insights into pathomechanisms, diagnosis, and management |journal=The Lancet. Respiratory Medicine |volume=11 |issue=9 |pages=820–835 |date=September 2023 |pmid=37591300 |doi=10.1016/S2213-2600(23)00259-X|url=https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(23)00259-X/abstract}}

Cognitive impairment is common in those with COPD as it is for other lung conditions that affect airflow. Cognitive impairment is associated with the declining ability to cope with the basic activities of daily living.{{sfn|Gold Report 2021|pp=121–126|loc=Chapter 6: COPD and comorbidities}}

It is unclear if those with COPD are at greater risk of contracting COVID-19, though if infected they are at risk of hospitalization and developing severe COVID-19. However, there are laboratory and clinical studies showing a possibility of certain inhaled corticosteroids for COPD providing a protective role against COVID-19.{{cite journal |vauthors=Singh D, Mathioudakis AG, Higham A |title=Chronic obstructive pulmonary disease and COVID-19: interrelationships |journal=Curr Opin Pulm Med |volume=28 |issue=2 |pages=76–83 |date=March 2022 |pmid=34690257 |pmc=8815646 |doi=10.1097/MCP.0000000000000834 }}

Differentiating COVID-19 symptoms from an exacerbation is difficult; mild prodromal symptoms may delay its recognition and where they include loss of taste or smell COVID-19 is to be suspected.{{cite journal |vauthors=Halpin DM, Criner GJ, Papi A, Singh D, Anzueto A, Martinez FJ, Agusti AA, Vogelmeier CF |title=Global Initiative for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease. The 2020 GOLD Science Committee Report on COVID-19 and Chronic Obstructive Pulmonary Disease |journal=Am J Respir Crit Care Med |volume=203 |issue=1 |pages=24–36 |date=January 2021 |pmid=33146552 |pmc=7781116 |doi=10.1164/rccm.202009-3533SO }}

Many definitions of COPD in the past have included chronic bronchitis and emphysema but these have never been included in GOLD report definitions.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Emphysema is defined as enlarged airspaces (alveoli) whose walls break down resulting in permanent damage to the lung tissue and is just one of the structural abnormalities that can limit airflow. The condition can exist without airflow limitation but commonly it does. Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years but does not always result in airflow limitation although the risk of developing COPD is great.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} These older definitions grouped the two types as type A and type B. Type A were emphysema types known as pink puffers due to their pink complexion, fast breathing rate and pursed lips. Type B were chronic bronchitic types referred to as blue bloaters due to low oxygen levels causing a bluish color to the skin and lips and swollen ankles.{{cite book | vauthors = Weinberger SE |title=Principles of pulmonary medicine |chapter=6. Chronic Obstructive Pulmonary Disease |chapter-url=https://www.sciencedirect.com/science/article/abs/pii/B978032352371400009X |date=2019 |publisher=Elsevier |isbn=978-0-323-52371-4 |page=104 |edition=7th|doi=10.1016/B978-0-323-52371-4.00009-X }} These differences were suggested to be due to the presence or not of collateral ventilation, evident in emphysema and lacking in chronic bronchitis.{{cite journal | vauthors = Delaunois L | title = Anatomy and physiology of collateral respiratory pathways | journal = The European Respiratory Journal | volume = 2 | issue = 9 | pages = 893–904 | date = October 1989 | doi = 10.1183/09031936.93.02090893 | pmid = 2680588 | s2cid = 7124561 | url = https://erj.ersjournals.com/content/2/9/893 | access-date = 30 August 2021 | doi-access = free }} This terminology was no longer accepted as useful, as most people with COPD have a combination of both emphysema and airway disease. These are now recognized as the two major phenotypes of COPD — the emphysematous phenotype and the chronic bronchitic phenotype.

It has since been recognized that COPD is more complex, with a diverse group of disorders of differing risk factors and clinical courses that has resulted in a number of subtypes or phenotypes of COPD being accepted and proposed.{{cite journal |vauthors=Ramírez-Venegas A, Torres-Duque CA, Guzmán-Bouilloud NE, González-García M, Sansores RH |title=SMALLa AIRWAY DISEASE IN COPD ASSOCIATED TO BIOMASS EXPOSURE |journal=Rev Invest Clin |volume=71 |issue=1 |pages=70–78 |date=2019 |pmid=30810542 |doi=10.24875/RIC.18002652 |url=|doi-access=free }}{{cite journal |vauthors=Corlateanu A, Mendez Y, Wang Y, Garnica RJ, Botnaru V, Siafakas N |title=Chronic obstructive pulmonary disease and phenotypes: a state-of-the-art |journal=Pulmonology |volume=26 |issue=2 |pages=95–100 |date=2020 |pmid=31740261 |doi=10.1016/j.pulmoe.2019.10.006|doi-access=free }} The two classic emphysematous and chronic bronchitic phenotypes are fundamentally different conditions with unique underlying mechanisms. Another subtype of COPD, categorized by some as a separate clinical entity, is asthma-COPD overlap, which is a condition sharing clinical features of both asthma and COPD.{{cite journal |last1=Postma |first1=Dirkje S. |last2=Rabe |first2=Klaus F. |title=The Asthma–COPD Overlap Syndrome |journal=New England Journal of Medicine |date=24 September 2015 |volume=373 |issue=13 |pages=1241–1249 |doi=10.1056/NEJMra1411863|pmid=26398072 }}{{cite journal |last1=Mekov |first1=Evgeni |last2=Nuñez |first2=Alexa |last3=Sin |first3=Don D |last4=Ichinose |first4=Masakazu |last5=Rhee |first5=Chin Kook |last6=Maselli |first6=Diego Jose |last7=Coté |first7=Andréanne |last8=Suppli Ulrik |first8=Charlotte |last9=Maltais |first9=François |last10=Anzueto |first10=Antonio |last11=Miravitlles |first11=Marc |title=Update on Asthma–COPD Overlap (ACO): A Narrative Review |journal=International Journal of Chronic Obstructive Pulmonary Disease |date=June 2021 |volume=16 |pages=1783–1799 |doi=10.2147/COPD.S312560|pmid=34168440 |pmc=8216660 |doi-access=free }} Spirometry measures are inadequate for defining phenotypes and chest X-ray, CT and MRI scans have been mostly employed. Most cases of COPD are diagnosed at a late stage and the use of imaging methods would allow earlier detection and treatment.

The identification and recognition of different phenotypes can guide appropriate treatment approaches. For example, the PDE4 inhibitor roflumilast is targeted at the chronic-bronchitic phenotype.

Two inflammatory phenotypes show a phenotype stability: the neutrophilic inflammatory phenotype and the eosinophilic inflammatory phenotype.{{cite journal |vauthors=Brightling C, Greening N |title=Airway inflammation in COPD: progress to precision medicine |journal=Eur Respir J |volume=54 |issue=2 |pages= |date=August 2019 |pmid=31073084 |doi=10.1183/13993003.00651-2019 |s2cid=149444134 |url=https://figshare.com/articles/journal_contribution/10221875/files/18436544.pdf}} Mepolizumab, a monoclonal antibody, has been shown to have benefit in treating the eosinophilic inflammatory type rather than the use of oral corticosteroids, but further studies have been called for.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Another recognized phenotype is the frequent exacerbator.{{cite journal |vauthors=Bai S, Zhao L |title=Imbalance Between Injury and Defense in the COPD Emphysematous Phenotype |journal=Frontiers in Medicine |volume=8 |issue= |pages=653332 |date=2021 |pmid=34026786 |pmc=8131650 |doi=10.3389/fmed.2021.653332 |url=|doi-access=free }} The frequent exacerbator has two or more exacerbations a year, has a poor prognosis and is described as a moderately stable phenotype.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

A pulmonary vascular COPD phenotype has been described due to cardiovascular dysfunction.{{cite journal |vauthors=Kumar A, Mahajan A, Salazar EA|display-authors=etal |title=Impact of human immunodeficiency virus on pulmonary vascular disease |journal=Glob Cardiol Sci Pract |volume=2021 |issue=2 |pages=e202112 |date=June 2021 |pmid=34285903 |pmc=8272407 |doi=10.21542/gcsp.2021.12 |url=}} A molecular phenotype of CFTR dysfunction is shared with cystic fibrosis. A combined phenotype of chronic bronchitis and bronchiectasis has been described with a difficulty noted of determining the best treatment.{{cite journal |vauthors=Osadnik CR, McDonald CF, Holland AE |title=Clinical issues of mucus accumulation in COPD |journal=Int J Chron Obstruct Pulmon Dis |volume=9 |issue= |pages=301–2 |date=2014 |pmid=24741301 |pmc=3970915 |doi=10.2147/COPD.S61797 |url= |doi-access=free }}

The only genotype is the alpha-1 antitrypsin deficiency (AATD) genetic subtype and this has a specific treatment.

The most common cause of the development of COPD is the exposure to harmful particles or gases, including tobacco smoke, that irritate the lung causing inflammation that interacts with a number of host factors. Such exposure needs to be significant or long-term.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} The greatest risk factor for the development of COPD is tobacco smoke. However, less than 50 percent of heavy smokers develop COPD, so other factors need to be considered, including exposure to indoor and outdoor pollutants, allergens, occupational exposure, and host factors.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} One of the known causes of COPD is exposure to construction dust. The three main types of construction dust are silica dust, non-silica dust (e.g., dust from gypsum, cement, limestone, marble and dolomite) and wood dust.{{cite web | url=https://www.hse.gov.uk/construction/faq-dust.htm | title=FAQs Dust - Health and Safety Executive (HSE)}} Host factors include a genetic susceptibility, factors associated with poverty, aging and physical inactivity. Asthma and tuberculosis are also recognized as risk factors, as the comorbidity of COPD is reported to be 12 times higher in patients with asthma after adjusting for smoking history.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} In Europe airway hyperresponsiveness is rated as the second most important risk factor after smoking.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}}

A host factor of an airway branching variation, arising during development has been described.{{cite journal |last1=Nikolić |first1=MZ |last2=Sun |first2=D |last3=Rawlins |first3=EL |title=Human lung development: recent progress and new challenges. |journal=Development |date=15 August 2018 |volume=145 |issue=16 |doi=10.1242/dev.163485 |pmid=30111617|pmc=6124546 }} The respiratory tree is a filter for harmful substances and any variant has the potential to disrupt this. A variation has been found to be associated with the development of chronic bronchitis and another with the development of emphysema. A branch variant in the central airway is specifically associated with an increased susceptibility for the later development of COPD. A genetic association for the variants has been sometimes found with FGF10.{{cite journal |display-authors=et al|vauthors=Smith BM, Traboulsi H, Austin JM|title=Human airway branch variation and chronic obstructive pulmonary disease |journal=Proc Natl Acad Sci U S A |volume=115 |issue=5 |pages=E974–E981 |date=January 2018 |pmid=29339516 |pmc=5798356 |doi=10.1073/pnas.1715564115 |bibcode=2018PNAS..115E.974S |url=|doi-access=free}}

Alcohol abuse can lead to alcoholic lung disease and is seen to be an independent risk factor for COPD.{{cite journal |vauthors=Bailey KL, Samuelson DR, Wyatt TA |title=Alcohol use disorder: A pre-existing condition for COVID-19? |journal=Alcohol |volume=90 |issue= |pages=11–17 |date=February 2021 |pmid=33080339 |pmc=7568767 |doi=10.1016/j.alcohol.2020.10.003 |url=}} Mucociliary clearance is disrupted by chronic exposure to alcohol; macrophage activity is diminished and an inflammatory response promoted.{{cite journal |vauthors=Arvers P |title=[Alcohol consumption and lung damage: Dangerous relationships] |language=French |journal=Rev Mal Respir |volume=35 |issue=10 |pages=1039–1049 |date=December 2018 |pmid=29941207 |doi=10.1016/j.rmr.2018.02.009 |s2cid=239523761 |url=}}{{cite journal |vauthors=Smith P, Jeffers LA, Koval M |title=Effects of different routes of endotoxin injury on barrier function in alcoholic lung syndrome |journal=Alcohol |volume=80 |issue= |pages=81–89 |date=November 2019 |pmid=31278041 |pmc=6613986 |doi=10.1016/j.alcohol.2018.08.007 |url=}} The damage leads to a susceptibility for infection, including COVID-19,{{cite journal |vauthors=Slovinsky WS, Romero F, Sales D, Shaghaghi H, Summer R |title=The involvement of GM-CSF deficiencies in parallel pathways of pulmonary alveolar proteinosis and the alcoholic lung |journal=Alcohol |volume=80 |issue= |pages=73–79 |date=November 2019 |pmid=31229291 |pmc=6592783 |doi=10.1016/j.alcohol.2018.07.006 |url=}} more so when combined with smoking; smoking induces the upregulation of the expression of ACE2, a receptor for the SARS-CoV-2 virus.

