by Aliza Becker, BA, MPS
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide according to the World Health Organization, having caused 3.23 million deaths in 2019, 80% of which occurred in low- and middle-income countries.7 COPD is a progressive condition characterized by an increased difficulty with breathing.1 In healthy lungs, small blood vessels known as capillaries run along the walls of air sacs at the ends of thousands of bronchioles, which branch off from the bronchial tubes.1 During healthy breathing, oxygen passes through the walls of the air sacs into blood in the capillaries and carbon dioxide gas moves from the capillaries into the air sacs for expulsion from the body during a process known as gas exchange.1 However, in an individual with COPD, a reduction in the elasticity of the airways and/or air sacs; damage to the air sacs; an inflammatory response to toxic particles or gases; or the creation of an overabundant amount of mucus, clogging the airways, can make it harder to breathe.2,3 While COPD and asthma have similar symptoms, COPD is progressive, while asthma is reversible or controllable, and COPD is primarily the result of damage caused by smoking, while asthma is considered a chronic inflammatory disorder resulting from an overreaction of the immune system.4
Signs and Symptoms
Common symptoms include chronic cough, greater production of sputum (a mixture of mucus and saliva coughed up from the respiratory tract), and/or increasing difficulty with breathing (dyspnea).5 Spirometry, a test that measures how much air is exhaled and the speed of exhalation, is the primary method used to confirm a COPD diagnosis.5 According to the Global Initiative for Chronic Obstructive Lung Disease,5 the presence of a post-bronchodilator forced expiratory volume (FEV1)/forced vital capacity (FVC) (i.e., how much air a person can force out of their lungs in one second after bronchodilator therapy/the total amount of air exhaled) ratio of less than 0.70 confirms the presence of a persistent airflow limitation and, thus, COPD. COPD severity is divided into four categories (A, B, C, and D) according to the level of their symptoms and the risk of future exacerbations of the disease.5 Two primary forms of COPD exist: 1) chronic bronchitis, which involves a long-term cough with excessive sputum as a result of airway inflammation, and 2) emphysema, which involves a loss of alveolar elasticity leading to chronic dyspnea.6
Risk Factors
Female sex. Past research suggests COPD has traditionally affected men more than women.8,9 However, some research indicates that the impact of COPD in women may be growing.10-12 These effects may be due to both differences in behavior and biology according to sex. Among 1,705 women in sub-Saharan Africa who were in charge of cooking in their household—a more common role for women relative to men—researchers found that COPD was higher among those using biomass for cooking and those who had been cooking for more than 30 years.10 Biomass is renewable organic material that comes from plants and/or animals (e.g., wood or other agricultural matter, solid waste, landfill gas and biogas, and alcohol fuels [e.g., ethanol, biodiesel]). Other researchers have concurred—a systematic review and meta-analysis of 35 studies revealed that exposure to biomass smoke indoors is strongly associated with COPD,14 biomass smoke pollution is an important contributing factor to the development of chronic airway diseases in nonsmoking women,15 and people with COPD who were exposed to biomass smoke were more likely to be female.16
In Australia, researchers noted that men and women exhibited a parallel increase in mortality from lung cancer and COPD from 1960 to 1980 in Australia, with a subsequent reduction thereafter among men but a continuing increase for women;17 the author argues this trend is the result of the long latent period between exposure to cigarette smoke and the development of both of these diseases combined with the reduction in smoking among men from 69 percent in 1955 to less than 30 percent in recent years versus the fairly constant rate of 30 percent among women during the same time period.17 Separately, other investigators found that a significantly faster annual decline in FEV1%, the amount of air you can force from your lungs in one second during a spirometry test, was predicted with increasing age among female current smokers more so than in male smokers;18 and lung function was lost at a rate of 32mL per year faster among women with COPD and an FEV1/FVC ratio of less than the median compared to women with less obstruction, yet the difference among men was just 8mL/year.19 Researchers have noted that women have smaller airways compared to men, which may make female airways more susceptible to the adverse effects of cigarette smoke.18
Smoking or exposure to second-hand smoke. Individuals with COPD often have a history of smoking. The U.S. CDC reported that, in 2017, the age-adjusted prevalence rates of COPD were 15.2 percent among current cigarette smokers, 7.6 percent among former smokers, and 2.8 percent among adults who had never smoked; the agency added that, though a strong positive correlation between the state prevalence of COPD and state prevalence of current smoking was expected among current and former smokers, a similar relationship among adults who had never smoked suggests secondhand smoke exposure remains a potential risk factor for COPD. Indeed, an estimated 25 percent of adults with COPD in the United States have never smoked.20
