Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term respiratory symptoms and airflow limitation.[8] The main symptoms include shortness of breath and a cough which may or may not produce mucus.[4] COPD progressively worsens with everyday activities such as walking or dressing becoming difficult.[3]

Chronic obstructive pulmonary disease
Other namesChronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD)
Section of a lung showing centrilobular emphysema, with enlarged airspaces in the centre of a lobule usually caused by smoking and a major feature of COPD
SymptomsShortness of breath, chronic cough[1]
ComplicationsAnxiety, depression, pulmonary heart disease, pneumothorax[2][1]
Usual onsetOver 35 years old[1]
DurationLong term[1]
CausesTobacco smoking, air pollution, genetics[3]
Diagnostic methodSpirometry[4]
Differential diagnosisAsthma, congestive heart failure, bronchiectasis, tuberculosis, obliterative bronchiolitis, diffuse panbronchiolitis[5]
PreventionStopping smoking, improving indoor and outdoor air quality, tobacco control measures[3][6]
TreatmentPulmonary rehabilitation, long-term oxygen therapy, lung volume reduction[6]
MedicationInhaled bronchodilators and steroids[6]
Frequency174.5 million (2015)[7]
Deaths3.2 million (2019)[3]

The two most common conditions of COPD are emphysema and chronic bronchitis, and they have been the two classic COPD phenotypes.[9] Emphysema is defined as enlarged airspaces (alveoli) whose walls break down resulting in permanent damage to the 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.[10][11] Chronic bronchitis does not always result in airflow limitation but in young adults who smoke the risk of developing COPD is high.[12] Many definitions of COPD in the past included emphysema, and chronic bronchitis but these have never been included in GOLD report definitions.[8]

The most common cause of COPD is tobacco smoking, other risk factors include indoor and outdoor pollution and genetics.[12] In developing countries, common sources of indoor air pollution are the use of biomass fuels such as wood and dry dung fuel for cooking and heating.[13][12] Most people living in European cities are exposed to damaging levels of air pollution.[14] A number of occupations and associated substances including cadmium dust or fumes, and dust from grains that promote respiratory symptoms has been published in the UK.[15] Long-term exposure to any of these irritants causes an inflammatory response in the lungs, resulting in narrowing of the small airways and breakdown of lung tissue.The diagnosis is based on poor airflow as measured by spirometry.[4]

Most cases of COPD can be prevented by reducing exposure to risk factors such as smoking and indoor and outdoor pollutants.[16] While treatment can slow worsening, there is no conclusive evidence that any medications can change the long-term decline in lung function.[6] COPD treatments include smoking cessation, vaccinations, pulmonary rehabilitation, inhaled bronchodilators, and corticosteroids.[6] Some people may benefit from long-term oxygen therapy, lung volume reduction (surgical) or (bronchoscopic), and lung transplantation.[17] In those who have periods of acute worsening, increased use of medications, antibiotics, corticosteroids, and hospitalization may be needed.[18]

As of 2015, COPD affected about 174.5 million people (2.4% of the global population).[7] It typically occurs in males and females over the age of 35–40.[1][3] In 2019 it caused 3.2 million deaths, 80% occurring in lower and middle income countries,[3] up from 2.4 million deaths in 1990.[19][20] The number of deaths is projected to increase further because of continued exposure to risk factors and an aging population.[8] In the US in 2010 the economic cost was put at 32.1 billion US dollars, and projected to rise to 49 billion dollars in 2020.[21] In the UK this cost is estimated at £3.8 billion annually.[22]

Signs and symptoms

Signs and symptoms of stages of COPD.