The primary risk factor for COPD globally is tobacco smoking with an increased rate of developing COPD shown in smokers and ex-smokers.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Of those who smoke, about 20% will get COPD,{{cite book| vauthors = Ward H |title=Oxford Handbook of Epidemiology for Clinicians|year=2012|publisher=Oxford University Press|isbn=978-0-19-165478-7|pages=289–290|url=https://books.google.com/books?id=dHLjLwru-l8C&pg=RA1-PT194 }} increasing to less than 50% in heavy smokers.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} In the United States and United Kingdom, of those with COPD, 80–95% are either current or previous smokers.{{cite book| vauthors = Rennard S |title=Clinical management of chronic obstructive pulmonary disease|year=2013|publisher=Informa Healthcare|isbn=978-0-8493-7588-0|page=23|url=https://books.google.com/books?id=DiTThQJkc0UC&pg=PA23|edition=2nd }}{{cite book| vauthors = Sharma A, Barclay J |title=COPD in primary care|year=2010|publisher=Radcliffe Pub.|isbn=978-1-84619-316-3|page=9|url=https://books.google.com/books?id=CrXFqhezbeMC&pg=PA9 }} Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke.{{cite journal | vauthors = Han MK, Martinez FJ | title = Host, Gender, and Early-Life Factors as Risks for Chronic Obstructive Pulmonary Disease | journal = Clinics in Chest Medicine | volume = 41 | issue = 3 | pages = 329–337 | date = September 2020 | pmid = 32800188 | pmc = 7993923 | doi = 10.1016/j.ccm.2020.06.009 }} For the same amount of cigarette smoking, women have a higher risk of COPD than men.{{cite journal | vauthors = Amaral AF, Strachan DP, Burney PG, Jarvis DL | title = Female Smokers Are at Greater Risk of Airflow Obstruction Than Male Smokers. UK Biobank | journal = American Journal of Respiratory and Critical Care Medicine | volume = 195 | issue = 9 | pages = 1226–1235 | date = May 2017 | pmid = 28075609 | doi = 10.1164/rccm.201608-1545OC | hdl-access = free | s2cid = 9360093 | hdl = 10044/1/45106 | url = https://openaccess.sgul.ac.uk/id/eprint/108529/7/AJRCCM-201608-1545OC-R1_supplement.pdf }} Women who smoke during pregnancy, and during the early life of the child is a risk factor for the later development of COPD in their child.{{cite journal | vauthors = Savran O, Ulrik CS | title = Early life insults as determinants of chronic obstructive pulmonary disease in adult life | journal = International Journal of Chronic Obstructive Pulmonary Disease | volume = 13 | issue = | pages = 683–693 | date = 2018 | pmid = 29520136 | pmc = 5834168 | doi = 10.2147/COPD.S153555 | doi-access = free }}

Inhaled smoke triggers the release of excessive proteases in lungs, which then degrades elastin, the major component of alveoli. Smoke also impairs the action of cilia, inhibiting mucociliary clearance that clears the bronchi of mucus, cellular debris and unwanted fluid.

Other types of tobacco smoke, such as from cigar, pipe, water-pipe and hookah use, also confer a risk.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Water-pipe or hookah smoke appears to be as harmful or even more harmful than smoking cigarettes.{{cite journal | vauthors = Patel MP, Khangoora VS, Marik PE | title = A Review of the Pulmonary and Health Impacts of Hookah Use | journal = Annals of the American Thoracic Society | volume = 16 | issue = 10 | pages = 1215–1219 | date = October 2019 | pmid = 31091965 | doi = 10.1513/AnnalsATS.201902-129CME | s2cid = 155103502 }}

Marijuana is the second most commonly smoked substance, but evidence linking its use to COPD is very limited. Limited evidence shows that marijuana does not accelerate lung function decline. A low use of marijuana gives a bronchodilatory effect rather than the bronchoconstrictive effect from tobacco use, but it is often smoked in combination with tobacco or on its own by tobacco smokers. Higher use however has shown a decline in the FEV1.{{cite journal |vauthors=Underner M, Urban T, Perriot J, Peiffer G, Harika-Germaneau G, Jaafari N |title=[Spontaneous pneumothorax and lung emphysema in cannabis users] |language=French |journal=Rev Pneumol Clin |volume=74 |issue=6 |pages=400–415 |date=December 2018 |pmid=30420278 |doi=10.1016/j.pneumo.2018.06.003 |s2cid=59233744 |url=}} There is evidence of it causing some respiratory problems and its use in combination may have a cumulative toxic effect suggesting it as a risk factor for spontaneous pneumothorax, bullous emphysema, COPD and lung cancer.{{cite journal |vauthors=Chatkin JM, Zabert G, Zabert I, Chatkin G, Jiménez-Ruiz CA, de Granda-Orive JI, etal | title=Lung Disease Associated With Marijuana Use |journal=Arch Bronconeumol |volume=53 |issue=9 |pages=510–515 |date=September 2017 |pmid=28483343 |doi=10.1016/j.arbres.2017.03.019 |url=}}{{cite journal |vauthors=Martinasek MP, McGrogan JB, Maysonet A |title=A Systematic Review of the Respiratory Effects of Inhalational Marijuana |journal=Respir Care |volume=61 |issue=11 |pages=1543–1551 |date=November 2016 |pmid=27507173 |doi=10.4187/respcare.04846 |url=|doi-access=free }} A noted difference between marijuana use and tobacco was that respiratory problems were resolved with stopping usage unlike the continued decline with stopping tobacco smoking. Respiratory symptoms reported with marijuana use included chronic cough, increased sputum production and wheezing but not shortness of breath. Also these symptoms were typically reported ten years ahead of their affecting tobacco smokers. Another study found that chronic marijuana smokers even with the additional use of tobacco developed similar respiratory problems, but did not seem to develop airflow limitation and COPD.{{cite journal |vauthors=Ribeiro LI, Ind PW |title=Effect of cannabis smoking on lung function and respiratory symptoms: a structured literature review |journal=npj Primary Care Respiratory Medicine |volume=26 |issue= |pages=16071 |date=October 2016 |pmid=27763599 |pmc=5072387 |doi=10.1038/npjpcrm.2016.71 |url=}}

{{Further|Energy poverty and cooking|Household air pollution}}

{{See also|Health effects of wood smoke}}

File:Access to clean fuels and technologies for cooking, OWID.svg and clean cooking facilities as of 2016{{cite web |title=Access to clean fuels and technologies for cooking |url=https://ourworldindata.org/grapher/access-to-clean-fuels-and-technologies-for-cooking |website=Our World in Data |access-date=15 February 2020}}]]

Exposure to particulates can bring about the development of COPD, or its exacerbations. Those with COPD are more susceptible to the harmful effects of particulate exposure that can cause acute exacerbations brought about by infections. Black carbon also known as soot, is an air pollutant associated with an increased risk of hospitalization due to the exacerbations caused. Long-term exposure is indicated as an increased rate of mortality in COPD. Studies have shown that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.{{cite journal | vauthors = Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM | title = Global burden of COPD: systematic review and meta-analysis | journal = The European Respiratory Journal | volume = 28 | issue = 3 | pages = 523–32 | date = September 2006 | pmid = 16611654 | doi = 10.1183/09031936.06.00124605 | doi-access = free }} Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD. Urban air pollution significantly effects the developing lung and its maturation, and contributes a potential risk factor for the later development of COPD. The overall effect in relation to smoking is believed to be small.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}}

Poorly ventilated fires used for cooking and heating, are often fueled by coal or biomass such as wood and dry dung, leading to indoor air pollution and are one of the most common causes of COPD in developing countries. Women are affected more as they have a greater exposure.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} These fuels are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.{{cite journal | vauthors = Pirozzi C, Scholand MB | title = Smoking cessation and environmental hygiene | journal = The Medical Clinics of North America | volume = 96 | issue = 4 | pages = 849–67 | date = July 2012 | pmid = 22793948 | doi = 10.1016/j.mcna.2012.04.014 }}

{{anchor|Occupational exposures}}

{{See also|Cadmium poisoning}}

Intense and prolonged exposure to workplace dusts, chemicals and fumes increases the risk of COPD in smokers, nonsmokers and never-smokers. Substances implicated in occupational exposure and listed in the UK, include organic and inorganic dusts such as cadmium, silica, dust from grains and flour and fumes from cadmium and welding that promote respiratory symptoms.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Workplace exposure is believed to be the cause in 10–20% of cases and in the United States, it is believed to be related to around 30% of cases among never smokers and probably represents a greater risk in countries without sufficient regulations.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}}{{cite book| vauthors = Hopper T |title=Mosby's Pharmacy Technician – E-Book: Principles and Practice|date=2014|publisher=Elsevier Health Sciences|isbn=978-0-323-29245-0|page=610|url=https://books.google.com/books?id=PtDsAwAAQBAJ&pg=PA610 }} The negative effects of dust exposure and cigarette smoke exposure appear to be cumulative.{{cite book | vauthors = Barnes PJ, Drazen JM, Rennard SI |year=2009 |chapter=Relationship between cigarette smoking and occupational exposures |chapter-url=https://books.google.com/books?id=HY9PiQL3kQMC&pg=PA464 | veditors = Barnes PJ, Drazen JM, Rennard SI, Thomson NC |title=Asthma and COPD: Basic Mechanisms and Clinical Management |publisher=Academic |isbn=978-0-12-374001-4 |page=464}}

Genetics play a role in the development of COPD. It is more common among relatives of those with COPD who smoke than unrelated smokers.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} The most well known genetic risk factor is alpha-1 antitrypsin deficiency (AATD) and this is the only genotype (genetic subtype) with a specific treatment.{{cite journal |vauthors=Silverman EK |title=Genetics of COPD |journal=Annu Rev Physiol |volume=82 |issue= |pages=413–431 |date=February 2020 |pmid=31730394 |pmc=7193187 |doi=10.1146/annurev-physiol-021317-121224 |url=}} This risk is particularly high if someone deficient in alpha-1 antitrypsin (AAT) also smokes.{{cite journal | vauthors = Foreman MG, Campos M, Celedón JC | title = Genes and chronic obstructive pulmonary disease | journal = The Medical Clinics of North America | volume = 96 | issue = 4 | pages = 699–711 | date = July 2012 | pmid = 22793939 | pmc = 3399759 | doi = 10.1016/j.mcna.2012.02.006 }} It is responsible for about 1–5% of cases{{cite journal | vauthors = Brode SK, Ling SC, Chapman KR | title = Alpha-1 antitrypsin deficiency: a commonly overlooked cause of lung disease | journal = CMAJ | volume = 184 | issue = 12 | pages = 1365–71 | date = September 2012 | pmid = 22761482 | pmc = 3447047 | doi = 10.1503/cmaj.111749 }} and the condition is present in about three to four in 10,000 people.{{cite book | vauthors = Reilly JJ, Silverman EK, Shapiro SD | chapter=Chronic Obstructive Pulmonary Disease | pages=2151–9 | veditors = Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J | year=2011 | title=Harrison's Principles of Internal Medicine | edition=18th | publisher=McGraw Hill | isbn=978-0-07-174889-6}}

Mutations in MMP1 gene that encodes for interstitial collagenase are associated with COPD.{{cite web |title=Home - Gene - NCBI |url=https://www.ncbi.nlm.nih.gov/gene |website=www.ncbi.nlm.nih.gov |access-date=17 July 2022}}

The COPDGene study is an ongoing longitudinal study into the epidemiology of COPD, identifying phenotypes and looking for their likely association with susceptible genes. Genome wide analyses in concert with the International COPD Genetics Consortium has identified more than 80 genome regions associated with COPD and further studies in these regions has been called for. Whole genome sequencing is an ongoing

collaboration (2019) with the National Heart, Lung and Blood Institute (NHLBI) to identify rare genetic determinants.{{cite journal | vauthors = Maselli DJ, Bhatt SP, Anzueto A, Bowler RP, DeMeo DL, Diaz AA, Dransfield MT, Fawzy A, Foreman MG, Hanania NA, Hersh CP, Kim V, Kinney GL, Putcha N, Wan ES, Wells JM, Westney GE, Young KA, Silverman EK, Han MK, Make BJ | display-authors = 6 | title = Clinical Epidemiology of COPD: Insights From 10 Years of the COPDGene Study | journal = Chest | volume = 156 | issue = 2 | pages = 228–238 | date = August 2019 | pmid = 31154041 | pmc = 7198872 | doi = 10.1016/j.chest.2019.04.135 }}

File:Copd 2010.jpgs shown in upper diagram. Lungs damaged by COPD in lower diagram with an inset showing a cross-section of bronchioles blocked by mucus and damaged alveoli.]]

