Condition Definition

Chronic obstructive pulmonary disease (COPD) is defined by a reduction in airflow that is not entirely reversible. Both current guidelines and the community standard for diagnostic spirometry in the United States require that fixed obstructive physiology be identified by a post-bronchodilator forced expiratory volume in 1 second (FEV₁)/forced vital capacity (FVC) less than 0.70.⁴ COPD is a progressive, chronic condition without a known cure. COPD is characterized by continual respiratory decline often associated with acute exacerbations that can result in hospitalization and ultimately death.^4–6 Although the degree of obstruction and symptoms (e.g., dyspnea, cough, fatigue) progress over time, the trajectory of decline can vary significantly among patients due to the complex interaction of genes with environmental exposures and other risk factors.^{7, 8}

COPD can be classified by the degree of obstruction, or symptoms, or both (Table 1). The degree of obstruction characterized by the post-bronchodilator FEV₁ percent predicted (i.e., ratio of volume exhaled in the first second over the volume predicted by any of a number of reference equations based on age, gender, race, and height).^{4, 9} In addition to the severity of airflow limitation (i.e., spirometric grade), the 2022 Global Initiative for Chronic Obstructive Lung Disease (GOLD) Global Strategy for the Diagnosis, Management and Prevention of COPD also recommends patients undergo assessment of their symptoms using standardized assessment tools (i.e., Modified British Medical Research Council [mMRC] questionnaire or COPD Assessment Test [CAT]).¹⁰ The mMRC is a dyspnea scale and the CAT captures a wider range of symptoms (e.g., cough, phlegm production, chest tightness, exercise tolerance, energy).

Table 1

Classification of COPD as Defined by Global Initiative for Chronic Obstructive Lung Disease (GOLD).

Prevalence and Risk Factors

In 2020, the Centers for Disease Control and Prevention (CDC) reported that chronic lower respiratory disease, composed chiefly of COPD, was the sixth leading cause of death in the United States, in spite of COPD-related mortality declining over the past 20 years.^{11, 12} The prevalence of COPD in U.S. adults varies from approximately 5 to 20 percent, depending on the populations studied and the disease criteria used. Measurements of the prevalence and burden of COPD are variable because prevalence estimates rely on a mix of self-report, spirometry, and administrative sources. Estimates from the 2020 Behavioral Risk Factor Surveillance System (BRFSS) showed that 6.2 percent of adults reported having been diagnosed with COPD.¹³ A 2019 systematic review estimated that the prevalence of all stages of COPD in the Americas was 14.5 percent.¹⁴

The major risk factor for developing COPD and COPD mortality is exposure to smoke or fumes, notably direct or indirect exposure to cigarette smoke.¹⁵ In 2017, the age-adjusted prevalence of COPD was 15.2 percent among current smokers, 7.6 percent among former smokers, and 2.8 percent among adults who had never smoked based on BRFSS estimates.¹⁶ Certain occupations, such as mining, farming and industrial work, which expose individuals to various inflammatory agents and irritants (e.g., respiratory crystalline silica, coal mine dust, toxins, organic dust, industrial chemicals), have been associated with the development of COPD. ^{17, 18} Occupational exposures are estimated to contribute to 15 percent of COPD cases. The most common environmental exposures linked to COPD include traffic pollutants and wood smoke.¹⁹ Additionally, exposure to secondhand smoke, heredity, a history of childhood respiratory infections, and asthma have been shown to increase the risk of developing the disease.^{15, 19–23} The higher prevalence of and morbidity from COPD in persons of low socioeconomic status (SES) is due to difference in health behaviors, sociopolitical factors, as well as social and structural environmental exposures.²⁴ And the higher prevalence of and morbidity from COPD in rural as compared to urban areas in the United States is, in part, related to SES (i.e., rural residents poorer and less education), as well as greater obstacles to care.²⁵

COPD prevalence also appears to vary by sex and racial and/or ethnic groups. Although prevalence and mortality are higher in men than women, the trend over time suggests more improvement for men than women. Data from the National Vital Statistics System (NVSS) found that age-adjusted COPD-related mortality for men declined from 57 deaths per 100,000 in 1999 to 40.5 in 2019; however, for women age-adjusted COPD-related mortality remained relatively stable, 35.3 deaths per 100,000 in 1999 and 34.3 in 2019.¹² This is thought to be due to a variety of factors, including increasing smoking rates among women, differences in environmental exposures, and potential biological or hormonal mechanisms affecting the susceptibility to COPD.²⁶ Data from the 2017 BRFSS found the highest rates of COPD were among Native American/Alaska Native populations (11.9%) followed by those identified as ‘other/multiracial’ (9.3%), White (6.7%), Black (6.6%), ‘Hispanic’ (3.6%), Native Hawaiian/Pacific Islander (3.3%), and Asian (1.7%).¹⁶ Analysis of data from BRFSS indicates that disproportionate socioeconomic challenges account for the comparatively high prevalence among Native American/Alaska Native populations.²⁷ Native Americans also have the highest prevalence of current smoking that most other racial and/or ethnic group in the United States. In 2019, 20.9 percent of Native American/Alaska Native adults in the United States smoked cigarettes compared with 14.0 percent of US adults overall.²⁸ According to 2018 data from the NVSS, age-adjusted death rates per 100,000 persons for chronic lower respiratory disease (mostly COPD) was highest in White adults (45.0), followed by Native American/Alaska Native adults (36.4), then Black (30.5), ‘Hispanic or Latino’ (17.0) and Asian/Pacific Islander (11.6) adults.²⁹ And although White adults have a higher prevalence of COPD than Black adults, Black adults experience higher hospitalizations rates, worse COPD-related quality of life, and their COPD-related mortality is not declining at the same rate as White adults.³⁰