Exposure to air pollution. Lung toxicity from sources other than tobacco smoke, such as environmental pollution, may also play a role. According to Adeloye et al.,9 comparing the percentage of increase in COPD cases from 1990 to 2010 between urban and rural residents yielded results of 90.5 percent vs. 44.6 percent, respectively.9 Ntritsos et al10 similarly observed a greater rate of COPD among urban dwellers compared to rural and mixed urban–rural dwellers. Chen et al21 compared the effects of fine and coarse particulate matter (PM) on lung function among the elderly in Taiwan, noting that long-term PM2.5 exposure primarily decreases the vital capacity of lung function, while PM2.5–10 exposure has a stronger negative effect on the function of conductive airways compared to PM2.5. Zhao et al22 also found that prolonged chronic exposure to PM2.5 in China led generally to reduced lung function, emphysematous lesions, and airway inflammation and, among patients with existing COPD, amplified cigarette smoke–induced changes. Elbarbary et al23 concurred using data from China that higher levels of exposure to ambient air pollution were associated with lower lung function, especially in individuals with existing COPD. Wang et al24 reported, following a study of six U.S. metropolitan regions, that long-term exposure to ambient air pollutants, especially ozone, was significantly associated with increasing rates of emphysema and worsening lung function. Finally, as reported by Hunt et al,25 following the great London fog of 1952, the incidence of COPD doubled (as demonstrated by autopsy results), suggesting that even short-term exposure to ambient air pollution may have adverse effects.
Associated health conditions. Given that individuals with COPD are often past or current smokers, many have an increased risk of developing lung cancer and cardiovascular diseases as a result of smoking-induced damage to the lungs and vasculature.26-28 In addition to lung cancer and cardiovascular events (e.g., heart diseases, heart failure, stroke), pneumonia, thoracic malignancies, respiratory failure, musculoskeletal dysfunction and depression, diabetes, and osteoporosis have also been associated with COPD.30-36
Managing COPD
Smoking cessation. Stopping smoking may be the most effective approach to managing COPD;37 up to 50 percent of patients with COPD continue to smoke following their diagnosis.38 In addition to avoiding further damage with continued smoking, cessation may also reduce the accelerated decline in FEV1 associated with COPD.39
Pharmacotherapy. Pharmaceutical options include bronchodilators, the mainstay option, and inhaled corticosteroids,40 as well as glucocorticoids (which may be nebulized, intravenous, inhaled, or given orally)41 and other drugs such as antibiotics, mucolytic agents, immunoregulators, and vasodilators.42 Appropriate inhaler technique can reduce symptoms such as cough and breathlessness during physical exertion by as much as 50 percent.43
Pulmonary rehabilitation. Pulmonary rehabilitation can also reduce symptoms of COPD,37 and may have other health benefits, such as reduced frailty44 and improved pulmonary muscle strength.45 Finally, some patients with COPD may undergo lung transplantation.3
Proper nutrition. According to the American Lung Association (ALA), diet can affect your breathing. For example, the body uses oxygen to metabolize food, a process that produces energy, as well as carbon dioxide, the waste product we exhale. Carbohydrate metabolism produces the most carbon dioxide compared to other food groups, whereas fat metabolism produces the least amount of carbon dioxide, suggesting that consuming less carbohydrates might improve breathing.46
The ALA recommends the following:46
- Choose complex carbohydrates over simple carbohydrates. Complex carbohydrates include whole grains (e.g., whole grain bread and pasta, oatmeal, brown rice) and whole fresh fruit and vegetables. Simple carbohydrates include highly processed foods, such as white breads and pastas, granulated sugar, candies, cakes, cookies, sugary soft drinks, and packaged baked goods.
- Get plenty of fiber. Eat 20 to 30 grams of fiber each day. Good sources of fiber include whole grains, nuts, seeds, beans, and fresh fruits and vegetables (leave the skin on when possible). Food processing removed nutrients, especially fiber, so avoid highly processed foods.
- Eat a good source of protein at least twice a day. Protein choices include milk, eggs, cheese, meat, fish, and poultry. For plant-based sources, consider tofu, tempeh, lentils, chickpeas, nuts, and beans or peas.
- Choose mono- and poly-unsaturated fats. These fats are plant-based, so they do not contain cholesterol. Avocados, nuts, seeds, olives, and olive and canola oils are examples of mono- and polyunsaturated fats.
- Limit foods that contain trans- and saturated fat. These fats come from animal-based foods (butter, meat fat, meat skin), highly processed foods, such as hydrogenated vegetable oils and packaged baked goods (e.g., cookies ,potato chips, cakes, crackers, and pastries).
- Monitor sodium intake. Too much salt intake can cause edema and raise blood pressure.
