View source for Chronic obstructive pulmonary disease

{{short description|Lung disease involving long-term poor airflow}}
{{good article}}
{{Infobox medical condition
| name          = Chronic obstructive pulmonary disease
| image         = Emphysema, centrilobular (4563270814).jpg
| caption       = Section of a lung showing [[centrilobular emphysema]], with enlarged airspaces in the centre of a [[pulmonary lobule|lobule]] usually caused by smoking and a major feature of COPD
| field         = [[Pulmonology]]
| synonyms      = Chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD)
| symptoms      = [[Shortness of breath]], chronic [[cough]]<ref name="CKSNice">{{cite web |title=Chronic obstructive pulmonary disease |url=https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/ |website=NICE |access-date=5 July 2021}}</ref>
| complications = [[Anxiety disorder|Anxiety]], [[Major depressive disorder|depression]], [[pulmonary heart disease]], [[Secondary spontaneous pneumothorax|pneumothorax]]<ref name="BMJbp"/><ref name="CKSNice"/>
| onset         = Over 35 years old<ref name="CKSNice"/>
| duration      = Long term<ref name="CKSNice" />
| causes        = [[Tobacco smoking]], [[air pollution]], [[genetics]]<ref name="WHO2021"/>
| risks         = 
| diagnosis     = [[Spirometry]]{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}    
| differential  = [[Asthma]], [[congestive heart failure]], [[bronchiectasis]], [[tuberculosis]], [[obliterative bronchiolitis]], [[diffuse panbronchiolitis]]{{sfn|Gold Report 2021|pp=33–35|loc=Chapter 2: Diagnosis and initial assessment}}
| prevention    = [[Smoking cessation|Stopping smoking]], improving indoor and outdoor [[air quality]], [[tobacco control]] measures<ref name="WHO2021"/>{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}
| treatment     = [[Pulmonary rehabilitation]], [[oxygen therapy|long-term oxygen therapy]], [[lung volume reduction surgery|lung volume reduction]]{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}
| medication    = [[Metered dose inhaler|Inhaled]] [[bronchodilator]]s and [[Corticosteroid|steroids]]{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}
| prognosis     = 
| frequency     = 174.5&nbsp;million (2015)<ref name=GBD2015Pre/>
| deaths        = 3.2&nbsp;million (2019)<ref name="WHO2021"/>
| alt           = 
}}

'''Chronic obstructive pulmonary disease''' ('''COPD''') is a type of progressive [[Obstructive lung disease|lung disease]] characterized by long-term respiratory symptoms and airflow limitation.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} The main symptoms include [[shortness of breath]] and a [[cough]], which may or may not produce [[mucus]].{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}} COPD [[progressive disease|progressively worsens]], with [[Activities of daily living|everyday activities]] such as walking or dressing becoming difficult.<ref name="WHO2021"/> While COPD is incurable, it is preventable and treatable.

The two most common conditions of COPD are [[emphysema]] and [[chronic bronchitis]] and they have been the two classic COPD [[Phenotype (clinical medicine)|phenotypes]].<ref name="Myc1">{{cite journal |vauthors=Myc LA, Shim YM, Laubach VE, Dimastromatteo J |title=Role of medical and molecular imaging in COPD |journal=Clin Transl Med |volume=8 |issue=1 |pages=12 |date=April 2019 |pmid=30989390 |pmc=6465368 |doi=10.1186/s40169-019-0231-z |url=}}</ref> Emphysema is defined as enlarged airspaces ([[Pulmonary alveolus|alveoli]]) whose [[Alveolar wall|walls]] have broken down resulting in permanent damage to the [[lung parenchyma|lung tissue]]. Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years. Both of these conditions can exist without airflow limitation when they are not classed as COPD. Emphysema is just one of the structural abnormalities that can limit airflow and can exist without airflow limitation in a significant number of people.<ref name="ICD11">{{cite web |title=ICD-11 - ICD-11 for Mortality and Morbidity Statistics |url=https://icd.who.int/browse11/l-m/en#/http%3a%2f%2fid.who.int%2ficd%2fentity%2f1948124976 |website=icd.who.int |access-date=30 June 2021}}</ref><ref name="Martini">{{cite journal |vauthors=Martini K, Frauenfelder T |title=Advances in imaging for lung emphysema |journal=Ann Transl Med |volume=8 |issue=21 |pages=1467 |date=November 2020 |pmid=33313212 |pmc=7723580 |doi=10.21037/atm.2020.04.44 |url=}}</ref> Chronic bronchitis does not always result in airflow limitation but in young adults who smoke the risk of developing COPD is high.{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Many definitions of COPD in the past included emphysema and chronic bronchitis, but these have never been included in [[Global Initiative for Chronic Obstructive Lung Disease|GOLD report]] definitions.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Emphysema and chronic bronchitis remain the predominant phenotypes of COPD but there is often overlap between them and a number of other phenotypes have also been described.<ref name="Myc1" /><ref name="De Rose">{{cite journal |vauthors=De Rose V, Molloy K, Gohy S, Pilette C, Greene CM |title=Airway Epithelium Dysfunction in Cystic Fibrosis and COPD |journal=Mediators Inflamm |volume=2018 |issue= |pages=1309746 |date=2018 |pmid=29849481 |pmc=5911336 |doi=10.1155/2018/1309746 |url=|doi-access=free }}</ref>

The most common cause of COPD is [[tobacco smoking]].<ref name="bmj22">{{cite web |title=Chronic obstructive pulmonary disease (COPD) - Aetiology {{!}} BMJ Best Practice |url=https://bestpractice.bmj.com/topics/en-gb/7/aetiology |website=bestpractice.bmj.com |access-date=25 November 2022}}</ref> Other [[risk factor]]s include [[household air pollution|indoor]] and [[air pollution|outdoor air pollution]] including [[dust]], exposure to occupational irritants such as dust from [[grain]]s, [[Cadmium poisoning|cadmium dust or fumes]], and [[genetics]], such as [[alpha-1 antitrypsin deficiency]] .{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}}<ref name="HSE">{{cite web |title=COPD causes - occupations and substances |url=https://www.hse.gov.uk/copd/causes.htm#substances |website=www.hse.gov.uk |access-date=3 July 2021}}</ref> In [[developing countries]], common sources of [[household air pollution|indoor air pollution]] are the use of coal and [[biomass]] such as wood and [[dry dung fuel|dry dung]] as fuel for [[Energy poverty and cooking|cooking and heating]].<ref name="Torres-Duque_2016">{{cite journal | vauthors = Torres-Duque CA, García-Rodriguez MC, González-García M | title = Is Chronic Obstructive Pulmonary Disease Caused by Wood Smoke a Different Phenotype or a Different Entity? | journal = Archivos de Bronconeumologia | volume = 52 | issue = 8 | pages = 425–31 | date = August 2016 | pmid = 27207325 | doi = 10.1016/j.arbres.2016.04.004 }}</ref>{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Most people living in European cities are exposed to damaging levels of air pollution.<ref name="EEA">{{cite web |title=Air pollution exposure in cities — European Environment Agency |url=https://www.eea.europa.eu/media/infographics/air-pollution-exposure-in-cities/view |website=www.eea.europa.eu |access-date=28 June 2021 |language=en}}</ref> The diagnosis is based on poor airflow as measured by [[spirometry]].{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}