Shortness of breath

A cardinal symptom of COPD is the chronic and progressive shortness of breath which is most characteristic of the condition.[4] Shortness of breath (breathlessness) is often the most distressing symptom.[23] In the advanced stages, or end stage pulmonary disease, it occurs during rest and may be always present.[24] Shortness of breath is a source of both anxiety and a poor quality of life in those with COPD.[25] 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.[4] Many people with more advanced COPD breathe through pursed lips, which can improve shortness of breath.[26] Shortness of breath is often responsible for reduced physical activity, and low levels of physical activity are associated with worse outcomes.[27][28] In severe and very severe cases there may be constant tiredness, weight loss, muscle loss, and anorexia.[4]


The most often first symptom of COPD is a chronic cough, which may or may not be productive of mucus as phlegm. An accompanying productive cough is only seen in up to 30% of cases. Sometimes limited airflow may develop in the absence of a cough.[4] Symptoms are usually worse in the morning.[29] When a cough persists for more than three months each year for at least two years, in combination with mucus production and without another explanation, it is by definition chronic bronchitis.[8] Chronic bronchitis can occur before the restricted airflow diagnostic of COPD.[8] The amount of phlegm coughed up as sputum can be intermittent.[4] Some people with COPD attribute the symptoms to a smoker's cough.[25] Sputum may be swallowed or spat out, depending often on social and cultural factors and is therefore difficult to evaluate.[4] In severe COPD, vigorous coughing may lead to rib fractures or to a brief loss of consciousness.[4] People with COPD often have increased breathlessness and frequent colds before seeking treatment.[4]


An acute exacerbation is a sudden worsening of signs and symptoms such as increased breathlessness, fast breathing, a fast heart rate, sweating, active use of muscles in the neck, a bluish tinge to the skin, and confusion or combative behavior in very severe exacerbations.[30][31] The usual cause of an exacerbation is a respiratory tract infection. Such infections can be bacterial or viral or even a combination, with the most common being the common cold virus.[12] Infections appear to be the cause of 50 to 75% of cases,[32][33] with bacteria in 30%, viruses in up to 50%,[34][35] and both in 25%.[36] Other risks include exposure to tobacco smoke (active and passive), and environmental pollutants – both indoor and outdoor.[37] During the COVID-19 pandemic, hospital admissions for COPD exacerbations sharply decreased which may be attributable to reduction of emissions and cleaner air.[38]

Smoke from wildfires are proving an increasing risk in many parts of the world, and government agencies have published protective advice on their websites. In the US the EPA advises that the use of dust masks do not give protection from the fine particles in wildfire, and instead advise the use of well-fitting particulate masks.[39] This same advice is offered in Canada to the effects of their forest fires.[40] Bushfires in Australia add to the high risk factors for COPD and its worsening for farmers.[41]

Cold temperatures may also play a role, with exacerbations occurring more commonly in winter.[42] Those with more severe underlying disease have more frequent exacerbations: in mild disease 1.8 per year, moderate 2 to 3 per year, and severe 3.4 per year.[43] Those with many exacerbations have a faster rate of deterioration of their lung function.[44] A pulmonary embolism (PE) (blood clot in the arteries of the lungs) can worsen symptoms in those with pre-existing COPD.[45] Signs of a PE in COPD include pleuritic chest pain and heart failure without signs of infection.[46]

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, depression, anxiety, and lung cancer.[47]

Anxiety, depression and muscle wasting are often complications of COPD.[2][1] Other complications include a reduced quality of life and increased disability, cor pulmonale, frequent chest infections including pneumonia, secondary polycythemia, respiratory failure, pneumothorax, lung cancer, and cachexia (muscle wasting).[1][2]

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.[48]

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 prodromal symptoms may delay its recognition and where they include loss of taste or smell COVID-19 is to be suspected.[38]


Many definitions of COPD in the past included chronic bronchitis and emphysema but these have never been included in GOLD report definitions.[8] Emphysema is defined as enlarged airspaces (alveoli) whose walls break down resulting in permanent damage to the lung tissue, and is just one of the structural abnormalities that can limit airflow. The condition can exist without airflow limitation but commonly it does.[10] 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.[12] These older definitions grouped the two types as type A and type B. Type A were emphysema types known as pink puffers due to their pink complexion, fast breathing rate, and pursed lips. Type B were chronic bronchitic types referred to as blue bloaters due to low oxygen levels causing a bluish color to the skin and lips, and swollen ankles.[49][50] This terminology was no longer accepted as useful, as most people with COPD have a combination of both emphysema and airway disease.[49] These are now recognized as the two major phenotypes of COPD – emphysematous phenotype and chronic bronchitic phenotype.[9]


The two classic emphysematous and chronic bronchitic phenotypes are fundamentally different conditions with unique underlying mechanisms.[9] 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.[51][52] 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.[9]