COPD is a progressive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and an inability to breathe out fully (air trapping) exist.{{cite journal |vauthors=Capron T, Bourdin A, Perez T, Chanez P |title=COPD beyond proximal bronchial obstruction: phenotyping and related tools at the bedside |journal=Eur Respir Rev |volume=28 |issue=152 |date=June 2019 |page=190010 |pmid=31285287 |doi=10.1183/16000617.0010-2019 |pmc=9488991 |s2cid=195844108 |url=https://hal.archives-ouvertes.fr/hal-02180604/file/190010.full.pdf}} The poor airflow is the result of small airways disease and emphysema (the breakdown of lung tissue).{{cite book |title=Robbins basic pathology |date=2018 |publisher=Elsevier |isbn=978-0-323-35317-5 |pages=498–502 |edition=10th| vauthors = Kumar V, Abbas AK, Aster JC }} The relative contributions of these two factors vary between people.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Air trapping precedes lung hyperinflation.{{cite journal |vauthors=D'Ascanio M, Viccaro F, Calabrò N, Guerrieri G, Salvucci C, Pizzirusso D, etal |title=Assessing Static Lung Hyperinflation by Whole-Body Plethysmography, Helium Dilution, and Impulse Oscillometry System (IOS) in Patients with COPD |journal=Int J Chron Obstruct Pulmon Dis |volume=15 |issue= |pages=2583–9 |date=2020 |pmid=33116475 |pmc=7585810 |doi=10.2147/COPD.S264261 |url= |doi-access=free }}

COPD develops as a significant and chronic inflammatory response to inhaled irritants which ultimately leads to bronchial and alveolar remodelling in the lung known as small airways disease.{{cite journal |vauthors=Knox-Brown B, Patel J, Potts J, Ahmed R, Aquart-Stewart A, Cherkaski H, etal |title=Small airways obstruction and its risk factors in the Burden of Obstructive Lung Disease (BOLD) study: a multinational cross-sectional study |journal=Lancet Glob Health |volume=11 |issue=1 |pages=e69–e82 |date=January 2023 |pmid=36521955 |doi=10.1016/S2214-109X(22)00456-9 |hdl=10044/1/100800 |s2cid=254665705 |url=|hdl-access=free }}{{cite journal |vauthors = Knox-Brown B, Patel J, Potts J |display-authors=et al.|title=The association of spirometric small airways obstruction with respiratory symptoms, cardiometabolic diseases, and quality of life: results from the Burden of Obstructive Lung Disease (BOLD) study |journal=Respiratory Research |date=23 May 2023 |volume=24 |issue=1 |page=137 |doi=10.1186/s12931-023-02450-1|pmid=37221593 |pmc=10207810 |doi-access=free }}{{cite journal |last1=Knox-Brown |first1=Ben |last2=Potts |first2=James |last3=Santofimio |first3=Valentina Quintero |last4=Minelli |first4=Cosetta |last5=Patel |first5=Jaymini |last6=Abass |first6=Najlaa Mohammed |last7=Agarwal |first7=Dhiraj |last8=Ahmed |first8=Rana |last9=Mahesh |first9=Padukudru Anand |last10=Bs |first10=Jayaraj |last11=Denguezli |first11=Meriam |last12=Franssen |first12=Frits |last13=Gislason |first13=Thorarinn |last14=Janson |first14=Christer |last15=Juvekar |first15=Sanjay K |last16=Koul |first16=Parvaiz |last17=Malinovschi |first17=Andrei |last18=Nafees |first18=Asaad Ahmed |last19=Nielsen |first19=Rune |last20=Paraguas |first20=Stefanni Nonna M |last21=Buist |first21=Sonia |last22=Burney |first22=Peter GJ |last23=Amaral |first23=Andre F S |title=Isolated small airways obstruction predicts future chronic airflow obstruction: a multinational longitudinal study |journal=BMJ Open Respiratory Research |date=November 2023 |volume=10 |issue=1 |pages=e002056 |doi=10.1136/bmjresp-2023-002056|pmid=37989490 |pmc=10660204 |hdl=20.500.11815/4593 |hdl-access=free }} Thus, airway remodelling with narrowing of peripheral airway and emphysema are responsible for the alteration of lung function. Mucociliary clearance is particularly altered with a dysregulation of cilia and mucus production.{{cite journal | vauthors = Lo Bello F, Ieni A, Hansbro PM, Ruggeri P, Di Stefano A, Nucera F, Coppolino I, Monaco F, Tuccari G, Adcock IM, Caramori G | display-authors = 6 | title = Role of the mucins in pathogenesis of COPD: implications for therapy | journal = Expert Review of Respiratory Medicine | volume = 14 | issue = 5 | pages = 465–483 | date = May 2020 | pmid = 32133884 | doi = 10.1080/17476348.2020.1739525 | hdl-access = free | s2cid = 212416323 | hdl = 10453/139160 }} Small airway disease sometimes called chronic bronchiolitis, appears to be the precursor for the development of emphysema.

The inflammatory cells involved include neutrophils and macrophages, two types of white blood cells. Those who smoke additionally have cytotoxic T cell involvement and some people with COPD have eosinophil involvement similar to that in asthma. Part of this cell response is brought on by inflammatory mediators such as chemotactic factors. Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells and breakdown of the connective tissue of the lungs by proteases (particularly elastase) that are insufficiently inhibited by protease inhibitors. The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow and finally, poor absorption and release of respiratory gases. General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}}

File:Emphysema low mag.jpg showing emphysema (left – large empty spaces) and lung tissue with relative preserved alveoli (right)]]

Narrowing of the airways occurs due to inflammation and subsequent scarring within them. This contributes to the inability to breathe out fully. The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time.{{cite journal | vauthors = Calverley PM, Koulouris NG | title = Flow limitation and dynamic hyperinflation: key concepts in modern respiratory physiology | journal = The European Respiratory Journal | volume = 25 | issue = 1 | pages = 186–99 | date = January 2005 | pmid = 15640341 | doi = 10.1183/09031936.04.00113204 | doi-access = free }} This can result in more air from the previous breath remaining within the lungs when the next breath is started, resulting in an increase in the total volume of air in the lungs at any given time, a process called air trapping which is closely followed by hyperinflation.{{cite book| vauthors = Currie GP |title=ABC of COPD|year=2010|publisher=Wiley-Blackwell, BMJ Books|isbn=978-1-4443-2948-3|page=32|url=https://books.google.com/books?id=eEoYQA4QD_wC&pg=PA32|edition=2nd }} Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled.{{cite journal | vauthors = O'Donnell DE | s2cid = 20644418 | title = Hyperinflation, dyspnea, and exercise intolerance in chronic obstructive pulmonary disease | journal = Proceedings of the American Thoracic Society | volume = 3 | issue = 2 | pages = 180–4 | date = April 2006 | pmid = 16565429 | doi = 10.1513/pats.200508-093DO }} Hyperinflation may also worsen during an exacerbation.{{cite journal | vauthors = Cooper CB | title = The connection between chronic obstructive pulmonary disease symptoms and hyperinflation and its impact on exercise and function | journal = The American Journal of Medicine | volume = 119 | issue = 10 Suppl 1 | pages = 21–31 | date = October 2006 | pmid = 16996896 | doi = 10.1016/j.amjmed.2006.08.004 }} There may also be a degree of airway hyperresponsiveness to irritants similar to those found in asthma.

Low oxygen levels and eventually, high carbon dioxide levels in the blood, can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation and a reduced desire to breathe.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow and worsening of gas transfer. This can lead to low blood oxygen levels which if present for a prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to the breakdown of capillaries in the lungs. Both of these conditions may result in pulmonary heart disease also classically known as cor pulmonale.

File:DoingSpirometry.JPG. Smaller handheld devices are available for office use.]]

The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who has shortness of breath, a chronic cough, sputum production, or frequent winter colds and a history of exposure to risk factors for the disease. Spirometry is then used to confirm the diagnosis.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}{{cite web |title=Chronic obstructive pulmonary disease - NICE Pathways |url=https://pathways.nice.org.uk/pathways/chronic-obstructive-pulmonary-disease#path=view%3A/pathways/chronic-obstructive-pulmonary-disease/diagnosing-and-assessing-copd.xml&content=view-node%3Anodes-prognosis-and-severity-assessment |website=pathways.nice.org.uk | date=9 April 2020 |access-date=29 June 2021}}

Spirometry measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator, a medication to open up the airways. Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in the first second of a breath and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath.{{cite book| vauthors = Young VB |title=Blueprints medicine|year=2010|publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins|isbn=978-0-7817-8870-0|page=69|url=https://books.google.com/books?id=_DHtahEUgXcC&pg=PA69|edition=5th }} Normally, 75–80% of the FVC comes out in the first second and a FEV1/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease.{{cite journal | vauthors = Qaseem A, Wilt TJ, Weinberger SE, Hanania NA, Criner G, van der Molen T, Marciniuk DD, Denberg T, Schünemann H, Wedzicha W, MacDonald R, Shekelle P | display-authors = 6 | title = Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society | journal = Annals of Internal Medicine | volume = 155 | issue = 3 | pages = 179–191 | date = August 2011 | pmid = 21810710 | doi = 10.7326/0003-4819-155-3-201108020-00008 | s2cid = 18830625 }} Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly. The National Institute for Health and Care Excellence criteria additionally require a FEV1 less than 80% of predicted.{{NICE|101|Chronic Obstructive Pulmonary Disease|June 2010|60–70}} People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide due to decreased surface area in the alveoli, as well as damage to the capillary bed.{{cite journal | vauthors = Bailey KL | title = The importance of the assessment of pulmonary function in COPD | journal = The Medical Clinics of North America | volume = 96 | issue = 4 | pages = 745–752 | date = July 2012 | pmid = 22793942 | pmc = 3998207 | doi = 10.1016/j.mcna.2012.04.011 }} Testing the peak expiratory flow (the maximum speed of expiration), commonly used in asthma diagnosis, is not sufficient for the diagnosis of COPD.

Screening using spirometry in those without symptoms has uncertain effects and is generally not recommended; however, it is recommended for those without symptoms but with a known risk factor.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}}

A number of methods can be used to assess the effects and severity of COPD.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}} The MRC breathlessness scale or the COPD assessment test (CAT) are simple questionnaires that may be used.{{cite journal |vauthors=Williams N |title=The MRC breathlessness scale |journal=Occup Med (Lond) |volume=67 |issue=6 |pages=496–497 |date=August 2017 |pmid=28898975 |doi=10.1093/occmed/kqx086 |url=|doi-access=free }} GOLD refers to a modified MRC scale that if used, needs to include other tests since it is simply a test of breathlessness experienced.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}} Scores on CAT range from 0–40 with the higher the score, the more severe the disease.{{cite web |title=COPD Assessment Test (CAT) |url=http://www.thoracic.org/assemblies/srn/questionaires/copd.php |publisher=American Thoracic Society |access-date=November 29, 2013 |url-status=live |archive-url=https://web.archive.org/web/20131203054054/http://www.thoracic.org/assemblies/srn/questionaires/copd.php |archive-date=December 3, 2013 }} Spirometry may help to determine the severity of airflow limitation.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} This is typically based on the FEV1 expressed as a percentage of the predicted "normal" for the person's age, gender, height and weight.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} Guidelines published in 2011 by American and European medical societies recommend partly basing treatment recommendations on the FEV1. The GOLD guidelines group people into four categories based on symptoms assessment, degree of airflow limitation and history of exacerbations.{{cite web |title=Chronic obstructive pulmonary disease (COPD) - Criteria {{!}} BMJ Best Practice |url=https://bestpractice.bmj.com/topics/en-gb/7/criteria |website=bestpractice.bmj.com |access-date=2 July 2021}} Weight loss, muscle loss and fatigue are seen in severe and very severe cases.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}}

Use of screening questionnaires, such as COPD diagnostic questionnaire (CDQ), alone or in combination with hand-held flow meters is appropriate for screening of COPD in primary care.{{cite journal | vauthors = Tyagi J, Moola S, Bhaumik S | title = Diagnostic accuracy of screening tools for chronic obstructive pulmonary disease in primary health care: Rapid evidence synthesis | journal = Journal of Family Medicine and Primary Care | volume = 10 | issue = 6 | pages = 2184–2194 | date = June 2021 | pmid = 34322411 | pmc = 8284240 | doi = 10.4103/jfmpc.jfmpc_2263_20 | doi-access = free }}

A chest X-ray is not useful to establish a diagnosis of COPD but it is of use in either excluding other conditions or including comorbidities such as pulmonary fibrosis and bronchiectasis. Characteristic signs of COPD on X-ray include hyperinflation (shown by a flattened diaphragm and an increased retrosternal air space) and lung hyperlucency.{{sfn|Gold Report 2021|pp=33–35|loc=Chapter 2: Diagnosis and initial assessment}} A saber-sheath trachea may also be shown that is indicative of COPD.{{cite web |title=saber sheath trachea |url=https://radiopaedia.org/search?utf8=✓&q=saber+sheath+trachea&scope=all&lang=gb |website=Radiopaedia |access-date=13 August 2021}}

A CT scan is not routinely used except for the exclusion of bronchiectasis.{{sfn|Gold Report 2021|pp=33–35|loc=Chapter 2: Diagnosis and initial assessment}} Pulse oximetry measurement of peripheral oxygen saturation is recommended in people with clinical signs of respiratory failure or right heart failure.{{sfn|Gold Report 2021|pp=33–35|loc=Chapter 2: Diagnosis and initial assessment}} An analysis of arterial blood is recommended in those with a peripheral oxygen saturation of 92% or less to determine actual blood oxygen level and assess for high levels of carbon dioxide in the blood, which may have therapeutic implications such as need for non-invasive ventilation or oxygen supplementation. WHO recommends that all those diagnosed with COPD be screened for alpha-1 antitrypsin deficiency.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}}

File:COPD.JPG|alt=A black and white image, with a small white heart in the middle and large black lungs around it|Chest X-ray demonstrating severe COPD, displaying small heart size in comparison to the lungs

File:Barrowchest.JPG|A lateral chest X-ray of a person with emphysema, displaying barrel chest and flat diaphragm

File:BullaCXR.PNG|Lung bulla as seen on chest X-ray in a person with severe COPD

Medical X-Ray imaging WFH07 nevit.jpg|A severe case of bullous emphysema

File:Bullus emphasemaCT.png|Axial CT image of the lung of a person with end-stage bullous emphysema

File:EmphysemaPlusLungCA.png|Very severe emphysema with lung cancer on the left (CT scan)

COPD may need to be differentiated from other conditions such as congestive heart failure, asthma, bronchiectasis, tuberculosis, obliterative bronchiolitis and diffuse panbronchiolitis.{{sfn|Gold Report 2021|pp=33–35|loc=Chapter 2: Diagnosis and initial assessment}} The distinction between asthma and COPD is made on the basis of the symptoms, smoking history and whether airflow limitation is reversible with bronchodilators at spirometry.{{cite web|author1=BTS COPD Consortium|title=Spirometry in practice – a practical guide to using spirometry in primary care|url=https://www.brit-thoracic.org.uk/document-library/delivery-of-respiratory-care/spirometry/spirometry-in-practice/|access-date=25 August 2014|pages=8–9|year=2005|url-status=dead|archive-url=https://web.archive.org/web/20140826120148/https://www.brit-thoracic.org.uk/document-library/delivery-of-respiratory-care/spirometry/spirometry-in-practice/|archive-date=26 August 2014}} Chronic bronchitis with normal airflow is not classified as COPD.

