Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible airway disorder usually caused by tobacco smoking. It is characterized by shortness of breath due to loss of elastic recoil of the lungs, leading to decreased total lung capacity and impaired gas exchange. It affects more than 5% of the population and is associated with high morbidity and mortality.[1] COPD is the third most common cause of death in the United States and the fifth most common cause of death worldwide. Its incidence and mortality rate are rising due to increasing worldwide cigarette use and air pollution.[2]

COPD pathophysiology involves chronic bronchitis and/or emphysema and sometimes poorly controlled chronic asthma (reversible airway hyperreactivity which can lead to remodeling and is now referred to as asthma-COPD overlap). Chronic bronchitis is characterized by airway inflammation and defined by the presence of a productive cough that lasts at least 3 months and occurs in more than 2 successive years. Emphysema entails abnormal and permanent enlargement of air spaces and destruction of the lung parenchyma, resulting in closure of small airways and loss of lung elasticity.

Risk Factors

Smoking. Cigarette smoking is the most important risk factor for COPD, causing more than 80% of cases.[3],[4] Secondhand smoke also contributes to COPD. However, relatively few smokers (< 15%) develop COPD. The amount and duration of smoking contributes to disease severity.

Genetics. Genetic factors play a role in the development of COPD, although it is unclear whether a genetic predisposition is a prerequisite for COPD to occur.

α1-antitrypsin deficiency. α1-antitrypsin is an inhibitor of the elastase enzyme. This inherited disorder predisposes affected individuals to emphysema due to the uncontrolled action of elastase, which destroys the lung parenchyma.

Airway hyperresponsivity.


Occupation. Certain occupational exposures (e.g., mining and agriculture) are linked to COPD.

Air pollution. The role of pollutants in the pathogenesis of COPD is unclear. However, the incidence of COPD and the frequency of acute exacerbations are significantly increased in areas of heavy air pollution.


Pulmonary function testing (spirometry) showing an obstructive pattern is the most reliable indicator for diagnosis. This would be a ratio of forced expiratory volume in 1 second to the forced vital capacity of < 70% (FEV1/FVC ratio < 70%). In addition, pulmonary function tests are used to determine severity of airflow limitation, assess response to medications, and follow disease progression.

Chest x-rays may reveal hyperinflation of the lungs—flattening of the diaphragm and radiolucency of the lung fields. However, x-rays may appear normal until the emphysema component is quite advanced. CT scans are more sensitive and specific and help determine whether the emphysema is centriacinar, panacinar, or paraseptal.

Hematocrit levels may be elevated due to chronic hypoxia.

Arterial blood gas concentration may reveal hypoxemia and, if severe, hypercapnia.

All patients diagnosed with COPD should be screened for α1-antitrypsin deficiency (ATTD), particularly in areas with high prevalence of ATTD.[5]


Smoking cessation is essential at any stage of the disease. Although lung damage will not be reversed, pulmonary function can improve.

Physical exercise, as part of a pulmonary rehabilitation program, can improve functional status in COPD. Exercise programs do not necessarily increase lung function, but they should increase patients’ ability to perform activities of daily living. Inspiratory muscle training in particular is associated with significant improvements in pulmonary capacity, endurance, exercise capacity, and dyspnea.[6] As with other forms of exercise, benefits are lost if patients do not maintain their efforts.[7]

Respiratory therapy and pulmonary rehabilitation improve quality of life and exercise capacity and reduce mortality.

Continuous or nighttime supplemental oxygen provides symptomatic relief and reduces the risk of mortality in patients with chronic hypoxemia.

Bronchodilators, including short-acting anticholinergics (e.g., ipratropium bromide) and β2-adrenergic agents (e.g., albuterol), may alleviate symptoms by reducing bronchial tone. Patients with spirometry that does not respond to bronchodilators may still have long-term improvement in symptoms with regular use. Anticholinergics, such as the long-acting agent tiotropium, may be combined with beta-agonists.