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.[53] Two inflammatory phenotypes show a phenotype stability; the neutrophilic inflammatory phenotype, and the eosinophilic inflammatory phenotype.[54] A pulmonary vascular COPD phenotype has been described due to cardiovascular dysfunction.[55] Another recognized phenotype is the frequent exacerbator.[56] The frequent exacerbator has two or more exacerbations a year, has a poor prognosis, and is described as a moderately stable phenotype.[57]


The cause of the development of COPD is the exposure to harmful particles or gases that irritate the lung causing inflammation. Such exposure needs to be significant or long-term.[8]

The most important risk factor for the development of COPD is tobacco smoke; other factors include exposure to indoor and outdoor pollutants, allergens, and occupational exposure.[29][12] In Europe airway hyperresponsiveness is rated as the second most important risk factor after smoking.[12] COPD develops from the inflammatory effects of toxic factors and their interaction with a number of host factors. Host factors include a genetic susceptibility, factors associated with poverty, aging and physical inactivity. Asthma and tuberculosis are also recognized as risk factors.[12]


Percentage of females smoking tobacco as of the late 1990s early 2000s
Percentage of males smoking tobacco as of the late 1990s and early 2000s. Note the scales used for females and males differ.[58]

The primary risk factor for COPD globally is tobacco smoking.[8] Of those who smoke, about 20% will get COPD,[59] and of those who are lifelong smokers, about half will get COPD.[60] In the United States and United Kingdom, of those with COPD, 80–95% are either current or previous smokers.[59][61][62] The likelihood of developing COPD increases with the number of cigarettes smoked.[63] Several studies indicate that women are more susceptible than men to the harmful effects of tobacco smoke.[64] In non-smokers, exposure to passive smoking (second-hand smoke) is the cause of 1.2 million deaths from the more than 8 million deaths worldwide due to tobacco smoke.[65] Other types of tobacco smoke, such as from cigar, pipe, water-pipe and hookah use, also confer a risk.[12] Water-pipe or hookah smoke appears to be as harmful or even more harmful as smoking cigarettes.[66]

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.[67] 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 FEV1.[68] 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.[67][69] 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.[67] 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.[67] 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.[70]

Women who smoke during pregnancy may increase the risk for the later development of COPD in their child.[71] For the same amount of cigarette smoking, women have a higher risk of COPD than men.[72]


Access to clean fuel and clean cooking facilities as of 2016.[73]

Poorly ventilated cooking fires, often fueled by coal or biomass fuels such as wood and dry dung fuel, lead to indoor air pollution and are one of the most common causes of COPD in developing countries.[74] These fires are a method of cooking and heating for nearly three billion people, with their health effects being greater among women due to greater exposure.[71][74] They are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.[75]

People who live in large cities have a higher rate of COPD compared to people who live in rural areas.[76] While urban air pollution is a contributing factor in exacerbations, its overall role as a cause of COPD is unclear.[71] Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD.[75] The overall effect in relation to smoking, however, is believed to be small.[71]

Occupational exposure

Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of COPD in both smokers and nonsmokers. A number of occupations and their associated substances including cadmium dust or fumes, and dust from grains that promote respiratory symptoms has been published in the UK.[15] Workplace exposure is believed to be the cause in 10–20% of cases.[77] In the United States, it is believed that it is related to more than 30% of cases among those who have never smoked and probably represents a greater risk in countries without sufficient regulations.[71]

A number of industries and sources have been implicated, including[75] high levels of dust in coal mining, gold mining (and mining in general, due to the common element of rock blasting, materials handling, and crushing), and the cotton textile industry, occupations involving silica and isocyanates, and fumes from welding.[78] Working in agriculture is also a risk.[75] In some professions, the risks have been estimated as equivalent to that of one-half to two packs of cigarettes a day.[79] Silica dust and fiberglass dust exposure can also lead to COPD, with the risk unrelated to that for silicosis.[80][81] The negative effects of dust exposure and cigarette smoke exposure appear to be additive or possibly synergistic (i.e. more than additive).[79]


Genetics play a role in the development of COPD.[71] It is more common among relatives of those with COPD who smoke than unrelated smokers.[71] Currently, the only clearly inherited risk factor is alpha-1 antitrypsin deficiency.[82] This risk is particularly high if someone deficient in alpha-1 antitrypsin also smokes.[82] It is responsible for about 1–5% of cases[82][83] and the condition is present in about three to four in 10,000 people.[84] Other genetic factors are being investigated,[82] of which many are likely.[75]


Normal lungs shown in upper diagram. Lungs damaged by COPD in lower diagram with an inset showing a cross-section of bronchioles blocked by mucus, and damaged alveoli.