Most cases of COPD can be prevented by reducing exposure to risk factors such as smoking and indoor and outdoor pollutants.{{sfn|Gold Report 2021|pp=80–83|loc=Chapter 4: Management of stable COPD}} While treatment can slow worsening, there is no conclusive evidence that any medications can change the long-term decline in lung function.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} COPD treatments include [[smoking cessation]], [[vaccination]]s, [[pulmonary rehabilitation]], [[Metered dose inhaler|inhaled]] [[bronchodilator]]s and [[corticosteroid]]s.{{sfn|Gold Report 2021|pp=40–46|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} Some people may benefit from long-term [[oxygen therapy]], [[lung volume reduction]] and [[lung transplantation]].{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}} In those who have periods of [[Acute exacerbation of chronic obstructive pulmonary disease|acute worsening]], increased use of medications, [[antibiotics]], corticosteroids and hospitalization may be needed.<ref>{{cite journal | vauthors = Dobler CC, Morrow AS, Beuschel B, Farah MH, Majzoub AM, Wilson ME, etal | title = Pharmacologic Therapies in Patients With Exacerbation of Chronic Obstructive Pulmonary Disease: A Systematic Review With Meta-analysis | journal = Annals of Internal Medicine | volume = 172 | issue = 6 | pages = 413–422 | date = March 2020 | pmid = 32092762 | doi = 10.7326/M19-3007 | s2cid = 211476101 }}</ref>

As of 2015, COPD affected about 174.5&nbsp;million people (2.4% of the global population).<ref name=GBD2015Pre>{{cite journal | author = ((GBD 2015 Disease and Injury Incidence and Prevalence Collaborators)) | title = Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1545–1602 | date = October 2016 | pmid = 27733282 | pmc = 5055577 | doi = 10.1016/S0140-6736(16)31678-6 }}</ref> It typically occurs in males and females over the age of 35–40.<ref name="CKSNice" /><ref name="WHO2021">{{cite web |title=Chronic obstructive pulmonary disease (COPD) |url=https://www.who.int/en/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd) |work=Fact Sheets |publisher=World Health Organization |access-date=1 July 2021 |language=en}}</ref> In 2019 it caused 3.2&nbsp;million deaths, 80% occurring in lower and middle income countries,<ref name="WHO2021"/> up from 2.4&nbsp;million deaths in 1990.<ref name=GBD2015De>{{cite journal | vauthors = Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, etal | collaboration = GBD 2015 Mortality and Causes of Death Collaborators | title = Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1459–1544 | date = October 2016 | pmid = 27733281 | pmc = 5388903 | doi = 10.1016/S0140-6736(16)31012-1 }}</ref><ref name=GDB2013>{{cite journal | author = ((GBD 2013 Mortality and Causes of Death Collaborators)) | title = Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 | journal = Lancet | volume = 385 | issue = 9963 | pages = 117–71 | date = January 2015 | pmid = 25530442 | pmc = 4340604 | doi = 10.1016/S0140-6736(14)61682-2 }}</ref> The number of deaths is projected to increase further because of continued exposure to risk factors and an aging population.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} In the United States in 2010 the economic cost was put at US$32.1&nbsp;billion and projected to rise to US$49&nbsp;billion in 2020.<ref name="CDCinfo">{{cite web |title=COPD Costs |url=https://www.cdc.gov/copd/infographics/copd-costs.html |website=www.cdc.gov |language=en-us |date=5 July 2019}}</ref> In the United Kingdom this cost is estimated at £3.8 billion annually.<ref name="toolkit">{{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}}</ref>   
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== Signs and symptoms ==
[[File:Symptoms of COPD.svg|thumb|[[Signs and symptoms]] of stages of COPD.]]
{{listen
| filename     = Wheeze2O.ogg   
| title        = Wheezing
| description  = The sound of wheezing as heard with a stethoscope.
| format       = [[Ogg]]
}}

=== Shortness of breath ===
A [[Signs and symptoms#Cardinal signs and symptoms|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 [[Pursed-lip breathing|breathe through pursed lips]], which can improve shortness of breath.<ref name="Mayer">{{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=}}</ref> 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}}<ref>{{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 }}</ref> In severe and very severe cases there may be [[fatigue|constant tiredness]], weight loss, muscle loss and [[anorexia]]. People with COPD often have increased breathlessness and frequent [[common cold|colds]] before seeking treatment.{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}

=== Cough ===
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.<ref name="Szalontai">{{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 }}</ref>

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 fracture]]s or to [[Syncope (medicine)|a&nbsp;brief loss of consciousness]].{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}

== Exacerbations ==
An [[Acute exacerbation of chronic obstructive pulmonary disease|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.<ref name="CDC2">{{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}}</ref> Other [[Upper respiratory infection|respiratory infections]] may be bacterial or in combination sometimes secondary to a viral infection.<ref name="Guo-Parke">{{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 }}</ref> The most common bacterial infection is caused by ''[[Haemophilus influenzae]]''.<ref name="Short">{{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=}}</ref> Other risks include exposure to tobacco smoke (active and [[Passive smoking|passive]]) and environmental [[Particulates|pollutants]]{{Snd}}both indoor and outdoor.<ref name="EPA">{{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}}</ref> During the [[COVID-19 pandemic]], hospital admissions for COPD exacerbations sharply decreased which may be attributable to reduction of emissions and cleaner air.<ref name="Halpin"/> There has also been a marked decrease in the number of cold and flu infections during this time.<ref name="Iacobucci">{{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 }}</ref>

[[Particulates#Wildfire smoke risk|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 mask]]s do not give protection from the fine particles in [[wildfire]]s and instead advise the use of well-fitting [[Respirator|''particulate masks'']].<ref name="USEPA">{{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}}</ref> This same advice is offered in Canada to the effects of their forest fires.<ref name="LACA">{{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}}</ref> Bushfires in Australia add to the high risk factors for COPD and its worsening for farmers.<ref name="farmer">{{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}}</ref>

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 syndrome|Frailty]] in ageing increases exacerbations and hospitalization.<ref name="Luo">{{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=}}</ref>

Acute exacerbations in COPD are often unexplained and thought to have many causes other than infections. A [[systematic review]] in collaboration with [[Cochrane (organisation)|Cochrane]] suggests that chronic acid reflux and microaspirations can lead to more frequent exacerbations.<ref>{{cite journal | vauthors = Raveling T, Vonk J, Struik FM, Goldstein R, Kerstjens HA, Wijkstra PJ, Duiverman ML | title = Chronic non-invasive ventilation for chronic obstructive pulmonary disease | journal = The Cochrane Database of Systematic Reviews | volume = 2021 | issue = 8 | pages = CD002878 | date = August 2021 | pmid = 34368950 | pmc = 8407093 | doi = 10.1002/14651858.CD002878.pub3 | collaboration = Cochrane Airways Group }}</ref> Another study emphasizes the possibility of a [[pulmonary embolism]] as sometimes being responsible in these cases. Signs can include [[Pleurisy|pleuritic]] [[chest pain]] and [[heart failure]] without signs of infection. Such emboli could respond to [[anticoagulant]]s.<ref>{{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 }}</ref>

== Other conditions ==
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]], [[Major depressive disorder|depression]], [[Anxiety disorder|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.<ref name="Edgar">{{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 |url=}}</ref> 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.<ref name="Clementi">{{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 |pages= |date=January 2019 |pmid=30704059 |pmc=6468691 |doi=10.3390/toxics7010006 |url=}}</ref> When comorbid with COPD there is more systemic inflammation.<ref name="Clementi"/> 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.<ref name="Chan">{{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 |url=}}</ref>

Anxiety and depression are often complications of COPD.<ref name="BMJbp">{{cite web |title=Chronic obstructive pulmonary disease (COPD) - Complications {{!}} BMJ Best Practice |url=https://bestpractice.bmj.com/topics/en-gb/7/complications |website=bestpractice.bmj.com |access-date=11 July 2021}}</ref><ref name="CKSNice" /> Other complications include a reduced quality of life and increased disability, [[cor pulmonale]], frequent chest infections including [[pneumonia]], [[secondary polycythemia]], [[Respiratory failure#Type 2|respiratory failure]], [[Secondary spontaneous pneumothorax|pneumothorax]], lung cancer, and [[cachexia]] (muscle wasting).<ref name="CKSNice"/><ref name="BMJbp"/><ref name="Forfia">{{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 |url=}}</ref>