Methylxanthines (e.g., theophylline) are a controversial treatment and are rarely used. They may be beneficial in refractory COPD cases by augmenting the action of the diaphragm during exhalation, improving gas exchange, and increasing airway caliber.

The role of corticosteroids is still under investigation. Inhaled steroids may decrease exacerbations and slow the progression of symptoms, but have little impact on lung function and mortality. Systemic steroids may help hospitalized patients with acute exacerbations.

Phosphodiesterase-4 (PDE-4) inhibitors (e.g., roflumilast) decrease inflammation and may promote smooth muscle relaxation, reducing the risk of COPD exacerbations.[8]

Antibiotics are generally not indicated for patients with stable COPD. However, for frequent exacerbations they might be helpful (e.g., azithromycin).

Because infections are a common cause of COPD exacerbation, pneumococcal and seasonal influenza vaccines are recommended for all patients.

Surgical intervention may be helpful in a minority of advanced cases. Lung-volume-reduction surgery may benefit selected end-stage patients by increasing elastic recoil, improving expiratory airflow, and improving the function of the diaphragm and intercostal muscles. Lung transplantation may also be considered.

Emergency Treatments

Acute exacerbations of COPD must be treated emergently. It is important to identify and treat the cause of the exacerbation (e.g., infection, excessive sedation), administer bronchodilator therapy (e.g., beta-agonists) and supplemental oxygen, ensure clearance of pulmonary secretions, and closely monitor for signs of respiratory failure. Caution is required for oxygen administration, as excessive oxygenation may cause a lethal hypercapnia.

If respiratory failure occurs, intubation may be necessary. Noninvasive positive pressure ventilation (BiPAP) is often used in deteriorating patients and may eliminate the need for intubation.

Use of oral or intravenous steroids and antibiotics is the standard of care during an acute exacerbation.

New treatment options for reducing inflammation and for blocking certain enzymes (e.g., anti-proteases) are under investigation.

Nutritional Considerations

While smoking and other exposures are strong contributors to COPD, nutritional factors may influence the likelihood of developing this condition, as well as its clinical course. A Western diet and excesses of certain macronutrients appear to increase risk. Protective roles have emerged for healthy dietary patterns to include consumption of antioxidants, anti-inflammatory foods like fruits and vegetables, other sources of dietary fiber (e.g., legumes), certain micronutrients (vitamins D and E), dietary supplements (i.e., N-acetylcysteine), and avoidance of unhealthful fats and simple carbohydrates.

Particularly essential factors are as follows:

Maintaining a healthy weight. Obesity, and particularly abdominal obesity, is associated with a decline in lung function and a higher risk for respiratory disease in general. The Canadian Health Survey found that the prevalence of obesity was significantly higher in COPD patients compared with those without COPD (24.6% versus 17.1%). Obese patients with COPD have more significant dyspnea and more inferior overall health status when compared with healthy-weight individuals, and loss of excess weight often results in improved functional status. However, while obese COPD patients with mild to moderate disease are at higher mortality risk, overweight patients with more severe disease are at lower mortality risk (see below).[9]

Avoiding Western diets. Consuming the most foods in a Western dietary pattern (high in animal products and refined carbohydrates) was associated with more than a 2-fold risk for developing COPD. By comparison, individuals consuming the most foods in a healthful dietary pattern had a 45% lower risk, compared with those eating the least amount of these foods.[10] Similarly, the Nurses’ Health and Health Professionals studies found that persons consuming the most foods on the Alternative Healthy Eating Index (AHEI-2010) reduced their risk for COPD by > 30%, compared with those who ate the least.[11]

An essential part of these healthier dietary patterns may be legumes (beans, peas, and lentils), which are associated with a reduced risk for COPD, possibly through effects on reducing systemic inflammation.[12] A plant-based diet may provide a similar benefit, due to the association of dietary fiber with better lung function, reduced respiratory symptoms, and lower risk for COPD.[13]