COPD is a type of obstructive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and inability to breathe out fully (air trapping) exist.[45] The poor airflow is the result of small airways disease – chronic bronchiolitis, and emphysema (the breakdown of lung tissue).[85] The relative contributions of these two factors vary between people.[8]

COPD develops as a significant and chronic inflammatory response to inhaled irritants which ultimately leads to bronchial and alveolar remodelling in the lung. Thus, airway remodelling with narrowing of peripheral airway and emphysema are responsible for the alteration of lung function.[54] The mucociliary clearance is particularly altered with a dysregulation of cilia and mucus production. [86][87][88][89] Chronic bacterial infections may also add to the inflammatory state.[44] The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who smoke additionally have Tc1 lymphocyte involvement and some people with COPD have eosinophil involvement similar to that in asthma. Part of this cell response is brought on by inflammatory mediators such as chemotactic factors. Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors. The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow, and finally, poor absorption and release of respiratory gases.[71] General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood.[71]

Micrograph showing emphysema (left – large empty spaces) and lung tissue with relative preserved alveoli (right).

Narrowing of the airways occurs due to inflammation and scarring within them. This contributes to the inability to breathe out fully. The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time.[90] 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 hyperinflation or air trapping.[90][91] Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled.[92] Hyperinflation may also worsen during an exacerbation.[93]

Some also have a degree of airway hyperresponsiveness to irritants similar to those found in asthma.[84]

Low oxygen levels, and eventually, high carbon dioxide levels in the blood, can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation, and a reduced desire to breathe.[71] During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow, and worsening of gas transfer. This can also lead to insufficient ventilation, and eventually low blood oxygen levels.[94] Low oxygen levels, if present for a prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to the breakdown of capillaries in the lungs.

Both of these changes result in increased blood pressure in the arteries of the lungs, which may cause secondary right-sided heart failure also known as cor pulmonale.[71][95][96] This leads to symptoms of leg swelling[25] and bulging neck veins.[94] Cor pulmonale has become less common since the use of supplemental oxygen.[84]


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 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.[4][97]


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.[98] Two main components are measured to make the diagnosis, the forced expiratory volume in one second FEV1, which is the greatest volume of air that can be breathed out in the first second of a breath, and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath.[99] Normally, 75–80% of the FVC comes out in the first second[99] and a FEV1/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease.[98] Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly.[98] The National Institute for Health and Care Excellence criteria additionally require a FEV1 less than 80% of predicted.[23] People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide (DLCO) due to decreased surface area in the alveoli, as well as damage to the capillary bed.[100] Testing the peak expiratory flow (the maximum speed of expiration), commonly used in asthma diagnosis, is not sufficient for the diagnosis of COPD.[23]

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.[47]


MRC shortness of breath scale[23]
GradeActivity affected
1Only strenuous activity
2Vigorous walking
3With normal walking
4After a few minutes of walking
5With changing clothing
GOLD criteria[25]
SeverityFEV1 % 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.[97][47] The MRC breathlessness scale or the COPD assessment test (CAT) are simple questionnaires that may be used.[101][97] GOLD refers to a modified MRC scale that if used, needs to include other tests since it is simply a test of breathlessness experienced.[47][102] Scores on CAT range from 0–40 with the higher the score, the more severe the disease.[103] Spirometry may help to determine the severity of airflow limitation.[25] This is typically based on the FEV1 expressed as a percentage of the predicted "normal" for the person's age, gender, height, and weight.[25] Both the American and European guidelines recommend partly basing treatment recommendations on the FEV1.[98] The GOLD guidelines group people into four categories based on symptoms assessment, degree of airflow limitation, and history of exacerbations.[102] Weight loss, muscle loss, and fatigue are seen in severe and very severe cases.[47]