[[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.
Differentiating COVID-19 symptoms from an exacerbation is difficult; mild [[Prodrome|prodromal symptoms]] may delay its recognition and where they include loss of taste or smell COVID-19 is to be suspected.<ref name="Halpin">{{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 |url=}}</ref>

===Definition===

Many definitions of COPD in the past included chronic bronchitis and [[emphysema]] but these have never been included in [[Global Initiative for Chronic Obstructive Lung Disease|GOLD report]] definitions.{{sfn|Gold Report 2021|pp=4–8|loc=Chapter 1: Definition and overview}} Emphysema is defined as enlarged airspaces ([[Pulmonary alveolus|alveoli]]) whose walls break down resulting in permanent damage to the [[lung parenchyma|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.<ref name="ICD11"/> 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 [[cyanosis|bluish color to the skin and lips]] and swollen ankles.<ref name="Weinberger">{{cite book | vauthors = Weinberger SE |title=Principles of pulmonary medicine |date=2019 |location=Philadelphia, PA |isbn=9780323523714 |page=104 |edition=Seventh}}</ref> These differences were suggested to be due to the presence or not of [[collateral ventilation]], evident in emphysema and lacking in chronic bronchitis.<ref name="Delaunois">{{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 }}</ref> This terminology was no longer accepted as useful, as most people with COPD have a combination of both emphysema and airway disease.<ref name="Weinberger"/> These are now recognized as the two major phenotypes of COPD – emphysematous phenotype and chronic bronchitic phenotype.<ref name="Myc1"/>

== Subtypes ==
The two classic emphysematous and chronic bronchitic [[Phenotype (clinical medicine)|phenotypes]] are fundamentally different conditions with unique underlying mechanisms.<ref name="Myc1"/> 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 other subtypes or phenotypes of COPD being accepted and proposed.<ref name="RIC">{{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 }}</ref><ref name="Corlateanu">{{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 }}</ref> 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.<ref name="Myc1"/>

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.<ref name="Halpin2"/>

Two inflammatory phenotypes show a phenotype stability; the [[neutrophil]]ic inflammatory phenotype and the [[eosinophil]]ic inflammatory phenotype.<ref name="Brightling">{{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://leicester.figshare.com/articles/journal_contribution/Airway_inflammation_in_COPD-_progress_to_precision_medicine/10221875/files/18436544.pdf}}</ref> [[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.<ref name="Bai">{{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 }}</ref> 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.<ref name="Kumar">{{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=}}</ref> A molecular phenotype of [[CFTR]] dysfunction is shared with [[cystic fibrosis]].<ref name="De Rose"/> A combined phenotype of chronic bronchitis and [[bronchiectasis]] has been described with a difficulty noted of determining the best treatment.<ref name="Osadnik">{{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=}}</ref>

The only [[genotype]] is the [[alpha-1 antitrypsin deficiency]] (AATD) genetic subtype and this has a specific treatment.<ref name="Silverman" />

==Cause==
The cause of the development of COPD is the exposure to harmful [[Particulates#Health effects|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.<ref name="bmj22"/> 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.<ref name="Szalontai"/>{{sfn|Gold Report 2021|pp=8–14|loc=Chapter 1: Definition and overview}} Host factors include a genetic susceptibility, [[Socioeconomic status#Health|factors associated with poverty]], aging and physical inactivity. [[Asthma]] and [[tuberculosis]] are also recognized as risk factors, as the cormorbidity 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 [[Anatomical variation|variation]] arising during [[Lung#Development|development]] has been described. 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]]''.<ref name="Nikolić">{{cite journal |vauthors=Nikolić MZ, Sun D, Rawlins EL |title=Human lung development: recent progress and new challenges |journal=Development |volume=145 |issue=16 |pages= |date=August 2018 |pmid=30111617 |pmc=6124546 |doi=10.1242/dev.163485 |url=}}</ref><ref name="Smith">{{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}}</ref>

[[Alcohol abuse]] can lead to [[alcoholic lung disease]] and is seen to be an independent risk factor for COPD.<ref name="Bailey">{{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=}}</ref><ref name="Smith1">{{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=}}</ref>
[[Mucociliary clearance]] is disrupted by chronic exposure to alcohol; [[Pulmonary macrophage|macrophage]] activity is diminished and an inflammatory response promoted.<ref name="Arvers">{{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=}}</ref><ref name="Smith1"/> The damage leads to a susceptibility for infection, including [[COVID-19]],<ref name="Slovinsky">{{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=}}</ref> more so when combined with smoking; smoking induces the upregulation of the expression of [[ACE2]] a recognized factor in the development of COVID-19.<ref name="Bailey"/>

===Smoking===
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}}<ref name="bmj22"/> Of those who smoke, about 20% will get COPD,<ref name=Ward2012>{{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 }}</ref> 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.<ref name=Ward2012/><ref name=Ren2013>{{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 }}</ref><ref name=Rich2010>{{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 }}</ref> Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke.<ref name="CCM">{{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 }}</ref> For the same amount of cigarette smoking, women have a higher risk of COPD than men.<ref>{{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 }}</ref> In non-smokers, exposure to [[second-hand smoke]] (passive smoking) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide due to [[tobacco smoke]].<ref name="WHO2020">{{cite web |title=Tobacco |url=https://www.who.int/news-room/fact-sheets/detail/tobacco |work=Fact Sheets |publisher=World Health Organization |access-date=12 July 2021 |language=en}}</ref> 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.<ref name="Savran">{{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 }}</ref>

Inhaled smoke triggers the release of excessive [[protease]]s in lungs, which then degrades [[elastin]], the major component of alveoli (which allows rapid gas exchange in the lungs).<ref>{{Cite web | vauthors = Hecht M |date=2018-11-26 |title=The Alveoli in Your Lungs |url=https://www.healthline.com/health/alveoli-function |url-status=live |archive-url=https://archive.today/20211018185705/https://www.healthline.com/health/alveoli-function |archive-date=2021-10-18 |access-date=2022-02-04 |website=[[Healthline]]}}</ref> Smoke also impairs the action of [[Cilium|cilia]], inhibiting [[mucociliary clearance]] that clears the bronchi of mucus, cellular debris and unwanted fluid.<ref name="bmj22"/>

Other types of tobacco smoke, such as from cigar, [[tobacco pipe|pipe]], [[Bong|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.<ref name="Patel">{{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 }}</ref>

[[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.<ref name="Chatkin" /> 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]].<ref name="Underner">{{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=}}</ref> 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.<ref name="Chatkin">{{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=}}</ref><ref name="RC">{{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 }}</ref> 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.<ref name="Chatkin" /> 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.<ref name="Chatkin" /> 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.<ref name="Ribeiro">{{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=}}</ref>

===Pollution===
{{Further|Energy poverty and cooking|Household air pollution}}
[[File:Access to clean fuels and technologies for cooking, OWID.svg|thumb|upright=1.4|Access to [[clean fuel]] and [[Energy poverty and cooking#Clean cooking facilities|clean cooking facilities]] as of 2016.<ref>{{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}}</ref>]]

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.<ref name="Clementi"/> [[Black carbon]] also known as ''soot'', is an [[air pollution|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.<ref name="Clementi"/> Studies have shown that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.<ref>{{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 }}</ref> Areas with poor outdoor air quality, including that from [[exhaust gas]], generally have higher rates of COPD.<ref name=Piro2012/>  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 fuel|dry dung]], leading to [[Household air pollution|indoor air pollution]] and are one of the most common causes of COPD in [[developing country|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]].<ref name=Piro2012>{{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 }}</ref>