Avoiding processed meats. Several studies have reported associations between processed meat consumption and risk for COPD.[14],[15],[16],[17] One of these studies also found a significantly higher (2-fold) risk for hospital readmission in COPD patients consuming the most processed meat, compared with those eating the lowest amount.[15] Dietary nitrites may be responsible for this effect by causing nitrosative stress that amplifies inflammatory processes in the airways. However, additional potential contributors to COPD are the advanced glycation end products (AGEs) found in meats. AGEs are elevated in the lungs of COPD patients compared with controls and increase the same biomarkers of inflammation linked to COPD risk and COPD exacerbations.[18],[19]

Fruits, vegetables, and tea. Several epidemiological studies have suggested a role for fruits and vegetables in COPD prevention.[20] Although clinical trials to test this hypothesis have been few and far between, one intervention study compared a group of COPD patients who significantly increased their fruit and vegetable intake with a control group that maintained its baseline consumption. The intervention group showed an annual increase in percentage predicted FEV1, compared with the control group, which exhibited a decrease in FEV1.[21]

The risk for COPD increases with decreasing levels of serum vitamin A, and NHANES III data revealed an inverse association between the intake of several carotenoids (as well as vitamin C) and COPD mortality.[22],[23] An increase in fruit intake by roughly 3.5 oz/day from baseline was associated with a 24% lower mortality risk in COPD patients followed over 20 years, and the Seven Countries Study found that the combined intakes of fruit and fish explained 67% of COPD mortality over 25 years.[10]

Green tea has antioxidant and anti-inflammatory effects. It reduces the risk of lung cancer and type 2 diabetes. A study between 2008 to 2015 of 13,750 participants looked at green tea intake and COPD risk. The study found reduced COPD risk with green tea intake more than 2 times per day.[24]

Vitamin E. Studies comparing COPD patients with healthy individuals have reported lower levels of alpha-tocopherol in plasma and peripheral skeletal muscle. In the COPD group, there is a lower mortality risk from respiratory disease with higher blood concentrations of vitamin E. In the Women’s Health Study, those who took vitamin E supplements (600 IU/day for 10 years) had a 10% lower risk for COPD when compared with a placebo group.[25]

Vitamin D. The prevalence of vitamin D deficiency is between 33% and 77% in those with advanced disease, and hypovitaminosis D is a risk factor for developing COPD. Supplementation of deficient patients has been found to strengthen airway muscles and reduce the incidence of moderate to severe COPD exacerbation in patients with COPD with baseline 25-hydroxyvitamin D levels of < 50 nmol/L.[26],[27]

N-acetylcysteine supplementation. N-acetylcysteine, a dietary supplement with mucolytic, antioxidant, and anti-inflammatory properties, reduces the number of COPD exacerbations when taken at a dosage of 600 mg twice daily.[28]

Follow suggestions for preventing and treating upper respiratory infection. Human rhinovirus infections cause roughly 80% of common colds and are a crucial trigger of COPD exacerbations.[29] (See Upper Respiratory Infection chapter.)

Nutritional Supplementation and COPD Mortality

Despite the risk represented by being obese, most patients with COPD are not overweight, and 25-40% are considered undernourished. It is essential to prevent excessive weight loss, as COPD patients with a body mass index of < 20 have a higher risk for disease exacerbations, compared with weight-stable individuals. Loss of excessive amounts of weight (particularly fat-free mass) in patients with COPD is multifactorial, and mechanisms include dyspnea, increased energy expenditure due to difficulty breathing, and an increase in proinflammatory cytokines that have diminishing effects on appetite and food intake.[30]

A joint statement published by the American Thoracic and European Respiratory Societies held that caloric supplementation should be considered in persons with a body mass index < 21 kg/m2, unintentional weight loss of > 5% in the past month or > 10% over 6 months, or depletion in fat-free or lean body mass.