Most cases of COPD are potentially preventable through decreasing exposure to tobacco smoke and other indoor and outdoor pollutants.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}}

{{See also|World No Tobacco Day}}

The policies of governments, public health agencies and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking. Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke and while many places have instituted bans, more are recommended.

In those who smoke, stopping smoking is the only measure shown to slow down the worsening of COPD.{{cite journal | vauthors = Jiménez-Ruiz CA, Fagerström KO | title = Smoking cessation treatment for COPD smokers: the role of counselling | journal = Monaldi Archives for Chest Disease| volume = 79 | issue = 1 | pages = 33–7 | date = March 2013 | pmid = 23741944 | doi = 10.4081/monaldi.2013.107 | doi-access = free }}{{Cite web|url=http://www.nice.org.uk/guidance/cg101/ifp/chapter/Chronic-obstructive-pulmonary-disease|title=Chronic obstructive pulmonary disease in over 16s: diagnosis and management {{!}} Guidance and guidelines {{!}} NICE|website=www.nice.org.uk|date=23 June 2010 |access-date=2018-06-05}} Even at a late stage of the disease, it can reduce the rate of worsening lung function and delay the onset of disability and death.{{cite book |vauthors=Kumar P, Clark M |title=Clinical Medicine |publisher=Elsevier Saunders |year=2005 |isbn=978-0-7020-2763-5 |pages=900–1 |edition=6th }} Often, several attempts are required before long-term abstinence is achieved.{{cite book |url=https://www.who.int/tobacco/resources/publications/tobacco_dependence/en/ |publisher=World Health Organization |title=Policy Recommendations for Smoking Cessation and Treatment of Tobacco Dependence |isbn=978-92-4-156240-9 |pages=15–40 |url-status=dead |archive-url=https://web.archive.org/web/20080915105015/http://www.who.int/tobacco/resources/publications/tobacco_dependence/en/ |archive-date=2008-09-15 |year=2003 }} Attempts over 5 years lead to success in nearly 40% of people.

Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive and many smokers need further support.{{cite web |title=Coping with cravings |url=https://www.nhs.uk/live-well/quit-smoking/stop-smoking-coping-with-cravings/ |website=nhs.uk |access-date=15 July 2021 |language=en |date=27 April 2018}} The chance of quitting is improved with social support, engagement in a smoking cessation program and the use of medications such as nicotine replacement therapy, bupropion, or varenicline.{{cite journal | vauthors = Tønnesen P | title = Smoking cessation and COPD | journal = European Respiratory Review | volume = 22 | issue = 127 | pages = 37–43 | date = March 2013 | pmid = 23457163 | doi = 10.1183/09059180.00007212 | pmc = 9487432 | doi-access = free }} Combining smoking-cessation medication with behavioral therapy is more than twice as likely to be effective in helping people with COPD stop smoking, compared with behavioral therapy alone.{{cite journal | vauthors = van Eerd EA, van der Meer RM, van Schayck OC, Kotz D | title = Smoking cessation for people with chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 8 | pages = CD010744 | date = August 2016 | volume = 2019 | pmid = 27545342 | doi = 10.1002/14651858.CD010744.pub2 | pmc = 6400424 }}

A number of measures have been taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction and stonemasonry—will develop COPD. Examples of these measures include the creation of public policy, education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators and dust control.{{cite book| vauthors = Smith BK, Timby NE |title=Essentials of nursing : care of adults and children|year=2005|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-5098-1|page=338|url=https://books.google.com/books?id=LJWDJMoStnMC&pg=PA338 }}{{cite book | veditors = Rom WN, Markowitz SB |title=Environmental and occupational medicine|year=2007|publisher=Wolters Kluwer/Lippincott Williams & Wilkins|isbn=978-0-7817-6299-1|pages=521–522|url=https://books.google.com/books?id=H4Sv9XY296oC&pg=PA521|edition=4th }} Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.{{cite web |url=http://www.hse.gov.uk/copd/casestudies/wetcut.htm |title=Wet cutting |publisher=Health and Safety Executive |access-date=November 29, 2013 |url-status=live |archive-url=https://web.archive.org/web/20131203004449/http://www.hse.gov.uk/copd/casestudies/wetcut.htm |archive-date=December 3, 2013 }} If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing their work role.{{cite book| vauthors = George RB |title=Chest medicine : essentials of pulmonary and critical care medicine |year=2005 |publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-5273-2 |page=172 |url= https://books.google.com/books?id=ZzlX2zJMbdgC&pg=PA172 |edition=5th }}

{{Further|Indoor air pollution in developing nations|Air pollution#Pollution control}}

Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease. This may be achieved by public policy efforts, cultural changes and personal involvement.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}} Many developed countries have successfully improved outdoor air quality through regulations which has resulted in improvements in the lung function of their populations. Individuals are also advised to avoid irritants of indoor and outdoor pollution.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}}

In developing countries one key effort is to reduce exposure to smoke from cooking and heating fuels through improved ventilation of homes and better stoves and chimneys.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}} Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is also effective. Using fuels such as kerosene or coal might produce less household particulate matter than traditional biomass such as wood or dung, but whether this is better health wise is unclear.

COPD currently has no cure,{{cite web|url=https://www.nhs.uk/conditions/chronic-obstructive-pulmonary-disease-copd/treatment/|title=Chronic obstructive pulmonary disease (COPD) - Treatment - NHS|date=20 October 2017 }} but the symptoms are treatable and its progression can be delayed, particularly by stopping smoking.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} The major goals of management are to reduce exposure to risk factors including offering non-pharmacological treatments such as help with stopping smoking. Stopping smoking can reduce the rate of lung function decline and also reduce mortality from smoking-related diseases such as lung cancer and cardiovascular disease.{{cite web |title=Chronic obstructive pulmonary disease |url=https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/ |website=nice.org |access-date=5 July 2021}} Other recommendations include pneumococcal vaccination and yearly influenza vaccination to help reduce the risk of exacerbations; as of 2024 CDC and GOLD also recommend RSV vaccine for individuals above 60 years.{{Cite web |last=CDC |date=2024-01-18 |title=RSV information for healthcare providers |url=https://www.cdc.gov/rsv/clinical/index.html |access-date=2024-02-23 |website=Centers for Disease Control and Prevention |language=en-us}} giving advice as to healthy eating and encouraging physical exercise. Guidance is also advised as to managing breathlessness and stress.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Other illnesses are also being managed. An action plan is drawn up and is to be reviewed.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}} Providing people with a personalized action plan, an educational session and support for use of their action plan in the event of an exacerbation, reduces the number of hospital visits and encourages early treatment of exacerbations.{{cite journal | vauthors = Howcroft M, Walters EH, Wood-Baker R, Walters JA | title = Action plans with brief patient education for exacerbations in chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 12 | pages = CD005074 | date = December 2016 | pmid = 27990628 | pmc = 6463844 | doi = 10.1002/14651858.CD005074.pub4 }} When self-management interventions, such as taking corticosteroids and using supplemental oxygen, is combined with action plans, health-related quality of life is improved compared to usual care.{{cite journal | vauthors = Lenferink A, Brusse-Keizer M, van der Valk PD, Frith PA, Zwerink M, Monninkhof EM, van der Palen J, Effing TW | display-authors = 6 | title = Self-management interventions including action plans for exacerbations versus usual care in patients with chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2017 | issue = 8 | pages = CD011682 | date = August 2017 | pmid = 28777450 | pmc = 6483374 | doi = 10.1002/14651858.CD011682.pub2 }} In those with COPD who are malnourished, supplementation with vitamin C, vitamin E, zinc and selenium can improve weight, strength of respiratory muscles and health-related quality of life.{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Significant vitamin D deficiency is common in those with COPD and can cause increased exacerbations. Supplementation when deficient can give a 50% reduction in the number of exacerbations.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}{{cite journal | vauthors = Jolliffe DA, Greenberg L, Hooper RL, Mathyssen C, Rafiq R, de Jongh RT, Camargo CA, Griffiths CJ, Janssens W, Martineau AR | display-authors = 6 | title = Vitamin D to prevent exacerbations of COPD: systematic review and meta-analysis of individual participant data from randomised controlled trials | journal = Thorax | volume = 74 | issue = 4 | pages = 337–345 | date = April 2019 | pmid = 30630893 | doi = 10.1136/thoraxjnl-2018-212092 | doi-access = free }}

A number of medical treatments are used in the management of stable COPD and exacerbations. These include bronchodilators, corticosteroids and antibiotics.

In those with a severe exacerbation, antibiotics improve outcomes.{{cite journal | vauthors = Vollenweider DJ, Frei A, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA | title = Antibiotics for exacerbations of chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD010257 | date = October 2018 | issue = 10 | pmid = 30371937 | pmc = 6517133 | doi = 10.1002/14651858.CD010257.pub2 }} A number of different antibiotics may be used including amoxicillin, doxycycline and azithromycin; whether one is better than the others is unclear.{{cite journal | vauthors = Mackay AJ, Hurst JR | title = COPD exacerbations: causes, prevention, and treatment | journal = The Medical Clinics of North America | volume = 96 | issue = 4 | pages = 789–809 | date = July 2012 | pmid = 22793945 | doi = 10.1016/j.mcna.2012.02.008 }} There is no clear evidence of improved outcomes for those with less severe cases. The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.{{cite web|title=Fluoroquinolone Antibacterial Drugs: Drug Safety Communication – FDA Advises Restricting Use for Certain Uncomplicated Infections|url=https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm500665.htm|website=FDA|access-date=16 May 2016|date=12 May 2016|url-status=live|archive-url=https://web.archive.org/web/20160516004228/https://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm500665.htm|archive-date=16 May 2016}}

In treating acute hypercapnic respiratory failure (acutely raised levels of carbon dioxide), bilevel positive airway pressure (BPAP) can decrease mortality and the need of intensive care.{{cite journal | vauthors = Decramer M, Janssens W, Miravitlles M | title = Chronic obstructive pulmonary disease | journal = Lancet | volume = 379 | issue = 9823 | pages = 1341–51 | date = April 2012 | pmid = 22314182 | doi = 10.1016/S0140-6736(11)60968-9 | pmc = 7172377 | citeseerx = 10.1.1.1000.1967 }}

In those with end-stage disease, palliative care is focused on relieving symptoms.{{cite journal | vauthors = Oliveira EP, Medeiros Junior P | title = Palliative care in pulmonary medicine | language = Portuguese | journal = Jornal Brasileiro de Pneumologia | volume = 46 | issue = 3 | pages = e20190280 | date = 2020 | pmid = 32638839 | pmc = 7572288 | doi = 10.36416/1806-3756/e20190280 }} Morphine can improve exercise tolerance.{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Non-invasive ventilation may be used to support breathing and also reduce daytime breathlessness.{{cite journal | vauthors = Wilson ME, Dobler CC, Morrow AS, Beuschel B, Alsawas M, Benkhadra R, Seisa M, Mittal A, Sanchez M, Daraz L, Holets S, Murad MH, Wang Z | display-authors = 6 | title = Association of Home Noninvasive Positive Pressure Ventilation With Clinical Outcomes in Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-analysis | journal = JAMA | volume = 323 | issue = 5 | pages = 455–465 | date = February 2020 | pmid = 32016309 | pmc = 7042860 | doi = 10.1001/jama.2019.22343 }}{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Inhaled short-acting bronchodilators are the primary medications used on an as needed basis; their use on a regular basis is not recommended.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} The two major types are beta2-adrenergic agonists and anticholinergics; either in long-acting or short-acting forms. Beta2–adrenergic agonists target receptors in the smooth muscle cells in bronchioles causing them to relax and allow improved airflow. They reduce shortness of breath, tend to reduce dynamic hyperinflation and improve exercise tolerance.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}{{cite journal | vauthors = Almadhoun K, Sharma S |title=Bronchodilators |url=https://www.ncbi.nlm.nih.gov/books/NBK519028/ |website=StatPearls |publisher=StatPearls Publishing |access-date=27 July 2021 |date=2021|pmid=30085570 }} Short-acting bronchodilators have an effect for four hours and for maintenance therapy long acting bronchodilators with an effect of over twelve hours are used. In times of more severe symptoms a short acting agent may be used in combination.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} An inhaled corticosteroid used with a long-acting beta-2 agonist is more effective than either one on its own.{{sfn|Gold Report 2021|pp=48–52|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Which type of long-acting agent, long-acting muscarinic antagonist (LAMA) such as tiotropium or long-acting beta agonist (LABA), is better is unclear and trying each and continuing with the one that works best may be advisable.{{cite journal|vauthors=Farne HA, Cates CJ|date=October 2015|title=Long-acting beta2-agonist in addition to tiotropium versus either tiotropium or long-acting beta2-agonist alone for chronic obstructive pulmonary disease|url=http://openaccess.sgul.ac.uk/2674/1/CD008989.pdf|journal=The Cochrane Database of Systematic Reviews|volume=2015 |issue=10|pages=CD008989|doi=10.1002/14651858.CD008989.pub3|pmc=4164463|pmid=26490945}} Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. The combination of LABA/LAMA may reduce COPD exacerbations and improve quality-of-life compared to long-acting bronchodilators alone.{{cite journal | vauthors = Oba Y, Keeney E, Ghatehorde N, Dias S | title = Dual combination therapy versus long-acting bronchodilators alone for chronic obstructive pulmonary disease (COPD): a systematic review and network meta-analysis | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD012620 | date = December 2018 | issue = 12 | pmid = 30521694 | pmc = 6517098 | doi = 10.1002/14651858.CD012620.pub2 | collaboration = Cochrane Airways Group }} The 2018 NICE guideline recommends use of dual long-acting bronchodilators with economic modelling suggesting that this approach is preferable to starting one long acting bronchodilator and adding another later.{{cite web |title=Chronic obstructive pulmonary disease in over 16s: diagnosis and management |url=https://www.nice.org.uk/guidance/ng115/chapter/Recommendations |website=www.nice.org.uk |date=5 December 2018 |access-date=1 August 2021}}