{{anchor|Occupational exposures}}

===Occupational exposure===
{{See also|Cadmium poisoning}}
Intense and prolonged exposure to workplace [[dust]]s, 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 compound|organic]] and [[inorganic compound|inorganic]] dusts such as [[cadmium]], [[silica]], dust from [[grain]]s and [[flour]] and fumes from cadmium and [[welding]] that promote respiratory symptoms.<ref name="HSE"/>{{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}}<ref>{{cite book| vauthors = Hopper T |title=Mosby's Pharmacy Technician – E-Book: Principles and Practice|date=2014|publisher=Elsevier Health Sciences|isbn=9780323292450|page=610|url=https://books.google.com/books?id=PtDsAwAAQBAJ&pg=PA610 }}</ref> The negative effects of dust exposure and cigarette smoke exposure appear to be cumulative.<ref name=Barn2009>{{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}}</ref>

===Genetics===
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.<ref name="Silverman">{{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=}}</ref> This risk is particularly high if someone deficient in [[alpha-1 antitrypsin]] (AAT) also smokes.<ref name=Foreman2012>{{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 }}</ref> It is responsible for about 1–5% of cases<ref name=Foreman2012/><ref name=Brode2012>{{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 }}</ref> and the condition is present in about three to four in 10,000 people.<ref name=Harr2012>{{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}}</ref>

Mutations in ''MMP1'' [[gene]] that encodes for [[interstitial collagenase]] are associated with COPD.<ref name="gene">{{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}}</ref>

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 association study|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|National Heart, Lung and Blood Institute]] (NHLBI) to identify rare genetic determinants.<ref name="COPDGene">{{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 }}</ref>

==Pathophysiology==
[[File:Copd 2010.jpg|thumb|Normal [[lung]]s shown in upper diagram. Lungs damaged by COPD in lower diagram with an inset showing a cross-section of [[bronchiole]]s blocked by [[mucus]] and damaged [[Pulmonary alveolus|alveoli]].]]
COPD is a progressive [[obstructive lung disease|lung disease]] in which chronic, incompletely reversible poor airflow (airflow limitation) and an inability to breathe out fully ([[air trapping]]) exist.<ref name="Capron">{{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}}</ref> The poor airflow is the result of small airways disease and [[emphysema]] (the breakdown of [[lung parenchyma|lung tissue]]).<ref name="Robbins1">{{cite book |title=Robbins basic pathology |date=2018 |location=Philadelphia, Pennsylvania |isbn=9780323353175 |pages=498–502 |edition=Tenth| vauthors = Kumar V, Abbas AK, Aster JC }}</ref> 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.<ref name="IJCOPD">{{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=2583–2589 |date=2020 |pmid=33116475 |pmc=7585810 |doi=10.2147/COPD.S264261 |url=}}</ref>

<!--Lung destruction  -->
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'''.<ref name="Lancet2023">{{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 |url=}}</ref> Thus, airway remodelling with narrowing of peripheral airway and emphysema are responsible for the alteration of lung function.<ref name="Brightling" /> [[Mucociliary clearance]] is particularly altered with a dysregulation of [[cilia]] and [[mucus]] production.<ref name="ERRM">{{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 }}</ref> Small airway disease sometimes called [[chronic bronchiolitis]], appears to be the precursor for the development of emphysema.<ref name="Higham" />
The inflammatory cells involved include [[neutrophil]]s and [[macrophage]]s, 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 [[chemotaxis|chemotactic factors]]. Other processes involved with lung damage include [[oxidative stress]] produced by high concentrations of [[Radical (chemistry)|free radicals]] in tobacco smoke and released by inflammatory cells and breakdown of the [[connective tissue]] of the lungs by [[protease]]s (particularly [[elastase]]) that are insufficiently inhibited by [[Protease inhibitor (biology)|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|thumb|left|[[Micrograph]] showing [[emphysema]] (left – large empty spaces) and [[lung parenchyma|lung tissue]] with relative preserved [[pulmonary alveolus|alveoli]] (right).]]
<!--Airway narrowing  -->
Narrowing of the airways occurs due to inflammation and scarring within them.<!--<ref name=GOLD2013Chp1/> --> This contributes to the inability to breathe out fully.<!--<ref name=GOLD2013Chp1/> --> The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time.<ref name=Cal2005>{{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 }}</ref> 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 [[Inhalation#Hyperinflation|hyperinflation]].<ref name=Cal2005/><ref>{{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 }}</ref><ref name="IJCOPD"/> Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled.<ref name=Odon2006>{{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 }}</ref> Hyperinflation may also worsen during an exacerbation.<ref name=Coop2006>{{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 }}</ref> There may also be a degree of [[Bronchial hyperresponsiveness|airway hyperresponsiveness]] to irritants similar to those found in asthma.<ref name=Harr2012/>

<!-- End stage -->
[[Hypoxemia|Low oxygen levels]] and eventually, [[hypercapnia|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 [[vasoconstriction|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''.<ref name="Forfia"/>

== Diagnosis ==
[[File:DoingSpirometry.JPG|alt=A person sitting and blowing into a device attached to a computer|thumb|upright=1.4|A person blowing into a [[spirometer]]. 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 [[dyspnea|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}}<ref name="NICE2021">{{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 |access-date=29 June 2021}}</ref>

===Spirometry===
[[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.<ref name=Qas2011/> 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 [[vital capacity|forced vital capacity]] (FVC), which is the greatest volume of air that can be breathed out in a single large breath.<ref name=Young2010>{{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 }}</ref> Normally, 75–80% of the FVC comes out in the first second<ref name=Young2010/> and a [[FEV1/FVC ratio]] less than 70% in someone with symptoms of COPD defines a person as having the disease.<ref name=Qas2011>{{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 }}</ref> Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly.<ref name=Qas2011/> The [[National Institute for Health and Care Excellence]] criteria additionally require a FEV1 less than 80% of predicted.<ref name=NICE2010P60>{{NICE|101|Chronic Obstructive Pulmonary Disease|June 2010|60–70}}</ref> People with COPD also exhibit a decrease in [[DLCO|diffusing capacity of the lung for carbon monoxide]] due to decreased surface area in the alveoli, as well as damage to the capillary bed.<ref>{{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 }}</ref> Testing the [[peak expiratory flow]] (the maximum speed of expiration), commonly used in asthma diagnosis, is not sufficient for the diagnosis of COPD.<ref name=NICE2010P60/>

[[Screening (medicine)|Screening]] using spirometry in those without symptoms has uncertain effect 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}}

===Assessment===
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
|+[[Medical Research Council (United Kingdom)|MRC]] shortness of breath scale<ref name=NICE2010P60/>
|-
! Grade!! Activity affected
|-
| 1 || Only strenuous activity
|-
| 2 || Vigorous walking
|-
| 3 || With normal walking
|-
| 4 || After a few minutes of walking
|-
| 5 || With changing clothing
|}
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
|+[[Global Initiative for Chronic Obstructive Lung Disease|GOLD]] criteria{{sfn|Gold Report 2021|pp=20-27|loc=Chapter 2: Diagnosis and initial assessment}}
|-
! Severity!! FEV1 % predicted
|-
| Mild (GOLD 1) || ≥80
|-
| Moderate (GOLD 2)|| 50–79
|-
| Severe (GOLD 3) || 30–49
|-
| Very severe (GOLD 4)|| <30
|}

A number of methods can be used to assess the affects and severity of COPD.<ref name=NICE2021/>{{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.<ref name="Williams">{{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 }}</ref><ref name=NICE2021/> 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}}<ref name="BMJ"/> Scores on CAT range from 0–40 with the higher the score, the more severe the disease.<ref>{{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 }}</ref> 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}} Both the American and European guidelines recommend partly basing treatment recommendations on the FEV1.<ref name=Qas2011/> The GOLD guidelines group people into four categories based on symptoms assessment, degree of airflow limitation and history of exacerbations.<ref name="BMJ">{{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}}</ref> 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 COPD Diagnostic Questionnaire alone or in combination with hand-held flow meters is appropriate for screening of COPD in primary care.<ref>{{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 }}</ref>

===Other tests===
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 [[Pathognomonic|indicative]] of COPD.<ref name="radiopedia">{{cite web |title=saber sheath trachea {{!}} Search {{!}} Radiopaedia.org |url=https://radiopaedia.org/search?utf8=✓&q=saber+sheath+trachea&scope=all&lang=gb |website=Radiopaedia |access-date=13 August 2021}}</ref>