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.[5] A saber-sheath trachea may also be shown that is indicative of COPD.[104]

A CT scan is not routinely used except for the exclusion of bronchiectasis.[5] An analysis of arterial blood is used to determine the need for oxygen supplementation, and assess for 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.[25] In areas of the world where alpha-1 antitrypsin deficiency is common, people with COPD (particularly those below the age of 45 and with emphysema affecting the lower parts of the lungs) should be considered for testing.[25]

Differential diagnosis

COPD may need to be differentiated from other conditions such as congestive heart failure, asthma, bronchiectasis, tuberculosis, obliterative bronchiolitis, and diffuse panbronchiolitis.[105] 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.[106] Tuberculosis may also present with a chronic cough and should be considered in locations where it is common.[25] Chronic bronchitis with normal airflow is not classified as COPD.[84]


Most cases of COPD are potentially preventable through decreasing exposure to smoke and improving air quality.[75]

Smoking cessation

Keeping people from starting smoking is a key aspect of preventing COPD.[107] The policies of governments, public health agencies, and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking.[108] Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke, and while many places have instituted bans, more are recommended.[75]

In those who smoke, stopping smoking is the only measure shown to slow down the worsening of COPD.[109][110] 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.[111] Often, several attempts are required before long-term abstinence is achieved.[108] Attempts over 5 years lead to success in nearly 40% of people.[112]

Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive, and many smokers need further support.[113] 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.[108][110][112] 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.[114]

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.[75] Examples of these measures include the creation of public policy,[75] education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators, and dust control.[115][116] Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation.[117] If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing their work role.[118]


Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease.[75] This may be achieved by public policy efforts, cultural changes, and personal involvement.[31]

Many developed countries have successfully improved outdoor air quality through regulations. This has resulted in improvements in the lung function of their populations.[75] Those with COPD may experience fewer symptoms if they stay indoors on days when outdoor air quality is poor.[94]

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.[31] Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is also effective. Using fuels such as kerosene or coal might be better than traditional biomass such as wood or dung .[75]


COPD is not curable, but the symptoms are treatable and its progression can be delayed.[1] The major goals of management are to reduce exposure to risk factors including offering treatments that help with stopping smoking. Stopping smoking has the greatest potential for slowing the disease progression.[6] 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.[1] Other recommendations include vaccinations 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. Other illnesses are also managed. An action plan is drawn up and is to be reviewed.[119] 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.[120] 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.[121] 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.[17]

In those with advanced disease, palliative care may reduce symptoms, with morphine improving the feelings of shortness of breath.[122] Noninvasive ventilation may be used to support breathing.[122][123]

Corticosteroids by mouth improve the chance of recovery and decrease the overall duration of symptoms.[45][31] They work equally well as intravenous steroids but appear to have fewer side effects.[124] Five days of steroids work as well as ten or fourteen.[125] In those with a severe exacerbation, antibiotics improve outcomes.[126] A number of different antibiotics may be used including amoxicillin, doxycycline and azithromycin; whether one is better than the others is unclear.[127] There is no clear evidence of improved outcomes for those with less severe cases.[126] The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.[128] For people with type 2 respiratory failure (acutely raised CO
levels) bilevel positive airway pressure (BPAP) decreases the probability of death or the need of intensive care admission.[45] Fewer than 20% of exacerbations require hospital admission.[31] In those without acidosis from respiratory failure, home care ("hospital at home") may be able to help avoid some admissions.[31]

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.[57][129]


Inhaled short-acting bronchodilators are the primary medications used on an as needed basis; their use on a regular basis is not recommended.[6] The two major types are beta2-adrenergic agonists and anticholinergics; either in long-acting or short-acting forms. Beta2–adrenergic agonists target receptors in the smooth muscle cells in bronchioles causing them to relax and allow improved airflow. They reduce shortness of breath, tend to reduce dynamic hyperinflation, and improve exercise tolerance.[6][130] Short acting bronchodilators have an effect over 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.[6] If long-acting bronchodilators become insufficient, then inhaled corticosteroids are typically added.[45]

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.[131] Both types of agent appear to reduce the risk of acute exacerbations by 15–25%.[45] A 2018 review found the combination of LABA/LAMA may reduce COPD exacerbations and improve quality-of-life compared to long-acting bronchodilators alone.[132] 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.[133]