Several short-acting β₂ agonists are available, including salbutamol (albuterol) and terbutaline.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} They provide relief of symptoms for four to six hours.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} A long-acting beta agonist (LABA) such as salmeterol, formoterol and indacaterol are often used as maintenance therapy, with a duration of action of 12 to 24 hours.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Some feel the evidence of benefits is limited,{{cite journal | vauthors = Cave AC, Hurst MM | title = The use of long acting β₂-agonists, alone or in combination with inhaled corticosteroids, in chronic obstructive pulmonary disease (COPD): a risk-benefit analysis | journal = Pharmacology & Therapeutics | volume = 130 | issue = 2 | pages = 114–143 | date = May 2011 | pmid = 21276815 | doi = 10.1016/j.pharmthera.2010.12.008 }} while others view the evidence of benefit as established.{{cite journal | vauthors = Spencer S, Karner C, Cates CJ, Evans DJ | title = Inhaled corticosteroids versus long-acting beta(2)-agonists for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 12 | pages = CD007033 | date = December 2011 | volume = 2011 | pmid = 22161409 | pmc = 6494276 | doi = 10.1002/14651858.CD007033.pub3 | veditors = Spencer S }}{{cite journal | vauthors = Wang J, Nie B, Xiong W, Xu Y | title = Effect of long-acting beta-agonists on the frequency of COPD exacerbations: a meta-analysis | journal = Journal of Clinical Pharmacy and Therapeutics | volume = 37 | issue = 2 | pages = 204–211 | date = April 2012 | pmid = 21740451 | doi = 10.1111/j.1365-2710.2011.01285.x | s2cid = 45383688 | doi-access = free }}{{cite journal | vauthors = Geake JB, Dabscheck EJ, Wood-Baker R, Cates CJ | title = Indacaterol, a once-daily beta2-agonist, versus twice-daily beta₂-agonists or placebo for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 1 | issue = 3 | pages = CD010139 | date = January 2015 | pmid = 25575340 | pmc = 6464646 | doi = 10.1002/14651858.CD010139.pub2 }} Long-term use of LABAs appears safe in COPD,{{cite journal | vauthors = Decramer ML, Hanania NA, Lötvall JO, Yawn BP | title = The safety of long-acting β2-agonists in the treatment of stable chronic obstructive pulmonary disease | journal = International Journal of Chronic Obstructive Pulmonary Disease | volume = 8 | pages = 53–64 | year = 2013 | pmid = 23378756 | pmc = 3558319 | doi = 10.2147/COPD.S39018 | doi-access = free }} with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks.{{cite journal | vauthors = Nannini LJ, Lasserson TJ, Poole P | title = Combined corticosteroid and long-acting beta(2)-agonist in one inhaler versus long-acting beta(2)-agonists for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 9 | issue = 9 | pages = CD006829 | date = September 2012 | pmid = 22972099 | pmc = 4170910 | doi = 10.1002/14651858.CD006829.pub2 | veditors = Nannini LJ }} There is some evidence that combined treatment of LABAs with long-acting muscarinic antagonists (LAMA), an anticholinergic, and LABA +ICS (inhaled corticosteroid) may be similar in benefits in terms of fewer exacerbation's and quality of life measures for moderate to severe COPD, but LAMA+LABA offers better improvements in forced expiratory volume (FEV1%) and a lower risk of pneumonia.{{Cite journal |last1=Fukuda |first1=Nobuhiko |last2=Horita |first2=Nobuyuki |last3=Kaneko |first3=Ayami |last4=Goto |first4=Atsushi |last5=Kaneko |first5=Takeshi |last6=Ota |first6=Erika |last7=Kew |first7=Kayleigh M. |date=2023-06-05 |title=Long-acting muscarinic antagonist (LAMA) plus long-acting beta-agonist (LABA) versus LABA plus inhaled corticosteroid (ICS) for stable chronic obstructive pulmonary disease |journal=The Cochrane Database of Systematic Reviews |volume=2023 |issue=6 |pages=CD012066 |doi=10.1002/14651858.CD012066.pub3 |issn=1469-493X |pmc=10241721 |pmid=37276335 }} All three together, LABA, LAMA and ICS, have some evidence of benefits.{{cite journal | vauthors = Zheng Y, Zhu J, Liu Y, Lai W, Lin C, Qiu K, Wu J, Yao W | display-authors = 6 | title = Triple therapy in the management of chronic obstructive pulmonary disease: systematic review and meta-analysis | journal = BMJ | volume = 363 | pages = k4388 | date = November 2018 | pmid = 30401700 | pmc = 6218838 | doi = 10.1136/bmj.k4388 }} Indacaterol requires an inhaled dose once a day and is as effective as the other long-acting β₂ agonist drugs that require twice-daily dosing for people with stable COPD.

The two main anticholinergics used in COPD are ipratropium and tiotropium. Ipratropium is a short-acting muscarinic antagonist (SAMA), while tiotropium is long-acting muscarinic antagonist (LAMA). Tiotropium is associated with a decrease in exacerbations and improved quality of life,{{cite journal | vauthors = Karner C, Chong J, Poole P | title = Tiotropium versus placebo for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 7 | pages = CD009285 | date = July 2014 | volume = 2016 | pmid = 25046211 | doi = 10.1002/14651858.CD009285.pub3 | pmc = 8934583 }} and tiotropium provides those benefits better than ipratropium.{{cite journal | vauthors = Cheyne L, Irvin-Sellers MJ, White J | title = Tiotropium versus ipratropium bromide for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 9 | pages = CD009552 | date = September 2015 | volume = 2015 | pmid = 26391969 | doi = 10.1002/14651858.CD009552.pub3 | pmc = 8749963 }} Tiotropium does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke.{{cite journal | vauthors = Singh S, Loke YK, Enright P, Furberg CD | title = Pro-arrhythmic and pro-ischaemic effects of inhaled anticholinergic medications | journal = Thorax | volume = 68 | issue = 1 | pages = 114–6 | date = January 2013 | pmid = 22764216 | doi = 10.1136/thoraxjnl-2011-201275 | doi-access = free }} Aclidinium, another long-acting agent, reduces hospitalizations associated with COPD and improves quality of life.{{cite journal | vauthors = Jones P | title = Aclidinium bromide twice daily for the treatment of chronic obstructive pulmonary disease: a review | journal = Advances in Therapy | volume = 30 | issue = 4 | pages = 354–68 | date = April 2013 | pmid = 23553509 | doi = 10.1007/s12325-013-0019-2 | s2cid = 3530290 }}{{cite journal | vauthors = Cazzola M, Page CP, Matera MG | title = Aclidinium bromide for the treatment of chronic obstructive pulmonary disease | journal = Expert Opinion on Pharmacotherapy | volume = 14 | issue = 9 | pages = 1205–14 | date = June 2013 | pmid = 23566013 | doi = 10.1517/14656566.2013.789021 | s2cid = 24973904 }}{{cite journal | vauthors = Ni H, Soe Z, Moe S | title = Aclidinium bromide for stable chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 9 | issue = 9 | pages = CD010509 | date = September 2014 | pmid = 25234126 | doi = 10.1002/14651858.CD010509.pub2 | pmc = 8922974 }} The LAMA umeclidinium bromide is another anticholinergic alternative.{{cite journal | vauthors = Ni H, Htet A, Moe S | title = Umeclidinium bromide versus placebo for people with chronic obstructive pulmonary disease (COPD) | journal = The Cochrane Database of Systematic Reviews | volume = 2017 | pages = CD011897 | date = June 2017 | issue = 6 | pmid = 28631387 | doi = 10.1002/14651858.CD011897.pub2 | pmc = 6481854 }} When compared to tiotropium, the LAMAs aclidinium, glycopyrronium, and umeclidinium appear to have a similar level of efficacy; with all four being more effective than placebo.{{cite journal | vauthors = Ismaila AS, Huisman EL, Punekar YS, Karabis A | title = Comparative efficacy of long-acting muscarinic antagonist monotherapies in COPD: a systematic review and network meta-analysis | journal = International Journal of Chronic Obstructive Pulmonary Disease | volume = 10 | pages = 2495–517 | date = 2015 | pmid = 26604738 | pmc = 4655912 | doi = 10.2147/COPD.S92412 | doi-access = free }} Further research is needed comparing aclidinium to tiotropium.

Inhaled corticosteroids are anti-inflammatories that are recommended by GOLD as a first-line maintenance treatment in COPD cases with repeated exacerbations.{{cite journal |vauthors=Chen H, Sun J, Huang Q, Liu Y, Yuan M, Ma C, et al |title=Inhaled Corticosteroids and the Pneumonia Risk in Patients With Chronic Obstructive Pulmonary Disease: A Meta-analysis of Randomized Controlled Trials |journal=Front Pharmacol |volume=12 |issue= |pages=691621 |date=2021 |pmid=34267661 |pmc=8275837 |doi=10.3389/fphar.2021.691621 |url=|doi-access=free }}{{cite journal | vauthors = Chinet T, Dumoulin J, Honore I, Braun JM, Couderc LJ, Febvre M, etal | title = [The place of inhaled corticosteroids in COPD] | journal = Revue des Maladies Respiratoires | volume = 33 | issue = 10 | pages = 877–891 | date = December 2016 | pmid = 26831345 | doi = 10.1016/j.rmr.2015.11.009 }} Their regular use increases the risk of pneumonia in severe cases.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}} Studies have shown that the risk of pneumonia is associated with all types of corticosteroids; is related to the disease severity and a dose-response relationship has been noted. Oral glucocorticoids can be effective in treating an acute exacerbation.{{sfn|Gold Report 2021|pp=48–52|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} They appear to have fewer side effects than those given intravenously.{{cite journal | vauthors = Walters JA, Tan DJ, White CJ, Gibson PG, Wood-Baker R, Walters EH | title = Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2014 | issue = 9 | pages = CD001288 | date = September 2014 | pmid = 25178099 | doi = 10.1002/14651858.CD001288.pub4 | doi-access = free | pmc = 11195634 }} Five days of steroids work as well as ten or fourteen days.{{cite journal | vauthors = Walters JA, Tan DJ, White CJ, Wood-Baker R | title = Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD006897 | date = March 2018 | issue = 3 | pmid = 29553157 | doi = 10.1002/14651858.CD006897.pub4 | pmc = 6494402 }}

The use of corticosteroids is associated with a decrease in the number of lymphoid follicles (in the bronchial lymphoid tissue).{{cite journal |vauthors=Higham A, Quinn AM, Cançado JE, Singh D |title=The pathology of small airways disease in COPD: historical aspects and future directions |journal=Respir Res |volume=20 |issue=1 |pages=49 |date=March 2019 |pmid=30832670 |pmc=6399904 |doi=10.1186/s12931-019-1017-y |url= |doi-access=free }} A triple inhaled therapy of LABA/LAMA/ICS improves lung function, reduces symptoms and exacerbations and is seen to be more effective than mono or dual therapies.{{Cite journal |last1=van Geffen |first1=Wouter H. |last2=Tan |first2=Daniel J. |last3=Walters |first3=Julia A.E. |last4=Walters |first4=E. Haydn |date=2023-12-06 |editor-last=Cochrane Airways Group |title=Inhaled corticosteroids with combination inhaled long-acting beta2-agonists and long-acting muscarinic antagonists for chronic obstructive pulmonary disease |journal=Cochrane Database of Systematic Reviews |volume=2023 |issue=12 |pages=CD011600 |doi=10.1002/14651858.CD011600.pub3 |pmc=10698842 |pmid=38054551}}{{sfn|Gold Report 2021|pp=48–52|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} NICE guidelines recommend the use of ICSs in people with asthmatic features or features suggesting steroid responsiveness.