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}} An [[arterial blood gas|analysis of arterial blood]] is used to determine the need for oxygen supplementation and assess for [[hypercapnia|high levels of carbon dioxide]] in the blood; this is recommended in those with an FEV1 less than 35% predicted, those with a peripheral oxygen saturation less than 92% and those with symptoms of congestive heart failure.<ref name="GOLD2013Chp2">{{cite journal | vauthors = Vestbo J, Hurd SS, Agustí AG | display-authors = etal | title = Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary | journal = American Journal of Respiratory and Critical Care Medicine | volume = 187 | issue = 4 | pages =350–352 | date = February 2013 | pmid = 22878278 | doi = 10.1164/rccm.201204-0596PP | url = http://ajrccm.atsjournals.org/content/187/4/347.full.pdf+html }}</ref> [[World Health Organization|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}}

<gallery>
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: Note the small heart size in comparison to the lungs.
File:Barrowchest.JPG|A lateral chest X-ray of a person with emphysema: Note the 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)
</gallery>

===Differential diagnosis===
COPD may need to be [[Differential diagnosis|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.<ref>{{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}}</ref> Chronic bronchitis with normal airflow is not classified as COPD.<ref name=Harr2012/>

==Prevention==
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}}

===Smoking cessation===
{{See also|World No Tobacco Day}} 
<!--Primary prevention  -->
The [[Tobacco smoking#Legal issues and regulation|policies]] of governments, public health agencies and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking.<ref name=WHO2003/> [[Smoking ban]]s 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.<ref name=Piro2012/>

<!--Secondary prevention  -->
In those who smoke, [[smoking cessation|stopping smoking]] is the only measure shown to slow down the worsening of COPD.<ref name=Jim2013>{{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 }}</ref><ref name=NICECG101>{{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|access-date=2018-06-05}}</ref> 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.<ref name=kc>{{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 }}</ref> Often, several attempts are required before long-term abstinence is achieved.<ref name=WHO2003>{{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 }}</ref> Attempts over 5 years lead to success in nearly 40% of people.<ref name=Ton2013/>

Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive and many smokers need further support.<ref name="NHS2018">{{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}}</ref> 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]].<ref name=WHO2003/><ref name=NICECG101/><ref name=Ton2013>{{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 }}</ref> 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.<ref>{{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 }}</ref>

===Occupational health===
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.<ref name=Piro2012/> Examples of these measures include the creation of public policy,<ref name=Piro2012/> education of workers and management about the risks, promoting smoking cessation, [[disease surveillance|checking]] workers for early signs of COPD, use of [[respirator]]s and dust control.<ref>{{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 }}</ref><ref>{{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 }}</ref> Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.<ref>{{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 }}</ref> If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing their work role.<ref>{{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 }}</ref>

===Pollution control===
{{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.<ref name=Piro2012/> This may be achieved by public policy efforts, cultural changes and personal involvement.<ref name="GOLD2013Chp3">{{cite journal | vauthors = Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C, Anzueto A, Barnes PJ, Fabbri LM, Martinez FJ, Nishimura M, Stockley RA, Sin DD, Rodriguez-Roisin R | display-authors = 6 | title = Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary | journal = American Journal of Respiratory and Critical Care Medicine | volume = 187 | issue = 4 | pages = 347–365 | date = February 2013 | pmid = 22878278 | doi = 10.1164/rccm.201204-0596PP | url = https://www.research.manchester.ac.uk/portal/en/publications/global-strategy-for-the-diagnosis-management-and-prevention-of-chronic-obstructive-pulmonary-disease-gold-executive-summary(514ccafe-04b0-43ab-9e75-048e50e075d5).html }}</ref> Many developed countries have successfully improved outdoor air quality through regulations which has resulted in improvements in the lung function of their populations.<ref name=Piro2012/> 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.<ref name="GOLD2013Chp3"/> Proper stoves may improve [[indoor air quality]] by 85%.<!--<ref name=Piro2012/> --> Using alternative energy sources such as [[solar cooking]] and electrical heating is also effective.<!--<ref name=Piro2012/> --> 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.<ref name=Piro2012/>

== Management ==
COPD is not curable, but the symptoms are treatable and its progression can be delayed, particularly by stopping smoking.<ref name="CKSNice"/>{{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.<ref name="CKSNice"/> Other recommendations include annual [[influenza vaccination]]s and [[Pneumococcal vaccine|pneumococcal vaccination]] to help reduce the risk of exacerbations; 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}}

[[Comorbidity|Other illnesses]] are also 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.<ref>{{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 }}</ref> 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.<ref>{{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 }}</ref> 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}}<ref>{{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 }}</ref>

A number of [[Pharmacotherapy|medical treatments]] are used in the management of stable COPD and exacerbations. These include [[bronchodilator]]s, [[corticosteroid]]s and [[antibiotics]].

In those with a severe exacerbation, antibiotics improve outcomes.<ref name="vol2018">{{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 }}</ref> A number of different antibiotics may be used including [[amoxicillin]], [[doxycycline]] and [[azithromycin]]; whether one is better than the others is unclear.<ref name=Mackay2012>{{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 }}</ref> There is no clear evidence of improved outcomes for those with less severe cases.<ref name="vol2018"/> The FDA recommends against the use of [[fluoroquinolones]] when other options are available due to higher risks of serious side effects.<ref>{{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}}</ref>
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 medicine|intensive care]].<ref name="Lancet2012">{{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 }}</ref> Fewer than 20% of exacerbations require hospital admission.<ref name="GOLD2013Chp3"/> In those without acidosis from respiratory failure, [[home care]] may be able to help avoid some admissions.<ref name="GOLD2013Chp3"/>

In those with [[End stage pulmonary disease|end-stage disease]], [[palliative care]] is focused on relieving symptoms.<ref name="Oliveira">{{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 }}</ref> [[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.<ref>{{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 }}</ref>{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}

===Bronchodilators===
Inhaled short-acting [[bronchodilator]]s are the primary medications used on an [[Pro re nata|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 agonist]]s and [[anticholinergics]]; either in long-acting or short-acting forms. Beta2–adrenergic agonists target [[beta-2 adrenergic receptor#Muscular system|receptors]] in the [[smooth muscle|smooth muscle cells]] in [[bronchiole]]s 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}}<ref name="Almadhoun">{{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 }}</ref> 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 a [[long-acting beta agonist]] (LABA) is better is unclear and trying each and continuing with the one that works best may be advisable.<ref name="Far2015">{{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}}</ref> Both types of agent appear to reduce the risk of acute exacerbations by 15–25%.<ref name=Lancet2012/> The combination of LABA/LAMA may reduce COPD exacerbations and improve quality-of-life compared to long-acting bronchodilators alone.<ref>{{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 }}</ref> 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.<ref name="NICE3">{{cite web |title=Recommendations {{!}} Chronic obstructive pulmonary disease in over 16s: diagnosis and management {{!}} Guidance {{!}} NICE |url=https://www.nice.org.uk/guidance/ng115/chapter/Recommendations |website=www.nice.org.uk |access-date=1 August 2021}}</ref>