- Stay hydrated. Drinking plenty of water helps keep bronchial mucus thin, making it easier to expel.
- Consult with a registered dietician nutritionist (RDN) or other qualified healthcare professional. An RDN can assess your nutritional needs and help you devise a nutrition plan that is right for you.
References
1. National Heart, Lung, and Blood Institute. How the lungs work. https://www.nhlbi.nih.gov/health-topics/how-lungs-work. Accessed November 9, 2021.
2. Hogg JC. Lung structure and function in COPD. Int J Tuberc Lung Dis. 2008;12(5):
467–479.
3. Hogg JC, Timens W. The pathology of chronic obstructive pulmonary disease. Annu Rev Pathol. 2009;4:435–459.
4. Cukic V, Lovre V, Dragisic D, Ustamujic A. Asthma and chronic obstructive pulmonary disease (COPD)—differences and similarities. Mater Sociomed. 2012;24(2):100–105.
5. Vestbo J, Hurd SS, Agustí AG, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. J Respir Crit Care Med. 2013;187(4):347–365.
6. Haddad M, Sharma S. Physiology, Lung. [Updated 2021 Jul 22]. In: StatPearls [Internet]. Treasure Island, Florida: StatPearls Publishing; 2021.
7. World Health Organization. Chronic obstructive pulmonary disease (COPD). https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd). Accessed November 15, 2021.
8. Adeloye D, Cha S, Lee C, et al. Global and regional estimates of COPD prevalence: systematic review and meta–analysis. J Glob Health. 2015;5(2):020415.
9. Varmaghani M, Dehghani M, Heidari E, et al. Global prevalence of chronic obstructive pulmonary disease: systematic review and meta-analysis. East Mediterr Health J. 2019;25(1):47–57.
10. Ntritsos G, Franek J, Belbasis L, et al. 11Gender-specific estimates of COPD prevalence: a systematic review and meta-analysis. Int J Chron Obstruct Pulmon Dis. 2018;13:1507–1514.
11. Rycroft CE, Heyes A, Lanza L, Becker K. Epidemiology of chronic obstructive pulmonary disease: a literature review. Int J Chron Obstruct Pulmon Dis. 2012;7:457–494.
12. Mannino DM, Homa DM, Akinbami LJ, et al. Chronic obstructive pulmonary disease surveillance—United States, 1971–2000. MMWR Surveill Summ. 2002;51(6):1–16.
13. Sana A, Meda N, Kafando B, et al. Prevalence of COPD among women and relation with cooking fuel choice in Ouagadougou, Burkina Faso. Int J Tuberc Lung Dis. 2020;24(9):928–933.
14. Pathak U, Gupta NC, Suri JC. Risk of COPD due to indoor air pollution from biomass cooking fuel: a systematic review and meta-analysis. Int J Environ Health Res. 2020;30(1):75–88.
15. Ekici A, Ekici M, Kurtipek E, et al. Obstructive airway diseases in women exposed to biomass smoke. Environ Res. 2005;99(1):93–98.
16. Ramírez-Venegas A, Sansores RH, Pérez-Padilla R, et al. Survival of patients with chronic obstructive pulmonary disease due to biomass smoke and tobacco. Am J Respir Crit Care Med. 2006;173(4):393–397.
17. Berend N. Epidemiological survey of chronic obstructive pulmonary disease and alpha-1-antitrypsin deficiency in Australia. Respirology. 2001;6 Suppl:S21–S25.
18. Gan WQ, Man SFP, Postma DS, et al. Female smokers beyond the perimenopausal period are at increased risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis. Respir Res. 2006;7(1):52.
19. Watson L, Vonk JM, Löfdahl CG, et al. Predictors of lung function and its decline in mild to moderate COPD in association with gender: results from the Euroscop study. Respir Med. 2006;100(4):746–753.
20. Wheaton AG, Liu Y, Croft JB, et al. Chronic Obstructive Pulmonary Disease and Smoking Status—United States, 2017. MMWR Morb Mortal Wkly Rep. 2019;68(24):533–538.
21. Chen C-H, Wu C-D, Chiang H-C, et al. The effects of fine and coarse particulate matter on lung function among the elderly. Sci Rep. 2019;9(1):14790.
22. Zhao J, Li M, Wang Z, et al. Role of PM 2.5 in the development and progression of COPD and its mechanisms. Respir Res. 2019;20(1):120.
23. Elbarbary M, Oganesyan A, Honda T, et al. Ambient air pollution, lung function and COPD: cross-sectional analysis from the WHO Study of AGEing and adult health wave 1. BMJ Open Respir Res. 2020;7(1):e000684.