Several short-acting β2 agonists are available, including salbutamol (albuterol) and terbutaline.[31] They provide some relief of symptoms for four to six hours.[31] LABAs such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited,[134] while others view the evidence of benefit as established.[135][136][137] Long-term use appears safe in COPD[138] with adverse effects include shakiness and heart palpitations.[45] When used with inhaled steroids they increase the risk of pneumonia.[45] While steroids and LABAs may work better together,[134] it is unclear if this slight benefit outweighs the increased risks.[139] There is some evidence that combined treatment of LABAs with long-acting muscarinic antagonists (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).[140] All three together, LABA, LAMA, and ICS, have some evidence of benefits.[141] Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β2 agonist drugs that require twice-daily dosing for people with stable COPD.[137]

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,[142] and tiotropium provides those benefits better than ipratropium.[143] It does not appear to affect mortality or the overall hospitalization rate.[142] Anticholinergics can cause dry mouth and urinary tract symptoms.[45] They are also associated with increased risk of heart disease and stroke.[144][145] Aclidinium, another long-acting agent, reduces hospitalizations associated with COPD and improves quality of life.[146][147][148] The LAMA umeclidinium bromide is another anticholinergic alternative.[149] 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.[150] Further research is needed comparing aclidinium to tiotropium.[148]


Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease.[151] By themselves, they have no effect on overall one-year mortality.[152][153] Whether they affect the progression of the disease is unknown.[45] When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone.[154][155] Inhaled steroids are associated with increased rates of pneumonia.[156] The use of corticosteroids is associated with a decrease in the number of lymphoid follicles (in the bronchial lymphoid tissue).[157]

The 2018 NICE guidelines recommend the use of ICS in people with asthmatic features or features suggesting steroid responsiveness. These include any previous diagnosis of asthma or atopy, a higher blood eosinophil count, substantial variation in FEV1 over time (at least 400 mL), and at least 20% diurnal variation in peak expiratory flow. "Higher" eosinophil count was chosen, rather than specifying a particular value as it is not clear what the precise threshold should be or on how many occasions or over what time period it should be elevated.[158]

PDE4 inhibitors

Phosphodiesterase-4 inhibitors (PDE4 inhibitors) are anti-inflammatories that improve lung function and reduce exacerbations in moderate to severe illness. Roflumilast is a PDE4 inhibitor used orally once daily to reduce inflammation, it has no direct bronchodilatory effects. It is essentially used in treating those with chronic bronchitis along with systemic corticosteroids.[159] 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 suffering from depression.[159]

Other medications

Long-term antibiotics, specifically those from the macrolide class such as erythromycin, reduce the frequency of exacerbations in those who have two or more a year.[160][161] This practice may be cost effective in some areas of the world.[162] Concerns include the potential for antibiotic resistance and side effects including hearing loss, tinnitus, and changes to the heart rhythm (long QT syndrome).[161] Annual influenza vaccinations in those with COPD reduce exacerbations, hospitalizations and death.[127][163] Pneumococcal vaccination may also be beneficial.[127] A review of an oral Haemophilus influenzae vaccine found 1.6 exacerbations per year as opposed to a baseline of 2.1 in those with COPD.[164] This small reduction was not deemed significant.[164]

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. [6] Methylxanthines are not recommended for use in exacerbations due to adverse effects.[57]

Mucolytics may help to reduce exacerbations in some people with chronic bronchitis; noticed by less hospitalization and less days of disability in one month.[165] Erdosteine is recommended by NICE.[166] 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.[159] Erdosteine has been shown to significantly reduce the risk of exacerbations, shorten their duration, and hospital stays.[167]

Cough medicines are not recommended.[168] Beta blockers are not contraindicated for those with COPD, and should only be used where there is concomitant cardiovascular disease.[159]

Oxygen therapy

Supplemental oxygen is recommended for those with low oxygen levels in respiratory failure at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%).[17] When taking into account complications including cor pulmonale and pulmonary hypertension, the levels involved are 56–59 mmHg.[169] 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.[169] 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.[170] 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.[171][172] 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%.[172]