<!--Beta agonists  -->
Several short-acting β<sub>2</sub> agonists are available, including [[salbutamol]] (albuterol) and [[terbutaline]].<ref name=GOLD2013Chp3/> They provide some relief of symptoms for four to six hours.<ref name=GOLD2013Chp3/> LABAs such as [[salmeterol]], [[formoterol]] and [[indacaterol]] are often used as maintenance therapy. Some feel the evidence of benefits is limited,<ref name="Cave2011">{{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 }}</ref> while others view the evidence of benefit as established.<ref>{{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 }}</ref><ref>{{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 }}</ref><ref name="Geake2015">{{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 }}</ref> Long-term use appears safe in COPD<ref name="Decr2013">{{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 }}</ref> with adverse effects include [[tremor|shakiness]] and [[Palpitation|heart palpitations]].<ref name=Lancet2012/> When used with inhaled steroids they increase the risk of pneumonia.<ref name=Lancet2012/> While steroids and LABAs may work better together,<ref name=Cave2011/> it is unclear if this slight benefit outweighs the increased risks.<ref>{{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 }}</ref> There is some evidence that combined treatment of LABAs with long-acting [[muscarinic antagonist]]s (LAMA), an anticholinergic, may result in less exacerbations, less pneumonia, an improvement in forced expiratory volume ([[FEV1%]]) and potential improvements in quality of life when compared to treatment with LABA and an inhaled corticosteriod (ICS).<ref>{{cite journal | vauthors = Horita N, Goto A, Shibata Y, Ota E, Nakashima K, Nagai K, Kaneko T | title = Long-acting muscarinic antagonist (LAMA) plus long-acting beta-agonist (LABA) versus LABA plus inhaled corticosteroid (ICS) for stable chronic obstructive pulmonary disease (COPD) | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | issue = 2 | pages = CD012066 | date = February 2017 | pmid = 28185242 | pmc = 6464543 | doi = 10.1002/14651858.CD012066.pub2 }}</ref> All three together, LABA, LAMA and ICS, have some evidence of benefits.<ref>{{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 }}</ref> Indacaterol requires an inhaled dose once a day and is as effective as the other long-acting β<sub>2</sub> agonist drugs that require twice-daily dosing for people with stable COPD.<ref name=Geake2015/>

<!--Anticholinergics  -->
The two main anticholinergics used in COPD are [[ipratropium]] and [[tiotropium]]. Ipratropium is a short-acting muscarinic antagonist (SAMA), while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life,<ref name=Karner2014>{{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 }}</ref> and tiotropium provides those benefits better than ipratropium.<ref>{{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 }}</ref> It does not appear to affect mortality or the overall hospitalization rate.<ref name=Karner2014/> Anticholinergics can cause dry mouth and urinary tract symptoms.<ref name=Lancet2012/> They are also associated with increased risk of heart disease and [[stroke]].<ref name=Singh2013>{{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 }}</ref> [[Aclidinium]], another long-acting agent, reduces hospitalizations associated with COPD and improves quality of life.<ref>{{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 }}</ref><ref>{{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 }}</ref><ref name="Ni2014">{{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 }}</ref> The LAMA [[umeclidinium bromide]] is another anticholinergic alternative.<ref>{{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 }}</ref> 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]].<ref>{{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 }}</ref> Further research is needed comparing aclidinium to tiotropium.<ref name=Ni2014/>

===Corticosteroids===
Inhaled [[corticosteroid]]s are anti-inflammatories that are recommended by GOLD as a first-line maintenance treatment in COPD cases with repeated exacerbations.<ref name="Chen3">{{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 }}</ref><ref>{{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 }}</ref> 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.<ref name="Chen3"/> Oral [[glucocorticoid]]s 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.<ref>{{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 = 9 | issue = 9 | pages = CD001288 | date = September 2014 | pmid = 25178099 | doi = 10.1002/14651858.CD001288.pub4 | url = https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001288.pub4/epdf/abstract }}</ref> Five days of steroids work as well as ten or fourteen days.<ref>{{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 }}</ref>

The use of corticosteroids is associated with a decrease in the number of lymphoid follicles (in the [[BALT|bronchial lymphoid tissue]]).<ref name="Higham">{{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=}}</ref> 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.{{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.<ref name="NICE3"/>

===PDE4 inhibitors===
[[Phosphodiesterase-4 inhibitor]]s (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}}

===Other medications===
Long-term [[Preventive healthcare|preventive use]] of [[antibiotic]]s, specifically those from the [[macrolide]] class such as [[erythromycin]], reduce the frequency of exacerbations in those who have two or more a year.<ref name=Mammen2012>{{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}}</ref><ref name=Her2018>{{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 }}</ref> This practice may be cost effective in some areas of the world.<ref>{{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 }}</ref> Concerns include the potential for [[antibiotic resistance]] and side effects including [[hearing loss]], [[tinnitus]] and changes to the heart rhythm known as [[Drug-induced QT prolongation|long QT syndrome]].<ref name=Her2018 />

[[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}}

[[Mucolytic]]s may help to reduce exacerbations in some people with chronic bronchitis; noticed by less hospitalization and less days of disability in one month.<ref>{{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 }}</ref> [[Erdosteine]] is recommended by NICE.<ref name="BNF">{{cite web |title=Erdosteine |url=https://bnf.nice.org.uk/drug/erdosteine.html |website=NICE |access-date=20 July 2021}}</ref> 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.<ref name="Meldrum">{{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 }}</ref>

[[Cough medicine]]s are not recommended.<ref name="NHS1">{{cite web |title=Bronchitis |url=https://www.nhs.uk/conditions/bronchitis/ |website=nhs.uk |language=en |date=17 October 2017}}</ref> [[Beta blocker]]s 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.<ref name="NIH">{{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 }}</ref>

===Oxygen therapy===
{{Further|Effect of oxygen on chronic obstructive pulmonary disease}}
[[Oxygen therapy|Supplemental oxygen]] is recommended for those with [[hypoxemia|low oxygen levels]] in [[respiratory failure]] at rest (a [[partial pressure of oxygen]] less than 50–55&nbsp;mmHg or [[Oxygen saturation (medicine)|oxygen saturation]]s 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.<ref name="Khor">{{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=}}</ref> 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.<ref name="Khor"/> 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.<ref>{{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 }}</ref> 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.<ref>{{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 }}</ref><ref name=BTS2008>{{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 }}</ref> 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%.<ref name=BTS2008/>

=== Rehabilitation ===
[[Pulmonary rehabilitation]] is a program of exercise, disease management and counseling, coordinated to benefit the individual.<ref name="medline2021">{{cite web |title=Pulmonary Rehabilitation |url=https://medlineplus.gov/pulmonaryrehabilitation.html |website=medlineplus.gov |access-date=9 September 2021}}</ref> A severe exacerbertion 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.<ref name="Halpin2">{{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=}}</ref>

The optimal exercise routine, use of noninvasive ventilation during exercise and intensity of exercise suggested for people with COPD, is unknown.<ref>{{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 }}</ref><ref>{{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 | pmid = 24823712 | doi = 10.1002/14651858.CD007714.pub2 }}</ref> Performing endurance arm exercises improves arm movement for people with COPD and may result in a small improvement in breathlessness.<ref name="McKeough2016" /> Performing arm exercises alone does not appear to improve quality of life.<ref name="McKeough2016">{{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 }}</ref> [[Pursed-lip breathing]] exercises may be useful.<ref name="Mayer" /> ''[[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.<ref name="Ngai2016" /> Tai Chi was not found to be more effective than other exercise intervention programs.<ref name="Ngai2016">{{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 }}</ref> Inspiratory and expiratory muscle training (IMT, EMT) is an effective method for improving activities of daily living (ADL). A combination of IMT and walking exercises at home may help limit breathlessness in cases of severe COPD.<ref>{{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 }}</ref> Additionally, the use of low amplitude high velocity joint mobilization together with exercise improves lung function and exercise capacity.<ref name="Wearing 108–114">{{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 }}</ref> 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.<ref name="Wearing 108–114"/><ref>{{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 }}</ref>

[[Airway clearance technique]]s (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.<ref name="Osadnik_2012">{{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 = 3 | issue = 3 | pages = CD008328 | date = March 2012 | pmid = 22419331 | doi = 10.1002/14651858.CD008328.pub2 }}</ref> 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 hospitalisations related to respiratory issues.<ref name="Osadnik_2012" />