24. Wang M, Aaron CP, Madrigano J, et al. Association between long-term exposure to ambient air pollution and change in quantitatively assessed emphysema and lung function. JAMA. 2019;322(6):546–556.
25. Hun At, Abraham JL, Judson B, Berry CL. Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues. Environ Health Perspect. 2003;111(9):1209–1214.
26. Durham AL, Adcock IM. The relationship between COPD and lung cancer. Lung Cancer. 2015;90(2):121–127.
27. Morgan AD, Zakeri R, Quint KJ. Defining the relationship between COPD and CVD: what are the implications for clinical practice?. Ther Adv Respir Dis. 2018;12:1753465817750524.
28. Carr LL, Jacobson S, Lynch DA, et al. Features of COPD as predictors of lung cancer. Chest. 2018;153(6):1326–1335.
29. Sandelin M, Mindus S, Thuresson M, et al. Factors associated with lung cancer in COPD patients. Int J Chron Obstruct Pulmon Dis. 2018;13:1833–1839.
30. Sidney S, Sorel M, Quesenberry Jr. CP, et al. COPD and incident cardiovascular disease hospitalizations and mortality: Kaiser Permanente Medical Care Program. Chest. 2005;128(4):2068–2075.
31. Curkendall SM, DeLuise C, Jones JK, et al. Cardiovascular disease in patients with chronic obstructive pulmonary disease, Saskatchewan Canada cardiovascular disease in COPD patients. Ann Epidemiol. 2006;16(1):63–70.
32. Holguin F, Folch E, Redd SC, Mannino DM. Comorbidity and mortality in COPD-related hospitalizations in the United States, 1979 to 2001. Chest. 2005;128(4):2005–2011.
33. Kinnunen T, Säynäjäkangas O, Tuuponen T, Keistinen T. Impact of comorbidities on the duration of COPD patients’ hospital episodes. Respir Med. 2003;97(2):143–146.
34. Nussbaumer-Ochsner Y, Rabe KF. Systemic manifestations of COPD. Chest. 2011;139(1):165–173.
35. Gayle A, Dichinson S, Poole C, et al. Incidence of type II diabetes in chronic obstructive pulmonary disease: a nested case–control study. NPJ Prim Care Respir Med. 2019;29(1):28.
36. Chen Y-W, Ramsook AH, Coxson HO, et al. Prevalence and risk factors for osteoporosis in individuals with COPD: a systematic review and meta-analysis. Chest. 2019;156(6):1092–1110.
37. Mulhall P, Criner G. Non-pharmacological treatments for COPD. Respirology. 2016;21(5):791–809.
38. Karadogan D, Onal O, Sahin DS, Kanbay Y. Factors associated with current smoking in COPD patients: A cross-sectional study from the Eastern Black Sea region of Turkey. Tob Induc Dis. 2018;16:22.
39. Kanner RE, Connett JE, Williams DE, Buist AS. Effects of randomized assignment to a smoking cessation intervention and changes in smoking habits on respiratory symptoms in smokers with early chronic obstructive pulmonary disease: the Lung Health Study. Am J Med. 1999;106(4):410–406.
40. Vianna EO, Martin RJ. Bronchodilators and corticosteroids in the treatment of asthma. Drugs Today (Barc). 1998;34(3):203–223.
41. Zhang J, Zheng J, Huang K, et al. Use of glucocorticoids in patients with COPD exacerbations in China: a retrospective observational study. Ther Adv Respir Dis. 2018;12:1753466618769514.
42. Montuschi P. Pharmacological treatment of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2006;1(4):409–423.
43. Gregoriano C, Dieterle T, Breitenstein A-L, et al. Use and inhalation technique of inhaled medication in patients with asthma and COPD: data from a randomized controlled trial. Respir Res. 2018;19(1):237.
44. Gephine S, Saey D, Grosbois J-M, et al. Home-based pulmonary rehabilitation is effective in frail COPD patients with chronic respiratory failure [published online ahead of print November 9, 2021]. Chronic Obstr Pulm Dis.
45. Santiworakul A, Piya-Amornphan N, Jianramas N. A Home-based multimedia pulmonary rehabilitation program improves clinical symptoms and physical performance of patients with chronic obstructive pulmonary disease. Int J Environ Res Public Health. 2021;18(21):11479.
46. American Lung Association. Nutrition and COPD. Updated 10 Jun 2021. https://www.lung.org/lung-health-diseases/lung-disease-lookup/copd/living-with-copd/nutrition. Accessed 24 Jan 2022.
About the Author
Ms. Becker is the managing editor of The Journal of Innovations in Cardiac Rhythm Management. She also works as a freelance editor and as a teaching assistant for the George Washington University’s Master of Professional Studies in Publishing program.