Systematic reviews and meta-analyses have shown that oral nutritional supplementation in COPD patients significantly improves body weight, inspiratory and expiratory muscle strength, handgrip strength, quality of life, exercise performance, and the effects of exercise rehabilitation programs.[31]


Smoking cessation.

See Basic Diet Orders chapter.

Nutritional supplements, if indicated and per the recommendation of a registered dietitian.

What to Tell the Family

COPD is preventable in most cases by not smoking or by quitting smoking early. The family can play an important role in preventing COPD by encouraging smokers in the family to quit and by following healthful diets.

A family member who has COPD may require medications to reduce lung inflammation, dilate the bronchi, and reduce airway obstruction. Eventually, supplemental oxygen becomes necessary. Making sure the patient stays active helps prevent deconditioning and slows the progression of symptoms.


  1. Centers for Disease Control and Prevention (CDC). Chronic obstructive pulmonary disease among adults--United States, 2011. MMWR Morb Mortal Wkly Rep. 2012;61(46):938-43.  [PMID:23169314]
  2. Miniño AM, Murphy SL, Xu J, Kochanek KD. Deaths: final data for 2008. Natl Vital Stat Rep . 2011;59:1-126.
  3. Kuempel ED, Wheeler MW, Smith RJ, et al. Contributions of dust exposure and cigarette smoking to emphysema severity in coal miners in the United States. Am J Respir Crit Care Med. 2009;180(3):257-64.  [PMID:19423717]
  4. Lamprecht B, McBurnie MA, Vollmer WM, et al. COPD in never smokers: results from the population-based burden of obstructive lung disease study. Chest. 2011;139(4):752-763.  [PMID:20884729]
  5. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: 2020 Report. Global Initiative for Chronic Obstructive Lung Disease website. Accessed January 14, 2020.
  6. Geddes EL, Reid WD, Crowe J, et al. Inspiratory muscle training in adults with chronic obstructive pulmonary disease: a systematic review. Respir Med. 2005;99(11):1440-58.  [PMID:15894478]
  7. Weiner P, Magadle R, Beckerman M, et al. Maintenance of inspiratory muscle training in COPD patients: one year follow-up. Eur Respir J. 2004;23(1):61-5.  [PMID:14738232]
  8. Calverley PM, Rabe KF, Goehring UM, et al. Roflumilast in symptomatic chronic obstructive pulmonary disease: two randomised clinical trials. Lancet. 2009;374(9691):685-94.  [PMID:19716960]
  9. Hanson C, Rutten EP, Wouters EFM, Rennard S. Influence of diet and obesity on COPD development and outcomes. Int J COPD . 2014;9:723-733.
  10. Zheng PF, Shu L, Si CJ, et al. Dietary Patterns and Chronic Obstructive Pulmonary Disease: A Meta-analysis. COPD. 2016;13(4):515-22.  [PMID:26678388]
  11. Varraso R, Chiuve SE, Fung TT, et al. Alternate Healthy Eating Index 2010 and risk of chronic obstructive pulmonary disease among US women and men: prospective study. BMJ. 2015;350:h286.  [PMID:25649042]
  12. Young RP, Hopkins RJ. A review of the Hispanic paradox: time to spill the beans? Eur Respir Rev. 2014;23(134):439-49.  [PMID:25445942]
  13. Fonseca Wald ELA, van den Borst B, Gosker HR, et al. Dietary fibre and fatty acids in chronic obstructive pulmonary disease risk and progression: a systematic review. Respirology. 2014;19(2):176-184.  [PMID:24372903]
  14. Kaluza J, Larsson SC, Linden A, et al. Consumption of Unprocessed and Processed Red Meat and the Risk of Chronic Obstructive Pulmonary Disease: A Prospective Cohort Study of Men. Am J Epidemiol. 2016;184(11):829-836.  [PMID:27789447]