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 [[malnutrition|malnourished]].{{sfn|Gold Report 2021|pp=60–65|loc=Chapter 3: Evidence supporting prevention and maintenance therapy}}<ref name="Ferr2012">{{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 = 12 | pages = CD000998 | date = December 2012 | pmid = 23235577 | doi = 10.1002/14651858.CD000998.pub3 | veditors = Ferreira IM }}</ref>

===Management of exacerbations===
People with COPD can experience [[Acute exacerbation of chronic obstructive pulmonary disease|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 [[Asthma spacer|spacer]] or via a [[nebulizer]], with both appearing to be equally effective.<ref name="GOLD2013Chp3"/><ref>{{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}}</ref> Nebulization may be easier for those who are more unwell.<ref name="GOLD2013Chp3"/> [[Oxygen supplementation]] can be useful.<!--<ref name=Merk2016/> --> Excessive oxygen; however, can result in [[Hypercapnia|increased {{CO2}} levels]] and a decreased level of consciousness.<ref name=Merk2016>{{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}}</ref> Corticosteroids [[Systemic administration|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}}

===Room temperatures===
Maintaining [[room temperature]]s of at least 21&nbsp;°C [70&nbsp;°F] for a minimum of nine hours a day was associated with better health in those with COPD, especially for smokers.<ref>{{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=}}</ref> The World Health Organization (WHO) recommends indoor temperatures of a slightly higher range between 18&nbsp;°C and 24&nbsp;°C [65&nbsp;°F and 75&nbsp;°F].<ref>{{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 }}</ref>

===Room humidity===
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.<ref>{{cite web |title=COPD and Humidity: COPD and outdoor activity|date= 6 November 2018|publisher=healthline |url=https://www.healthline.com/health/copd/humidity#outdoor-activity }}</ref><ref>{{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}}</ref>

Keeping the indoor relative humidity above 40% RH significantly reduces the infectivity of aerosolized viruses.<ref>{{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 }}</ref>

==Procedures for emphysema==
{{Main|Lung volume reduction}}
There are a number of procedures to [[Lung volume reduction|reduce the volume of a lung]] in cases of severe emphysema with hyperinflation.

=== Surgical ===
{{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}}<ref name="Lancet2019">{{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 }}</ref> LVRS involves the removal of damaged tissue, which improves lung function by allowing the rest of the lungs to expand.<ref name=Lancet2012/><ref name=GOLD2013Chp3/> It is considered when the emphysema is in the upper lobes and when there are no comorbidities.<ref name="Duffy">{{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 }}</ref>

===Bronchoscopic===
{{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}}<ref name="NICE2">{{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 |access-date=7 July 2021}}</ref> [[Endobronchial valve]]s 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 [[atelectasis|collapse]] of the lobe that ensures a reduction in residual volume that improves lung function, the capacity for exercise and quality of life.<ref name="Klooster">{{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=}}</ref>

The placement of [[nitinol]] coils instead of valves is recommended where there is collateral ventilation that would prevent the use of valves.<ref name="Welling">{{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=}}</ref> Nitinol is a [[Nitinol biocompatibility|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.<ref name="Valipour">{{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 }}</ref>

===Other surgeries===
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.<ref name="Harr2012" /> [[Ventilation/perfusion scintigraphy]] is another imaging method that may be used to evaluate cases for surgical interventions and also to evaluate post-surgery responses.<ref name="seminars">{{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 }}</ref> A [[bullectomy]] may be carried out when a giant [[Focal lung pneumatosis|bulla]] occupies more than a third of a hemithorax.<ref name="Duffy"/>

==Prognosis==
[[File:Chronic obstructive pulmonary disease world map-Deaths per million persons-WHO2012.svg|thumb|upright=1.3|Chronic obstructive pulmonary disease deaths per million persons in 2012 {{refbegin|3}}{{legend|#ffff20|9–63}}{{legend|#ffe820|64–80}}{{legend|#ffd820|81–95}}{{legend|#ffc020|96–116}}{{legend|#ffa020|117–152}}{{legend|#ff9a20|153–189}}{{legend|#f08015|190–235}}{{legend|#e06815|236–290}}{{legend|#d85010|291–375}}{{legend|#d02010|376–1089}}{{refend}}]]
[[File:Chronic obstructive pulmonary disease world map - DALY - WHO2004.svg|upright=1.3|thumb|[[Disability-adjusted life year]]s lost to chronic obstructive pulmonary disease per 100,000&nbsp;inhabitants in 2004.<ref>{{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 }}</ref>
{{Col-begin}}
{{Col-break}}
{{legend|#b3b3b3|no data}}
{{legend|#ffff65|≤110}}
{{legend|#fff200|110–220}}
{{legend|#ffdc00|220–330}}
{{legend|#ffc600|330–440}}
{{legend|#ffb000|440–550}}
{{legend|#ff9a00|550–660}}
{{Col-break}}
{{legend|#ff8400|660–770}}
{{legend|#ff6e00|770–880}}
{{legend|#ff5800|880–990}}
{{legend|#ff4200|990–1100}}
{{legend|#ff2c00|1100–1350}}
{{legend|#cb0000|≥1350}}
{{col-end}}]]
COPD is progressive and can lead to premature death. It is estimated that 3% of [[disability adjusted life years|all disability]] is related to COPD.<ref name=DALY2012/> The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia.<ref name=DALY2012>{{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 }}</ref> The overall number of years lived with disability from COPD, however, has increased.<ref name=YLD2012>{{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 }}</ref>

There are many variables affecting the long-term outcome in COPD and GOLD recommends the use of a composite test ([[BODE index|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 assessment}}

NICE recommends against the use of BODE for the prognosis assessment in stable COPD; factors such as exacerbations and [[Frailty syndrome|frailty]] need to be considered.<ref name="NICE2" /> 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 admittance.{{sfn|Gold Report 2021|pp=104–109|loc=Chapter 5: Management of exacerbations}}

==Epidemiology==
Estimates of prevalence have considerable variation due to differences in analytical and surveying approach and the choice of diagnostic criteria.<ref name="CKS2">{{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}}</ref> An estimated 384 million people had 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.<ref name="WHO2021"/> 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.<ref name=Lancet2012/> Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence.<ref name=Lancet2012/>

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.<ref name=Ryc2012>{{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 }}</ref> This is most likely due to rates of smoking in women and men becoming more similar.<ref name=Harr2012/> 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.<ref>{{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 }}</ref>

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.<ref name="CKS2" /> 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.<ref name="CDCbasics">{{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}}</ref>

In 2011, there were approximately 730,000 hospitalizations in the United States for COPD.<ref name=Tor2013>{{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 }}</ref> 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.<ref name="WHO2019">{{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}}</ref>

==History==
{{Further|Emphysema#History|Chronic bronchitis#History}}
[[File:Giambattista morgagni.gif|thumb|upright=1.4|[[Giovanni Battista Morgagni]], 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.<ref name=History2006/> 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'', ''diffuse obstructive pulmonary syndrome''.<ref name=History2006/>

The terms ''emphysema'' and ''chronic bronchitis'' were formally defined as components of COPD in 1959 at the [[Novartis|CIBA]] guest symposium and in 1962 at the [[American Thoracic Society]] Committee meeting on Diagnostic Standards.<ref name=History2006/>

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".<ref name=History2006>{{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 }}</ref><ref name=Fish2008>{{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 }}</ref> In 1721 the first drawings of emphysema were made by Ruysh.<ref name=Fish2008 /> [[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.<ref name=History2006/> In 1842, [[John Hutchinson (surgeon)|John Hutchinson]] invented the [[spirometer]], which allowed the measurement of [[vital capacity]] of the lungs.<!--<ref name=History2006/> --> However, his spirometer could only measure volume, not airflow.<!--<ref name=History2006/> --> Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.<ref name=History2006/>

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.<ref name=woolcock84>{{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}}</ref> In 1953, Dr. 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.<ref>{{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 }}</ref>