Pulmonary rehabilitation is a program of exercise, disease management, and counseling, coordinated to benefit the individual.[173] 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.[53]

The optimal exercise routine, use of noninvasive ventilation during exercise, and intensity of exercise suggested for people with COPD, is unknown.[174][175] Performing endurance arm exercises improves arm movement for people with COPD, and may result in a small improvement in breathlessness.[176] Performing arm exercises alone does not appear to improve quality of life.[176] Pursed-lip breathing exercises may be useful.[26] 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.[177] Tai Chi was not found to be more effective than other exercise intervention programs.[177] 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.[178] Additionally, the use of low amplitude high velocity joint mobilization together with exercise improves lung function and exercise capacity.[179] The goal of spinal manipulation therapy (SMT) is to improve thoracic mobility in an effort to reduce the work on the lungs during respiration, to in turn increase exercise capacity as indicated by the results of a systemic medical review.[179]

Airway clearance techniques (ACTs), such as postural drainage, percussion/vibration, autogenic drainage, hand-held positive expiratory pressure (PEP) devices and other mechanical devices, may reduce the need for increased ventilatory assistance, the duration of ventilatory assistance, and the length of hospital stay in people with acute COPD.[180] 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.[180]

Being either underweight or overweight can affect the symptoms, degree of disability, and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.[17][181]

Management of exacerbations

People with COPD can experience exacerbations (flare-ups) that are commonly caused by respiratory tract infections. The symptoms that worsen are not specific to COPD and differential diagnoses need to be considered.[57] 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.[57] These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer, with both appearing to be equally effective.[31][182] Nebulization may be easier for those who are more unwell.[31] Oxygen supplementation can be useful. Excessive oxygen; however, can result in increased CO
and a decreased level of consciousness.[183]

Lung volume reduction


Where there is severe emphysema with significant hyperinflation that has proved unresponsive to other therapies lung volume reduction surgery (LVRS) may be an option.[184][185] LVRS involves the removal of tissue from a lobe damaged most by emphysema, which allows the rest of the lungs to expand and give improved function.[45][31] It seems to be particularly effective if emphysema predominantly involves the upper lobe, but the procedure increases the risks of adverse events and early death for people who have diffuse emphysema.[186] In very severe cases lung transplantation might be considered.[184] A CT scan may be useful in surgery considerations.[84] Ventilation/perfusion scintigraphy is another imaging method that may be used to evaluate cases for surgical interventions and also to evaluate post-surgery responses.[187]


Minimally invasive bronchoscopic procedures may be carried out to reduce lung volume. These include the use of valves, coils, or thermal ablation.[17][188] Endobronchial valves are one-way valves that may be used in those with severe hyperinflation resulting from advanced emphysema; a suitable target lobe, and no collateral ventilation are required for this procedure. The placement of one or more valves in the lobe induces a partial collapse of the lobe that ensures a reduction in residual volume that improves lung function, the capacity for exercise, and quality of life.[189]

The placement of nitinol coils instead of valves is recommended where there is collateral ventilation that would prevent the use of valves. [190] Nitinol is a biocompatible alloy.

Both of these techniques are associated with adverse effects including persistent air leaks and cardiovascular complications. Thermal vapor ablation has an improved profile. Heated water vapor is used to target lobe regions which leads to permanent fibrosis and volume reduction. The procedure is able to target individual lobe segments, can be carried out regardless of collateral ventilation, and can be repeated with the natural advance of emphysema.[191]


Chronic obstructive pulmonary disease deaths per million persons in 2012
Disability-adjusted life years lost to chronic obstructive pulmonary disease per 100,000 inhabitants in 2004.[192]

COPD is usually progressive and can lead to premature death. It is estimated that 3% of all disability is related to COPD.[193] The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia.[193] The overall number of years lived with disability from COPD, however, has increased.[194]

There are many variables affecting the long-term outcome in COPD, and GOLD recommends the use of a composite test (BODE) that includes the main variables of body-mass index, obstruction of airways, dyspnea (breathlessness), and exercise, and not just spirometry results.[195]

NICE recommends against the use of BODE for the prognosis assessment in stable COPD; factors such as exacerbations and frailty need to be considered.[188] 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.[57]