  15. de Batlle J, Mendez M, Romieu I, et al. Cured meat consumption increases risk of readmission in COPD patients. Eur Respir J. 2012;40(3):555-60.  [PMID:22408205]
  16. Jiang R, Paik DC, Hankinson JL, et al. Cured meat consumption, lung function, and chronic obstructive pulmonary disease among United States adults. Am J Respir Crit Care Med. 2007;175(8):798-804.  [PMID:17255565]
  17. Varraso R, Jiang R, Barr RG, et al. Prospective study of cured meats consumption and risk of chronic obstructive pulmonary disease in men. Am J Epidemiol. 2007;166(12):1438-45.  [PMID:17785711]
  18. DeChristopher LR, Uribarri J, Tucker KL. Intake of high fructose corn syrup sweetened soft drinks is associated with prevalent chronic bronchitis in U.S. Adults, ages 20-55 y. Nutr J. 2015;14:107.  [PMID:26474970]
  19. Varraso R, Camargo CA. Processed meat consumption and lung health: more evidence for harm. Eur Respir J. 2014;43(4):943-6.  [PMID:24687660]
  20. Kobayashi J, Ohtake K, Uchida H. NO-Rich Diet for Lifestyle-Related Diseases. Nutrients. 2015;7(6):4911-37.  [PMID:26091235]
  21. Keranis E, Makris D, Rodopoulou P, et al. Impact of dietary shift to higher-antioxidant foods in COPD: a randomised trial. Eur Respir J. 2010;36(4):774-80.  [PMID:20150206]
  22. Caram LM, Amaral RA, Ferrari R, et al. Serum Vitamin A and Inflammatory Markers in Individuals with and without Chronic Obstructive Pulmonary Disease. Mediators Inflamm. 2015;2015:862086.  [PMID:26339144]
  23. Ford ES, Li C, Cunningham TJ, et al. Associations between antioxidants and all-cause mortality among US adults with obstructive lung function. Br J Nutr. 2014;112(10):1662-73.  [PMID:25315508]
  24. Oh CM, Oh IH, Choe BK, et al. Consuming Green Tea at Least Twice Each Day Is Associated with Reduced Odds of Chronic Obstructive Lung Disease in Middle-Aged and Older Korean Adults. J Nutr. 2018;148(1):70-76.  [PMID:29378037]
  25. Agler AH, Kurth T, Gaziano JM, et al. Randomised vitamin E supplementation and risk of chronic lung disease in the Women's Health Study. Thorax. 2011;66(4):320-5.  [PMID:21257986]
  26. Hejazi ME, Modarresi-Ghazani F, Entezari-Maleki T. A review of Vitamin D effects on common respiratory diseases: Asthma, chronic obstructive pulmonary disease, and tuberculosis. J Res Pharm Pract. 2016;5(1):7-15.  [PMID:26985430]
  27. Martineau AR, James WY, Hooper RL, et al. Vitamin D3 supplementation in patients with chronic obstructive pulmonary disease (ViDiCO): a multicentre, double-blind, randomised controlled trial. Lancet Respir Med. 2015;3(2):120-130.  [PMID:25476069]
  28. Cazzola M, Calzetta L, Page C, et al. Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a meta-analysis. Eur Respir Rev. 2015;24(137):451-61.  [PMID:26324807]
  29. George SN, Garcha DS, Mackay AJ, et al. Human rhinovirus infection during naturally occurring COPD exacerbations. Eur Respir J. 2014;44(1):87-96.  [PMID:24627537]
  30. Itoh M, Tsuji T, Nemoto K, et al. Undernutrition in patients with COPD and its treatment. Nutrients. 2013;5(4):1316-35.  [PMID:23598440]
  31. Collins PF, Elia M, Stratton RJ. Nutritional support and functional capacity in chronic obstructive pulmonary disease: a systematic review and meta-analysis. Respirology. 2013;18(4):616-29.  [PMID:23432923]
Last updated: February 3, 2023