Modern treatments were developed during the second half of the 20th century.<!--<ref name=History2005> --> Evidence supporting the use of [[steroid]]s in COPD was published in the late 1950s.<!--<ref name=History2005> --> [[Bronchodilator]]s came into use in the 1960s following a promising trial of [[isoprenaline]].<!--<ref name=History2005> --> Further bronchodilators, such as short-acting [[salbutamol]], were developed in the 1970s and the use of [[Long-acting beta-adrenoceptor agonist|long-acting bronchodilators]] began in the mid-1990s.<ref name=History2005>{{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 }}</ref>

==Society and culture==
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.<ref name="CAM">{{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}}</ref>

===Economics===
Globally, as of 2010, COPD is estimated to result in economic costs of $2.1&nbsp;trillion, half of which occurring in the developing world.<ref name=Cost2013>{{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 }}</ref> Of this total an estimated $1.9&nbsp;trillion are direct costs such as medical care, while $0.2&nbsp;trillion are indirect costs such as missed work.<ref>{{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}}</ref> This is expected to more than double by 2030.<ref name=Cost2013/> In Europe, COPD represents 3% of healthcare spending.<ref name="GOLD2013Chp3"/> In the United States, costs of the disease are estimated at $50&nbsp;billion, most of which is due to exacerbation.<ref name="GOLD2013Chp2"/> COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7&nbsp;billion.<ref name=Tor2013/>

==Research==
{{See also|COPD: Journal of Chronic Obstructive Pulmonary Disease}}
[[Hyaluronan]] is a [[Glycosaminoglycan#Hyaluronic acid|natural sugar]] in the [[extracellular matrix]] that provides a protective coating for cells. It has been shown that on exposure to pollution the hyaluronan in the lungs breaks down into fragments causing irritation and activation of the immune system. There follows subsequent airway constriction and inflammation. The study showed that the inhalation of unfragmented hyaluronan overcame the effects of fragmented HA and reduced inflammation. Inhaled HA only acts locally in the bronchial tree and does not interfere with any drug. It improves mucus clearance by allowing it to move more freely. Further studies are to be carried out in the 
US to determine optimum dosage levels.<ref name="NIEHS">{{cite web |title=NIH study shows hyaluronan is effective in treating chronic lung disease |url=https://www.nih.gov/news-events/news-releases/nih-study-shows-hyaluronan-effective-treating-chronic-lung-disease |website=National Institutes of Health (NIH) |access-date=7 August 2021 |language=EN |date=1 February 2021}}</ref>

A new [[Cryotherapy|cryogenic treatment]] aimed at the chronic bronchitic subtype using a ''liquid nitrogen metered cryospray'' is being trialled and was due to complete in September 2021.<ref name="Poggi">{{cite journal |vauthors=Poggi C, Mantovani S, Pecoraro Y, Carillo C, Bassi M, D'Andrilli A, Anile M, Rendina EA, Venuta F, Diso D |title=Bronchoscopic treatment of emphysema: an update |journal=J Thorac Dis |volume=10 |issue=11 |pages=6274–6284 |date=November 2018 |pmid=30622803 |pmc=6297441 |doi=10.21037/jtd.2018.10.43 |url=}}</ref><ref name="NCT">{{cite web |title=A Prospective Safety and Feasibility Study of the RejuvenAir™ System Metered Cryospray Therapy for Chronic Bronchitis Patients |url=https://clinicaltrials.gov/ct2/show/NCT02483637 |publisher=clinicaltrials.gov |access-date=16 August 2021 |date=25 January 2021}}</ref>

[[Stem-cell therapy]] using [[mesenchymal stem cell]]s has the potential to restore lung function and thereby improve quality of life. In June 2021 eight [[clinical trial]]s had been completed and seventeen were underway. Overall, stem cell therapy has proved to be safe. The trials include the use of stem cells from different sources such as [[adipose tissue]], [[bone marrow]] and [[Cord blood|umbilical cord blood]].<ref name="Chen1">{{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=}}</ref>

A procedure known as [[targeted lung denervation]] is being trialled and has been used as part of a clinical trial (2021) in a hospital in the UK. The new [[minimally invasive procedure]] which takes about an hour to carry out, places electrodes to destroy branches of the [[vagus nerve]] in the lungs. The vagus nerve is responsible for both [[muscle contraction]] and mucus secretion, which results in narrowing the airways. In those with COPD these nerves are overactive, usually as a result of smoking damage and the constant mucus secretion and airway constriction leads to the symptoms of cough, shortness of breath, wheeze and tightness of the chest.<ref name="rbht">{{cite web |title=First UK patients get pioneering new treatment for serious lung disease {{!}} Royal Brompton & Harefield hospitals |url=https://www.rbht.nhs.uk/first-uk-patients-get-pioneering-new-treatment-for-serious-lung-disease |website=www.rbht.nhs.uk |access-date=4 August 2021}}</ref>

The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have [[alpha-1 antitrypsin deficiency]] is unclear.<ref>{{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 }}</ref> A later clinical trial of double-dosing has shown some improvements in slowing the breakdown of elastin and the progression of emphysema with further studies being called for.<ref name="Campos">{{cite journal | vauthors = Campos MA, Geraghty P, Holt G, Mendes E, Newby PR, Ma S, Luna-Diaz LV, Turino GM, Stockley RA | display-authors = 6 | title = The Biological Effects of Double-Dose Alpha-1 Antitrypsin Augmentation Therapy. A Pilot Clinical Trial | journal = American Journal of Respiratory and Critical Care Medicine | volume = 200 | issue = 3 | pages = 318–326 | date = August 2019 | pmid = 30965011 | pmc = 6680306 | doi = 10.1164/rccm.201901-0010OC }}</ref>

[[Mass spectrometry]] is being studied as a diagnostic tool in COPD.<ref>{{cite journal | vauthors = Nambiar S, Bong How S, Gummer J, Trengove R, Moodley Y | title = Metabolomics in chronic lung diseases | journal = Respirology | volume = 25 | issue = 2 | pages = 139–148 | date = February 2020 | pmid = 30907495 | doi = 10.1111/resp.13530 | doi-access = free }}</ref>

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.<ref name=McLean2011>{{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 | url = http://discovery.dundee.ac.uk/ws/files/1821515/Telehealthcare_for_chronic_obstructive_pulmonary_disease.pdf }}</ref>

Evidence is growing for the effectiveness of [[Astaxanthin]] against lung disease including COPD. Astaxanthin is a potent antioxidant with anti-inflammatory properties and more trials are said to be needed into its use.<ref name="Cheng">{{cite journal |vauthors=Cheng J, Eroglu A |title=The Promising Effects of Astaxanthin on Lung Diseases |journal=Adv Nutr |volume=12 |issue=3 |pages=850–864 |date=June 2021 |pmid=33179051 |doi=10.1093/advances/nmaa143 |pmc=8166543 |url=}}</ref>

American COPD patients and their caregivers consider the following COPD-related research areas as the most important: family/social/community research, patients' well‐being, curative research, biomedical therapies, policy and holistic therapies.<ref>{{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 }}</ref>

==Other animals==
Chronic obstructive pulmonary disease may occur in a number of other animals and may be caused by exposure to tobacco smoke.<ref>{{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 }}</ref> Most cases of the disease, however, are relatively mild.<ref>{{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 }}</ref> In [[horse]]s 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.<ref name="MSDVet">{{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}}</ref> COPD is also commonly found in old dogs.<ref name=Miller1989>{{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 }}</ref>

==See also==
*[[Extracorporeal membrane oxygenation]]
*[[Dahl's sign]]

== References ==
{{Reflist}}

===Works cited===
{{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}}

== External links ==
{{commons category|Chronic obstructive pulmonary disease}}
*{{curlie|Health/Conditions_and_Diseases/Respiratory_Disorders/Chronic_Obstructive_Pulmonary_Disease/}}
* {{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]]
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[[Category:Wikipedia medicine articles ready to translate (full)]]
[[Category:Occupational safety and health]]