Phosphodiesterase-4 inhibitors (PDE4 inhibitors) are anti-inflammatories that improve lung function and reduce exacerbations in moderate to severe illness. Roflumilast is a PDE4 inhibitor used orally once daily to reduce inflammation, it has no direct bronchodilatory effects. It is essentially used in treating those with chronic bronchitis along with systemic corticosteroids.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Reported adverse effects of roflumilast appear early in treatment, become less with continued treatment and are reversible. One effect is dramatic weight loss and its use is to be avoided in underweight people. It is also advised to be used with caution in those who have depression.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Long-term preventive use of antibiotics, specifically those from the macrolide class such as erythromycin, reduce the frequency of exacerbations in those who have two or more a year.{{cite journal | vauthors = Mammen MJ, Sethi S | s2cid = 35183033 | title = Macrolide therapy for the prevention of acute exacerbations in chronic obstructive pulmonary disease | journal = Polskie Archiwum Medycyny Wewnetrznej | volume = 122 | issue = 1–2 | pages = 54–9 | year = 2012 | pmid = 22353707 | doi=10.20452/pamw.1134}}{{cite journal | vauthors = Herath SC, Normansell R, Maisey S, Poole P | title = Prophylactic antibiotic therapy for chronic obstructive pulmonary disease (COPD) | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | pages = CD009764 | date = October 2018 | issue = 10 | pmid = 30376188 | pmc = 6517028 | doi = 10.1002/14651858.CD009764.pub3 }} This practice may be cost effective in some areas of the world.{{cite journal | vauthors = Simoens S, Laekeman G, Decramer M | title = Preventing COPD exacerbations with macrolides: a review and budget impact analysis | journal = Respiratory Medicine | volume = 107 | issue = 5 | pages = 637–48 | date = May 2013 | pmid = 23352223 | doi = 10.1016/j.rmed.2012.12.019 | doi-access = free }} Concerns include the potential for antibiotic resistance and side effects including hearing loss, tinnitus and changes to the heart rhythm known as long QT syndrome.

Methylxanthines such as theophylline are widely used. Theophylline is seen to have a mild bronchodilatory effect in stable COPD. Inspiratory muscle function is seen to be improved but the causal effect is unclear. Theophylline is seen to improve breathlessness when used as an add-on to salmeterol. All instances of improvement have been reported using sustained release preparations.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Methylxanthines are not recommended for use in exacerbations due to adverse effects.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

Mucolytics may help to reduce exacerbations in some people with chronic bronchitis; noticed by less hospitalization and less days of disability in one month.{{cite journal | vauthors = Poole P, Sathananthan K, Fortescue R | title = Mucolytic agents versus placebo for chronic bronchitis or chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 5 | pages = CD001287 | date = May 2019 | issue = 3 | pmid = 31107966 | pmc = 6527426 | doi = 10.1002/14651858.CD001287.pub6 }} Erdosteine is recommended by NICE.{{cite web |title=Erdosteine |url=https://bnf.nice.org.uk/drug/erdosteine.html |website=NICE |access-date=20 July 2021}} GOLD also supports the use of some mucolytics that are advised against when inhaled corticosteroids are being used and singles out erdosteine as having good effects regardless of corticosteroid use. Erdosteine also has antioxidant properties but there is not enough evidence to support the general use of antioxidants.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Erdosteine has been shown to significantly reduce the risk of exacerbations, shorten their duration and hospital stays.{{cite journal |vauthors=Meldrum OW, Chotirmall SH |title=Mucus, Microbiomes and Pulmonary Disease |journal=Biomedicines |volume=9 |issue=6 |date=June 2021 |page=675 |pmid=34199312 |pmc=8232003 |doi=10.3390/biomedicines9060675 |url=|doi-access=free }}

Cough medicines are not recommended.{{cite web |title=Bronchitis |url=https://www.nhs.uk/conditions/bronchitis/ |website=nhs.uk |language=en |date=17 October 2017}} Beta blockers are not contraindicated for those with COPD and should only be used where there is concomitant cardiovascular disease.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

Recent studies show that metformin plays a role in reducing systemic inflammation by reducing biomarker levels that are increased during COPD exacerbations.{{cite journal |vauthors=Zhu A, Teng Y, Ge D, Zhang X, Hu M, Yao X |date=October 2019|title=Role of metformin in treatment of patients with chronic obstructive pulmonary disease: a systematic review |journal=Journal of Thoracic Disease |volume=11 |issue=10 |pages=4371–4378 |doi=10.21037/jtd.2019.09.84 |pmid=31737323 |pmc=6837976 |url=|doi-access=free }}

{{Further|Effect of oxygen on chronic obstructive pulmonary disease}}

Supplemental oxygen is recommended for those with low oxygen levels in respiratory failure at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%).{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} When taking into account complications including cor pulmonale and pulmonary hypertension, the levels involved are 56–59 mmHg.{{cite journal |vauthors=Khor YH, Renzoni EA, Visca D, McDonald CF, Goh NS |title=Oxygen therapy in COPD and interstitial lung disease: navigating the knowns and unknowns |journal=ERJ Open Res |volume=5 |issue=3 |pages= |date=July 2019 |pmid=31544111 |pmc=6745413 |doi=10.1183/23120541.00118-2019 |url=}} Oxygen therapy is to be used for between 15 and 18 hours per day and is said to decrease the risk of heart failure and death. In those with normal or mildly low oxygen levels, oxygen supplementation (ambulatory) may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life.{{cite journal | vauthors = Ekström M, Ahmadi Z, Bornefalk-Hermansson A, Abernethy A, Currow D | title = Oxygen for breathlessness in patients with chronic obstructive pulmonary disease who do not qualify for home oxygen therapy | journal = The Cochrane Database of Systematic Reviews | volume = 11 | pages = CD006429 | date = November 2016 | issue = 8 | pmid = 27886372 | pmc = 6464154 | doi = 10.1002/14651858.CD006429.pub3 }} During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes.{{cite book| vauthors = Jindal SK |title=Chronic Obstructive Pulmonary Disease|year=2013|publisher=Jaypee Brothers Medical|isbn=978-93-5090-353-7 |page=139| url= https://books.google.com/books?id=PTgIAQAAQBAJ&pg=PA139 }}{{cite journal | vauthors = O'Driscoll BR, Howard LS, Davison AG | title = BTS guideline for emergency oxygen use in adult patients | journal = Thorax | volume = 63 | issue = 6 | pages = vi1-68 | date = October 2008 | pmid = 18838559 | doi = 10.1136/thx.2008.102947 | author4 = British Thoracic, Society | doi-access = free }} In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%. Once prescribed long-term oxygen therapy, patients should be re-assessed after 60 to 90 days, to determine whether supplemental oxygen is still indicated and if prescribed supplemental oxygen is effective.{{Cite journal |last=Venkatesan |first=Priya |date=January 2024 |title=GOLD COPD report: 2024 update |url=https://linkinghub.elsevier.com/retrieve/pii/S2213260023004617 |journal=The Lancet Respiratory Medicine |language=en |volume=12 |issue=1 |pages=15–16 |doi=10.1016/S2213-2600(23)00461-7|pmid=38061380 |s2cid=265751322 }}

Pulmonary rehabilitation is a program of exercise, disease management and counseling, coordinated to benefit the individual.{{cite web |title=Pulmonary Rehabilitation |url=https://medlineplus.gov/pulmonaryrehabilitation.html |website=medlineplus.gov |access-date=9 September 2021}} A severe exacerbation leads to hospital admission, high mortality and a decline in the ability to carry out daily activities. Following a hospital admission pulmonary rehabilitation has been shown to significantly reduce future hospital admissions, mortality and improve quality of life.{{cite journal |vauthors=Halpin DM, Miravitlles M, Metzdorf N, Celli B |title=Impact and prevention of severe exacerbations of COPD: a review of the evidence |journal=Int J Chron Obstruct Pulmon Dis |volume=12 |issue= |pages=2891–2908 |date=2017 |pmid=29062228 |pmc=5638577 |doi=10.2147/COPD.S139470 |url= |doi-access=free }}

The optimal exercise routine, use of noninvasive ventilation during exercise and intensity of exercise suggested for people with COPD, is unknown.{{cite journal | vauthors = McNamara RJ, McKeough ZJ, McKenzie DK, Alison JA | title = Water-based exercise training for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 12 | pages = CD008290 | date = December 2013 | pmid = 24353107 | doi = 10.1002/14651858.CD008290.pub2 }}{{cite journal | vauthors = Menadue C, Piper AJ, van 't Hul AJ, Wong KK | title = Non-invasive ventilation during exercise training for people with chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 5 | pages = CD007714 | date = May 2014 | volume = 2014 | pmid = 24823712 | doi = 10.1002/14651858.CD007714.pub2 | pmc = 10984247 }} Performing endurance arm exercises improves arm movement for people with COPD and may result in a small improvement in breathlessness. Performing arm exercises alone does not appear to improve quality of life.{{cite journal | vauthors = McKeough ZJ, Velloso M, Lima VP, Alison JA | title = Upper limb exercise training for COPD | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | pages = CD011434 | date = November 2016 | issue = 11 | pmid = 27846347 | doi = 10.1002/14651858.CD011434.pub2 | pmc = 6464968 }} Pursed-lip breathing exercises may be useful. Tai chi exercises appear to be safe to practice for people with COPD and may be beneficial for pulmonary function and pulmonary capacity when compared to a regular treatment program. Tai Chi was not found to be more effective than other exercise intervention programs.{{cite journal | vauthors = Ngai SP, Jones AY, Tam WW | title = Tai Chi for chronic obstructive pulmonary disease (COPD) | journal = The Cochrane Database of Systematic Reviews | issue = 6 | pages = CD009953 | date = June 2016 | volume = 2016 | pmid = 27272131 | doi = 10.1002/14651858.CD009953.pub2 | pmc = 8504989 }} Inspiratory and expiratory muscle training (IMT, EMT) have been suggested and may provide some improvements when compared to no treatment.{{Cite journal |last1=Ammous |first1=Omar |last2=Feki |first2=Walid |last3=Lotfi |first3=Tamara |last4=Khamis |first4=Assem M |last5=Gosselink |first5=Rik |last6=Rebai |first6=Ahmed |last7=Kammoun |first7=Samy |date=2023-01-06 |editor-last=Cochrane Airways Group |title=Inspiratory muscle training, with or without concomitant pulmonary rehabilitation, for chronic obstructive pulmonary disease (COPD) |url= |journal=Cochrane Database of Systematic Reviews |language=en |volume=2023 |issue=1 |pages=CD013778 |doi=10.1002/14651858.CD013778.pub2 |pmc=9817429 |pmid=36606682}} A combination of IMT and walking exercises at home may help limit breathlessness in cases of severe COPD.{{cite journal | vauthors = Thomas MJ, Simpson J, Riley R, Grant E | title = The impact of home-based physiotherapy interventions on breathlessness during activities of daily living in severe COPD: a systematic review | journal = Physiotherapy | volume = 96 | issue = 2 | pages = 108–19 | date = June 2010 | pmid = 20420957 | doi = 10.1016/j.physio.2009.09.006 }} Additionally, the use of low amplitude high velocity joint mobilization together with exercise improves lung function and exercise capacity.{{cite journal | vauthors = Wearing J, Beaumont S, Forbes D, Brown B, Engel R | title = The Use of Spinal Manipulative Therapy in the Management of Chronic Obstructive Pulmonary Disease: A Systematic Review | journal = Journal of Alternative and Complementary Medicine | volume = 22 | issue = 2 | pages = 108–14 | date = February 2016 | pmid = 26700633 | pmc = 4761829 | doi = 10.1089/acm.2015.0199 }} The goal of spinal manipulation therapy is to improve thoracic mobility in an effort to reduce the work on the lungs during respiration, however, the evidence supporting manual therapy for people with COPD is very weak.{{cite journal | vauthors = Simonelli C, Vitacca M, Vignoni M, Ambrosino N, Paneroni M | title = Effectiveness of manual therapy in COPD: A systematic review of randomised controlled trials | journal = Pulmonology | volume = 25 | issue = 4 | pages = 236–247 | date = 2019 | pmid = 30738792 | doi = 10.1016/j.pulmoe.2018.12.008 | doi-access = free }}

Airway clearance techniques (ACTs), such as postural drainage, percussion/vibration, autogenic drainage, hand-held positive expiratory pressure (PEP) devices and other mechanical devices, may reduce the need for increased ventilatory assistance, the duration of ventilatory assistance and the length of hospital stay in people with acute COPD.{{cite journal | vauthors = Osadnik CR, McDonald CF, Jones AP, Holland AE | title = Airway clearance techniques for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2012 | issue = 3 | pages = CD008328 | date = March 2012 | pmid = 22419331 | doi = 10.1002/14651858.CD008328.pub2 | pmc = 11285303 }} In people with stable COPD, ACTs may lead to short-term improvements in health-related quality of life and a reduced long-term need for hospitalizations related to respiratory issues.

Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}{{cite journal | vauthors = Ferreira IM, Brooks D, White J, Goldstein R | title = Nutritional supplementation for stable chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2012 | pages = CD000998 | date = December 2012 | issue = 12 | pmid = 23235577 | doi = 10.1002/14651858.CD000998.pub3 | veditors = Ferreira IM | pmc = 11742366 }}

People with COPD can experience exacerbations (flare-ups) that are commonly caused by respiratory tract infections. The symptoms that worsen are not specific to COPD and differential diagnoses need to be considered.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}} Acute exacerbations are typically treated by increasing the use of short-acting bronchodilators including a combination of a short-acting inhaled beta agonist and short-acting anticholinergic.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}} These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer, with both appearing to be equally effective.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}{{cite journal|title=Bronchodilators delivered by nebuliser versus inhalers for lung attacks of chronic obstructive pulmonary disease|date=29 August 2016 |pmid=27569680 |pmc=8487315 |doi=10.1002/14651858.CD011826.pub2 |journal=Cochrane Database of Systematic Reviews| vauthors = Van Geffen WH, Douma WR, Slebos DJ, Kerstjens HA |volume=29|issue=8|page=011826|hdl=11370/95fc3e6e-ebd0-440f-9721-489729f80add}} Nebulization may be easier for those who are more unwell.{{sfn|Gold Report 2021|pp=54–58|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Oxygen supplementation can be useful. Excessive oxygen; however, can result in increased {{CO2}} levels and a decreased level of consciousness.{{cite web| vauthors = Wise R |title=Chronic Obstructive Pulmonary Disease (COPD) |work=Pulmonary Disorders: Merck Manuals Professional Edition |url=https://www.merckmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd |access-date=16 December 2016|url-status=live|archive-url=https://web.archive.org/web/20161228151904/https://www.merckmanuals.com/professional/pulmonary-disorders/chronic-obstructive-pulmonary-disease-and-related-disorders/chronic-obstructive-pulmonary-disease-copd|archive-date=28 December 2016}} Corticosteroids given orally can improve lung function and shorten hospital stays but their use is recommended for only five to seven days; longer courses increase the risk of pneumonia and death.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

Maintaining room temperature of at least {{convert|21|°C|°F|abbr=on}} for a minimum of nine hours a day was associated with better health in those with COPD, especially for smokers.{{cite journal |vauthors=Osman LM, Ayres JG, Garden C, Reglitz K, Lyon J, Douglas JG |title=Home warmth and health status of COPD patients |journal=Eur. J. Public Health |volume=18 |issue= 4|pages=399–405 |date=2008 |doi=10.1093/eurpub/ckn015 |pmid=18367496 |url=|doi-access=free }} The World Health Organization (WHO) recommends indoor temperatures of a slightly higher range between {{convert|18|and|24|C|F}}.{{cite journal |vauthors=Mu Z, Chen PL, Geng FH, Ren L, Gu WC, Ma JY, Peng L, Li QY |title=Synergistic effects of temperature and humidity on the symptoms of COPD patients |journal=Int J Biometeorol |volume=61 |issue=11 |pages=1919–25 |date=2017 |doi=10.1007/s00484-017-1379-0 |pmid=28567499|bibcode=2017IJBm...61.1919M |s2cid=25962322 }}

For people with COPD, the ideal indoor humidity levels are 30–50% RH. Maintaining indoor humidity can be difficult in the winter, especially in cold climates where the heating system is constantly running.{{cite web |title=Humidifiers: Ease skin, breathing symptoms |publisher=Mayo Clinic |url=https://www.mayoclinic.org/diseases-conditions/common-cold/in-depth/humidifiers/art-20048021}}

Keeping the indoor relative humidity above 40% RH significantly reduces the infectivity of aerosolized viruses.{{cite journal |vauthors=Noti JD, Blachere FM, McMillen CM, Lindsley WG, Kashon ML, Slaughter DR, Beezhold DH |title=High humidity leads to loss of infectious influenza virus from simulated coughs |journal=PLOS ONE |volume=8 |issue=2 |pages=e57485 |date=2013 |doi=10.1371/journal.pone.0057485 |pmid=23460865 |pmc=3583861|bibcode=2013PLoSO...857485N |doi-access=free }}

{{Main|Lung volume reduction}}

There are a number of procedures to reduce the volume of a lung in cases of severe emphysema with hyperinflation.

{{Main|Lung volume reduction surgery}}

For severe emphysema that has proved unresponsive to other therapies lung volume reduction surgery (LVRS) may be an option.{{sfn|Gold Report 2021|pp=92–96|loc=Chapter 4: Management of stable COPD}}{{cite journal | vauthors = van Geffen WH, Slebos DJ, Herth FJ, Kemp SV, Weder W, Shah PL | title = Surgical and endoscopic interventions that reduce lung volume for emphysema: a systemic review and meta-analysis | journal = The Lancet. Respiratory Medicine | volume = 7 | issue = 4 | pages = 313–324 | date = April 2019 | pmid = 30744937 | doi = 10.1016/S2213-2600(18)30431-4 | s2cid = 73428098 | url = https://pure.rug.nl/ws/files/81829213/1_s2.0_S2213260018304314.pdf }} LVRS involves the removal of damaged tissue, which improves lung function by allowing the rest of the lungs to expand. It is considered when the emphysema is in the upper lobes and when there are no comorbidities.{{cite journal | vauthors = Duffy S, Marchetti N, Criner GJ | title = Surgical Therapies for Chronic Obstructive Pulmonary Disease | journal = Clinics in Chest Medicine | volume = 41 | issue = 3 | pages = 559–566 | date = September 2020 | pmid = 32800206 | doi = 10.1016/j.ccm.2020.06.011 | s2cid = 221145423 }}

{{Further|Bronchoscopic lung volume reduction}}

Minimally invasive bronchoscopic procedures may be carried out to reduce lung volume. These include the use of valves, coils, or thermal ablation.{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}{{cite web |title=1 Recommendations {{!}} Endobronchial valve insertion to reduce lung volume in emphysema {{!}} Guidance {{!}} NICE |url=https://www.nice.org.uk/guidance/ipg600/chapter/1-Recommendations |website=www.nice.org.uk |date=20 December 2017 |access-date=7 July 2021}} Endobronchial valves are one-way valves that may be used in those with severe hyperinflation resulting from advanced emphysema; a suitable target lobe and no collateral ventilation are required for this procedure. The placement of one or more valves in the lobe induces a partial collapse of the lobe that ensures a reduction in residual volume that improves lung function, the capacity for exercise and quality of life.{{cite journal |vauthors=Klooster K, Slebos DJ |title=Endobronchial Valves for the Treatment of Advanced Emphysema |journal=Chest |volume=159 |issue=5 |pages=1833–1842 |date=May 2021 |pmid=33345947 |pmc=8129734 |doi=10.1016/j.chest.2020.12.007 |url=}}

The placement of nitinol coils instead of valves is recommended where there is collateral ventilation that would prevent the use of valves.{{cite journal |vauthors=Welling JB, Slebos DJ |title=Lung volume reduction with endobronchial coils for patients with emphysema |journal=J Thorac Dis |volume=10 |issue=Suppl 23 |pages=S2797–S2805 |date=August 2018 |pmid=30210833 |pmc=6129816 |doi=10.21037/jtd.2017.12.95 |url= |doi-access=free }} Nitinol is a biocompatible alloy.

Both of these techniques are associated with adverse effects including persistent air leaks and cardiovascular complications. Thermal vapor ablation has an improved profile. Heated water vapor is used to target lobe regions which leads to permanent fibrosis and volume reduction. The procedure is able to target individual lobe segments, can be carried out regardless of collateral ventilation and can be repeated with the natural advance of emphysema.{{cite journal | vauthors = Valipour A | title = Bronchoscopic Thermal Vapour Ablation: Hot Stuff to Treat Emphysema Patients! | journal = Archivos de Bronconeumologia | volume = 53 | issue = 1 | pages = 1–2 | date = January 2017 | pmid = 27916315 | doi = 10.1016/j.arbr.2016.11.009 | s2cid = 78181696 }}

In very severe cases lung transplantation might be considered.{{sfn|Gold Report 2021|pp=92–96|loc=Chapter 4: Management of stable COPD}} A CT scan may be useful in surgery considerations. Ventilation/perfusion scintigraphy is another imaging method that may be used to evaluate cases for surgical interventions and also to evaluate post-surgery responses.{{cite journal | vauthors = Mortensen J, Berg RM | title = Lung Scintigraphy in COPD | journal = Seminars in Nuclear Medicine | volume = 49 | issue = 1 | pages = 16–21 | date = January 2019 | pmid = 30545511 | doi = 10.1053/j.semnuclmed.2018.10.010 | s2cid = 56486118 | doi-access = free }} A bullectomy may be carried out when a giant bulla occupies more than a third of a hemithorax.

File:Chronic obstructive pulmonary disease world map-Deaths per million persons-WHO2012.svg

File:Chronic obstructive pulmonary disease world map - DALY - WHO2004.svgs lost to chronic obstructive pulmonary disease per 100,000 inhabitants in 2004:{{cite web |url=https://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html |title=WHO Disease and injury country estimates |year=2009 |work=World Health Organization |access-date=Nov 11, 2009 |url-status=live |archive-url=https://web.archive.org/web/20091111101009/http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html |archive-date=2009-11-11 }}

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COPD is progressive and can lead to premature death. It is estimated that 3% of all disability is related to COPD. The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia.{{cite journal | vauthors = Murray CJ, Vos T, Lozano R, Naghavi M, Flaxman AD, Michaud C, etal | title = Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010 | journal = Lancet | volume = 380 | issue = 9859 | pages = 2197–2223 | date = December 2012 | pmid = 23245608 | doi = 10.1016/S0140-6736(12)61689-4 | s2cid = 205967479 }} The overall number of years lived with disability from COPD, however, has increased.{{cite journal | vauthors = Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, etal | title = Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010 | journal = Lancet | volume = 380 | issue = 9859 | pages = 2163–2196 | date = December 2012 | pmid = 23245607 | pmc = 6350784 | doi = 10.1016/S0140-6736(12)61729-2 }}

There are many variables affecting the long-term outcome in COPD and GOLD recommends the use of a composite test (BODE) that includes the main variables of body-mass index, obstruction of airways, dyspnea (breathlessness) and exercise and not just spirometry results.{{sfn|Gold Report 2021|pp=26-33|loc=Chapter 2: Diagnosis and initial assessment}} NICE recommends against the use of BODE for the prognosis assessment in stable COPD; factors such as exacerbations and frailty need to be considered. Other factors that contribute to a poor outcome include older age, comorbidities such as lung cancer and cardiovascular disease and the number and severity of exacerbations needing hospital admission.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

Estimates of prevalence have considerable variation due to differences in analytical and surveying approach and the choice of diagnostic criteria.{{cite web |title=COPD prevalence |url=https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/background-information/prevalence-incidence/ |website=NICE |access-date=18 July 2021}} An estimated 213 million people had COPD in 2021, corresponding to a global prevalence of 2.7%, whereas epidemiological studies indicated an estimation of 384 million having COPD in 2010, corresponding to a global prevalence of 12%.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} The disease affects men and women. The increase in the developing world between 1970 and the 2000s is believed to be related to increasing rates of smoking in this region, an increasing population and an aging population due to fewer deaths from other causes such as infectious diseases. Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence.

Around three million people die of COPD each year.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} In some countries, mortality has decreased in men but increased in women.{{cite journal | vauthors = Rycroft CE, Heyes A, Lanza L, Becker K | title = Epidemiology of chronic obstructive pulmonary disease: a literature review | journal = International Journal of Chronic Obstructive Pulmonary Disease | volume = 7 | pages = 457–94 | year = 2012 | pmid = 22927753 | pmc = 3422122 | doi = 10.2147/COPD.S32330 | doi-access = free }} This is most likely due to rates of smoking in women and men becoming more similar. A higher rate of COPD is found in those over 40 years and this increases greatly with advancing age with the highest rate found in those over 60 years.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Sex differences in the anatomy of the respiratory system include smaller airway lumens and thicker airway walls in women, which contribute to a greater severity of COPD symptoms like dyspnea and frequency of COPD exacerbation.{{cite journal |vauthors=Martinez FJ, Curtis JL, Sciurba F, Mumford J, Giardino ND, Weinmann G, Kazerooni E, Murray S, Criner GJ, Sin DD, Hogg J, Ries AL, Han M, Fishman AP, Make B, Hoffman EA, Mohsenifar Z, Wise R |date=April 2007|title=Sex differences in severe pulmonary emphysema |journal=American Journal of Respiratory and Critical Care Medicine |volume=176 |issue=3 |pages=243–252 |doi=10.1164/rccm.200606-828OC |pmid=17431226 |pmc=1994221 |url=|doi-access=free }}

In the UK, three million people are reported to be affected by COPD{{Snd}}two million of these being undiagnosed. On average, the number of COPD-related deaths between 2007 and 2016 was 28,600. The estimated number of deaths due to occupational exposure was estimated to be about 15% at around 4,000. In the United States in 2018, almost 15.7 million people had been diagnosed with COPD and it is estimated that millions more have not been diagnosed.{{cite web |title=Basics About COPD |work=Chronic Obstructive Pulmonary Disease (COPD) |url=https://www.cdc.gov/copd/basics-about.html |publisher=Center for Disease Control |access-date=18 July 2021 |language=en-us |date=9 June 2021}}

In 2011, there were approximately 730,000 hospitalizations in the United States for COPD.{{cite journal | vauthors = Torio CM, Andrews RM | title = National Inpatient Hospital Costs: The Most Expensive Conditions by Payer, 2011: Statistical Brief #160 | journal = Healthcare Cost and Utilization Project (HCUP) Statistical Briefs | year = 2006 | pmid = 24199255 | url = http://hcup-us.ahrq.gov/reports/statbriefs/sb160.jsp | archive-url = https://web.archive.org/web/20170314171958/https://www.hcup-us.ahrq.gov/reports/statbriefs/sb160.jsp | url-status = live | archive-date = 2017-03-14 }} Globally, COPD in 2019 was the third-leading cause of death. In low-income countries, COPD does not appear in the Top 10 causes of death; in other income groups, it is in the Top 5.{{cite web |title=The top 10 causes of death |url=https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death |work=Fact Sheets |publisher=World Health Organization |language=en}}

{{Further|Emphysema#History|Chronic bronchitis#History}}

File:Giambattista morgagni.gif, who made one of the earliest recorded descriptions of emphysema in 1769]]

The name chronic obstructive pulmonary disease is believed to have first been used in 1965. Previously it has been known by a number of different names, including chronic obstructive bronchopulmonary disease, chronic airflow obstruction, chronic obstructive lung disease, nonspecific chronic pulmonary disease, and diffuse obstructive pulmonary syndrome.