Estimates of prevalence have considerable variation due to differences in analytical and surveying approach, and the choice of diagnostic criteria.[196] An estimated 384 million people had COPD in 2010, corresponding to a global prevalence of 12%.[8] The disease affects men and women almost equally, as there has been increased tobacco use among women in the developed world.[197] 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.[45] Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence.[45] The global numbers are expected to continue increasing as risk factors remain common and the population continues to get older.[107]

Around three million people die of COPD each year.[8] In some countries, mortality has decreased in men but increased in women.[198] This is most likely due to rates of smoking in women and men becoming more similar.[84] COPD is more common in older people.[71]

In the UK three million people are reported to be affected by COPD – 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.[196] 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.[199]

In 2011, there were approximately 730,000 hospitalizations in the United States for COPD.[200] 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.[201]


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.[202] Previously it has been known by a number of different names, including chronic obstructive bronchopulmonary disease, chronic obstructive respiratory disease, chronic airflow obstruction, chronic airflow limitation, chronic obstructive lung disease, nonspecific chronic pulmonary disease, diffuse obstructive pulmonary syndrome, and chronic obstructive airways disease.[202][203]

The terms emphysema, and chronic bronchitis were formally defined in 1959 at the CIBA guest symposium and in 1962 at the American Thoracic Society Committee meeting on Diagnostic Standards.[202] The word emphysema is derived from the Greek ἐμφυσᾶν emphysan meaning inflate – itself composed of ἐν en, meaning "in", and φυσᾶν physan, meaning "breath, blast".[204] The term chronic bronchitis came into use in 1808[205] Early descriptions of probable emphysema include: 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".[202][206] In 1721 the first drawings of emphysema were made by Ruysh.[206] These were followed with pictures by Matthew Baillie in 1789 and descriptions of the destructive nature of the condition. In 1814 Charles Badham used catarrh to describe the cough and excess mucus in chronic bronchitis. René Laennec, the physician who invented the stethoscope, used the term emphysema in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.[202]

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.[207] 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.[208]

Early treatments of chronic bronchitis included garlic, cinnamon and ipecac, among others.[205] Modern treatments were developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators came into use in the 1960s following a promising trial of isoprenaline. Further bronchodilators, such as short-acting salbutamol, were developed in the 1970s, and the use of long-acting bronchodilators began in the mid-1990s.[209]

Society and culture

COPD is known colloquially as smoker's lung, but it also occurs in people who have never smoked.[210] People with emphysema have been known as pink puffers or "type A" due to their frequent pink complexion, fast respiratory rate and pursed lips,[49] and people with chronic bronchitis have been referred to as blue bloaters or "type B" due to the often bluish color of the skin and lips from low oxygen levels and their swollen ankles.[211] This terminology is no longer used, as most people with COPD have a combination of both emphysema and airway disease.[84][49]

It is generally accepted that COPD is widely underdiagnosed, and many people remain untreated. In the US the NIH promoted November as COPD Awareness Month to be an annual focus on increasing awareness of the condition.[212]


Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world.[213] Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work.[214] This is expected to more than double by the year 2030.[213] In Europe, COPD represents 3% of healthcare spending.[71] In the United States, costs of the disease are estimated at $50 billion, most of which is due to exacerbation.[71] COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7 billion.[200]


Mass spectrometry is being studied as a diagnostic tool in COPD.[215]

Several new long-acting agents are under development.[45] Treatment with stem cells is under study.[216] While there is tentative data that it is safe, and the animal data is promising, there is little human data as of 2017.[217][218][219][220] The small amount of human data there is has shown poor results.[217][221]

A procedure known as targeted lung denervation, which involves decreasing the parasympathetic nervous system supply of the lungs, is being studied but does not have sufficient data to determine its use.[222] The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have alpha-1 antitrypsin deficiency is unclear.[223]

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.[224]

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.[225]

Other animals

Chronic obstructive pulmonary disease may occur in a number of other animals and may be caused by exposure to tobacco smoke.[226] Most cases of the disease, however, are relatively mild.[227] In horses it is known as recurrent airway obstruction (RAO) or heaves. RAO can be quite severe, and most often is linked to exposure to common allergens.[228] COPD is also commonly found in old dogs.[229]


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