The terms emphysema and chronic bronchitis were formally defined as components of COPD in 1959 at the CIBA guest symposium and in 1962 at the American Thoracic Society Committee meeting on Diagnostic Standards.

Early descriptions of probable emphysema began in 1679 by T. Bonet of a condition of "voluminous lungs" and in 1769 by Giovanni Morgagni of lungs which were "turgid particularly from air".{{cite journal | vauthors = Petty TL | title = The history of COPD | journal = International Journal of Chronic Obstructive Pulmonary Disease | volume = 1 | issue = 1 | pages = 3–14 | year = 2006 | pmid = 18046898 | pmc = 2706597 | doi = 10.2147/copd.2006.1.1.3 | doi-access = free }}{{cite book | vauthors = Wright JL, Churg A |chapter=Pathologic Features of Chronic Obstructive Pulmonary Disease: Diagnostic Criteria and Differential Diagnosis |chapter-url=http://www.mhprofessional.com/downloads/products/0071457399/0071457399_chap40.pdf |pages=693–705 | veditors = Fishman A, Elias J, Fishman J, Grippi M, Senior R, Pack A |year=2008 |title=Fishman's Pulmonary Diseases and Disorders |edition=4th |publisher=McGraw-Hill |isbn=978-0-07-164109-8 |access-date=2008-11-11 |archive-date=2016-03-03 |archive-url=https://web.archive.org/web/20160303202744/http://www.mhprofessional.com/downloads/products/0071457399/0071457399_chap40.pdf |url-status=dead }} In 1721 the first drawings of emphysema were made by Ruysh. René Laennec, used the term emphysema in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.

Air pollution and the increase in cigarette smoking in Great Britain at the start of the 20th century led to high rates of chronic lung disease, though it received little attention until the Great Smog of London in December 1952. This spurred epidemiological research in the United Kingdom, Holland and elsewhere.{{cite journal |vauthors=Woolcock A |title=The Search for Words to Describe the Bad Blowers |journal=Chest |date=1984 |volume=85 |issue=6 |pages=73S–74S |doi=10.1378/chest.85.6_Supplement.73S}} In 1953, George L. Waldbott, an American allergist, first described a new disease he named smoker's respiratory syndrome in the 1953 Journal of the American Medical Association. This was the first association between tobacco smoking and chronic respiratory disease.{{cite book| vauthors = Waldbott GL | title = A struggle with Titans |date=1965|publisher=Carlton Press|page=6|url=https://books.google.com/books?id=hLRpAAAAMAAJ }}

Modern treatments were developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators came into use in the 1960s following a promising trial of isoprenaline. Further bronchodilators, such as short-acting salbutamol, were developed in the 1970s and the use of long-acting bronchodilators began in the mid-1990s.{{cite journal | vauthors = Fishman AP | title = One hundred years of chronic obstructive pulmonary disease | journal = American Journal of Respiratory and Critical Care Medicine | volume = 171 | issue = 9 | pages = 941–8 | date = May 2005 | pmid = 15849329 | doi = 10.1164/rccm.200412-1685OE }}

It is generally accepted that COPD is widely underdiagnosed and many people remain untreated. In the US the NIH has promoted November as COPD Awareness Month to be an annual focus on increasing awareness of the condition.{{cite web |title=November is National COPD Awareness Month {{!}} NHLBI, NIH |url=https://www.nhlbi.nih.gov/health-topics/education-and-awareness/copd-learn-more-breathe-better/copd-awareness-month |website=www.nhlbi.nih.gov |access-date=21 July 2021}}

Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world.{{cite book | vauthors = Lomborg B | title=Global problems, local solutions : costs and benefits | year=2013 | publisher=Cambridge University Press | isbn=978-1-107-03959-9 | page=143 | url=https://books.google.com/books?id=cRZaAQAAQBAJ&pg=PA143 }} Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work.{{cite book| vauthors = Bloom D |title=The Global Economic Burden of Noncommunicable Diseases|year=2011|publisher=World Economic Forum|page=24|url=http://www3.weforum.org/docs/WEF_Harvard_HE_GlobalEconomicBurdenNonCommunicableDiseases_2011.pdf|url-status=live|archive-url=https://web.archive.org/web/20150204162753/http://www3.weforum.org/docs/WEF_Harvard_HE_GlobalEconomicBurdenNonCommunicableDiseases_2011.pdf|archive-date=2015-02-04}} This is expected to more than double by 2030. In Europe, COPD represents 3% of healthcare spending.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} In the United States, costs of the disease were estimated at $50 billion in 2010, most of which is due to exacerbation.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} In the United Kingdom this cost was in 2021 estimated at £3.8 billion annually.{{cite web |title=COPD commissioning toolkit |url=https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/212876/chronic-obstructive-pulmonary-disease-COPD-commissioning-toolkit.pdf |website=www.assets.publishing.service.gov.uk |access-date=18 July 2021}}

{{See also|COPD: Journal of Chronic Obstructive Pulmonary Disease}}

Stem-cell therapy using mesenchymal stem cells was in June 2021 studied in eight clinical trials had been completed and seventeen were underway.{{cite journal |vauthors=Chen YT, Miao K, Zhou L, Xiong WN |title=Stem cell therapy for chronic obstructive pulmonary disease |journal=Chin Med J (Engl) |volume=134 |issue=13 |pages=1535–1545 |date=June 2021 |pmid=34250959 |pmc=8280064 |doi=10.1097/CM9.0000000000001596 |url=}}

The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have alpha-1 antitrypsin deficiency is unclear.{{cite journal | vauthors = Gøtzsche PC, Johansen HK | title = Intravenous alpha-1 antitrypsin augmentation therapy for treating patients with alpha-1 antitrypsin deficiency and lung disease | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 9 | pages = CD007851 | date = September 2016 | pmid = 27644166 | pmc = 6457738 | doi = 10.1002/14651858.CD007851.pub3 }}

Metabolomic approaches to diagnosing and differentiating subtypes of COPD are being studied.{{Cite journal |last1=Gea |first1=Joaquim |last2=Enríquez-Rodríguez |first2=César J. |last3=Agranovich |first3=Bella |last4=Pascual-Guardia |first4=Sergi |date=2023 |title=Update on metabolomic findings in COPD patients |journal=ERJ Open Research |volume=9 |issue=5 |pages=00180–2023 |doi=10.1183/23120541.00180-2023 |issn=2312-0541 |pmc=10613990 |pmid=37908399}}{{Cite journal |last1=Dasgupta |first1=Sanjukta |last2=Ghosh |first2=Nilanjana |last3=Bhattacharyya |first3=Parthasarathi |last4=Roy Chowdhury |first4=Sushmita |last5=Chaudhury |first5=Koel |date=2023-02-17 |title=Metabolomics of asthma, COPD, and asthma-COPD overlap: an overview |journal=Critical Reviews in Clinical Laboratory Sciences |language=en |volume=60 |issue=2 |pages=153–170 |doi=10.1080/10408363.2022.2140329 |pmid=36420874 |issn=1040-8363}}{{Cite journal |last1=Zeng |first1=Xiaoyin |last2=Lan |first2=Yanting |last3=Xiao |first3=Jing |last4=Hu |first4=Longbo |last5=Tan |first5=Long |last6=Liang |first6=Mengdi |last7=Wang |first7=Xufei |last8=Lu |first8=Shaohua |last9=Peng |first9=Tao |last10=Long |first10=Fei |date=2022-12-02 |title=Advances in phosphoproteomics and its application to COPD |journal=Expert Review of Proteomics |language=en |volume=19 |issue=7–12 |pages=311–324 |doi=10.1080/14789450.2023.2176756 |pmid=36730079 |issn=1478-9450}}

Research continues into the use of telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely may reduce the number of emergency-room visits and improve the person's quality of life.{{cite journal | vauthors = McLean S, Nurmatov U, Liu JL, Pagliari C, Car J, Sheikh A | title = Telehealthcare for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | issue = 7 | pages = CD007718 | date = July 2011 | volume = 2012 | pmid = 21735417 | doi = 10.1002/14651858.CD007718.pub2 | pmc = 8939044 | url = http://discovery.dundee.ac.uk/ws/files/1821515/Telehealthcare_for_chronic_obstructive_pulmonary_disease.pdf }}

American people with COPD and their caregivers consider the following COPD-related research areas as the most important: family/social/community research, well-being of people with COPD, curative research, biomedical therapies, policy, and holistic therapies.{{cite journal | vauthors = Gruß I, McCreary GM, Ivlev I, Houlihan ME, Yawn BP, Pasquale C, Clark W, Mularski RA | display-authors = 6 | title = Developing a patient-driven chronic obstructive pulmonary disease (COPD) research agenda in the U.S. | journal = Journal of Patient-Reported Outcomes | volume = 5 | issue = 1 | pages = 126 | date = December 2021 | pmid = 34865193 | pmc = 8643383 | doi = 10.1186/s41687-021-00399-7 | doi-access = free }}

Chronic obstructive pulmonary disease may occur in a number of other animals and may be caused by exposure to tobacco smoke.{{cite book| vauthors = Akers RM, Denbow DM |title=Anatomy and Physiology of Domestic Animals|year=2008|publisher=Wiley|isbn=978-1-118-70115-7|page=852|url=https://books.google.com/books?id=Ze6J2znDg38C&pg=PT852 }} Most cases of the disease, however, are relatively mild.{{cite book | vauthors = Churg A, Wright JL | chapter = Animal models of cigarette smoke-induced chronic obstructive lung disease | volume = 14 | pages = 113–25 | year = 2007 | pmid = 17684336 | doi = 10.1159/000107058 | isbn = 978-3-8055-8332-9 | series = Contributions to Microbiology | title = Models of Exacerbations in Asthma and COPD }} In horses it is known as recurrent airway obstruction (RAO) or heaves. RAO can be quite severe and most often is linked to exposure to common allergens.{{cite web |title=Recurrent Airway Obstruction in Horses - Respiratory System |url=https://www.msdvetmanual.com/respiratory-system/respiratory-diseases-of-horses/recurrent-airway-obstruction-in-horses |website=Veterinary Manual |access-date=7 July 2021 |language=en}} COPD is also commonly found in old dogs.{{cite journal | vauthors = Miller MS, Tilley LP, Smith FW | title = Cardiopulmonary disease in the geriatric dog and cat | journal = The Veterinary Clinics of North America. Small Animal Practice | volume = 19 | issue = 1 | pages = 87–102 | date = January 1989 | pmid = 2646821 | doi = 10.1016/S0195-5616(89)50007-X }}

{{Reflist}}

{{refbegin}}

• {{cite book |title=Global Strategy for Prevention, Diagnosis and Management of COPD: 2021 Report |date=25 November 2020|publisher=Global Initiative for Chronic Obstructive Lung Disease |url=https://goldcopd.org/wp-content/uploads/2020/11/GOLD-REPORT-2021-v1.1-25Nov20_WMV.pdf |access-date=28 June 2021|ref={{harvid|Gold Report 2021}}}}

{{refend}}

{{commons category|Chronic obstructive pulmonary disease}}

• [https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd) WHO fact sheet on COPD]
• {{cite web | url = https://medlineplus.gov/copd.html | publisher = U.S. National Library of Medicine | work = MedlinePlus | title = COPD }}

{{Medical resources

| DiseasesDB = 2672

| ICD10 = {{ICD10|J|40||j|40}}–{{ICD10|J|44||j|40}}, {{ICD10|J|47||j|40}}

| ICD9 = {{ICD9|490}}–{{ICD9|492}}, {{ICD9|494}}–{{ICD9|496}}

| OMIM = 606963

| MedlinePlus = 000091

| eMedicineSubj = med

| eMedicineTopic = 373

| eMedicine_mult = {{eMedicine2|emerg|99}}

| MeshName = COPD

| MeshNumber = C08.381.495.389

| SNOMED CT = 13645005

}}

{{Respiratory pathology}}

{{Authority control}}

{{DEFAULTSORT:Chronic Obstructive Pulmonary Disease}}

Category:Aging-associated diseases

Category:Chronic lower respiratory diseases

Category:Health effects of tobacco

Category:Occupational diseases

Category:Wikipedia emergency medicine articles ready to translate

Category:Wikipedia medicine articles ready to translate (full)