Screening and Active Case Finding

Many patients with COPD go undetected despite having symptoms for multiple reasons, including under-recognition and/or under-reporting of mild symptoms (e.g., dyspnea) or nonspecific symptoms (e.g., fatigue). Therefore, screening or active case finding (i.e., systematically assessing for symptoms and/or risk factors and performing spirometry) would detect persons otherwise not diagnosed with opportunistic case finding as part of routine care. Earlier diagnosis of COPD may help prevent poorer outcomes and higher economic costs typically associated with persons diagnosed at more advanced stages.^31–33 Earlier COPD diagnosis may result in better disease management with non-pharmacologic interventions (e.g., smoking cessation, exercise) and medications to reduce dyspnea, exacerbations, and to improve quality of life. Overall, adults with yet undiagnosed COPD generally have fewer symptoms and/or better lung function than their diagnosed counterparts.^{34, 35} One recent and large prospective Danish cohort study examined the rates of undiagnosed COPD in individuals considered at risk for COPD (defined as age 40 years or older, with cumulative tobacco consumption of ten years or greater). Eleven percent of at-risk participants met the COPD criteria, 78 percent of whom were yet undiagnosed.³⁶ Of those who were yet undiagnosed, 89 percent had mild to moderate COPD and 71 percent of were symptomatic. However, most of those who were symptomatic yet undiagnosed, had minimal symptoms, 73 percent had an mMRC score of less than 2. Adults with asymptomatic undiagnosed COPD had a mean FEV₁ of around 71 percent predicted, compared with an FEV₁ of around 66 percent predicted in persons with symptoms, yet undiagnosed. All adults with undiagnosed COPD had an increased risk of exacerbations and pneumonia, including those who were asymptomatic.³⁶ Other studies have demonstrated that screening or active case finding typically identifies persons with mild to moderate COPD or mean population FEV₁ ≥ 60 percent.^37–39

Screening or active case finding for COPD in primary care may involve screening those at risk (e.g., based on age and smoking status) for COPD using spirometry or using screening questionnaires for more detailed risk and symptoms assessment to inform who receives spirometry. These questionnaires can typically be quickly administered or self-administered (e.g., the Lung Function Questionnaire [LFQ],^{40, 41} the COPD Diagnostic Questionnaire [CDQ],^{42, 43} the COPD population screener [COPD-PS],⁴⁴ and the Salzburg COPD-screening questionnaire [SCSQ]).⁴⁵ Other brief screening questionnaires can incorporate peak expiratory flow (PEF) (e.g., COPD Assessment in Primary Care to Identify Undiagnosed Respiratory Disease and Exacerbation Risk [CAPTURE TM]).^{46, 47}Other ‘pre-screeners’ can include point of care tools measuring FEV known as ‘handheld spirometry’ (e.g., COPD-6 device [Vitalograph Ltd, Ireland]).⁴⁸ Screening spirometry, either preceded by risk assessment or not, is administered without medication (i.e., pre-bronchodilator spirometry).⁴ Since the diagnosis of COPD requires persistent airway obstruction, all abnormal screening spirometry should be followed up with spirometry testing following the administration of an inhaled medication like albuterol (i.e., post-bronchodilator spirometry).^{4, 9} This step can be done with screening or in a separate step depending on the setting, training of staff, and equipment available. The previous systematic review found evidence to suggest that externally validated questionnaires (i.e., COPD Diagnostic Questionnaire [CDQ]) had adequate test performance for the detection of COPD and more limited evidence to demonstrate that spirometry (both screening and post-bronchodilator) could identify COPD.¹

Treatment Approaches

The management and treatment of mild to moderate or minimally symptomatic COPD includes both pharmacologic and non-pharmacologic interventions. Smoking cessation is by far the most important secondary prevention intervention for individuals with COPD because combustible cigarette smoking accelerates the deterioration of lung function in patients with the disease.^{4, 49} The Lung Health Study demonstrated that smoking cessation counseling in adults with mostly asymptomatic mild to moderate COPD reduced all-cause mortality.^{50, 51} In addition to smoking cessation, many non-pharmacologic interventions address self-management of disease, diet, exercise, and uptake of recommended preventive services like influenza and pneumococcal immunizations. Although pulmonary rehabilitation has been evaluated in persons with low symptom burden, in the United States it is currently used for COPD patients who remain symptomatic, despite optimal pharmacological therapy. Pharmacologic management of mild to moderate COPD primarily treats symptoms and may improve functioning and quality of life but does not appear to prevent the progression of disease. Medications used in the management of COPD include bronchodilators and anti-inflammatory therapies. The mainstay of pharmacologic treatment of mild to moderate COPD is bronchodilators, i.e., short acting beta-agonists (SABA), long-acting beta-agonists (LABA), short-acting muscarinic antagonists (SAMA), and long-acting muscarinic antagonists (LAMA).⁵² Typically short-acting bronchodilators are used in those with the least symptom burden, then long-acting bronchodilators in those who are more symptomatic, and combination LABA/LAMA in those with high initial symptom burden or history of exacerbations. The addition of inhaled corticosteroids (ICS) is generally used in persons with high symptom burden, co-existing asthma, and/or eosinophilia.

Current Clinical Practice and Recommendations of Others

Major clinical practice guidelines recommend against routine general screening for COPD in asymptomatic patients; however, they do recommend case finding in patients presenting with respiratory symptoms associated with the disease (e.g., dyspnea, chronic cough, sputum production). GOLD recommends active case finding in patients with symptoms and/or risk factors (Table 2).

Table 2

Selected COPD Guidelines on Screening or Active Case-Finding.

Generally, screening for COPD using pre-bronchodilator spirometry is not widely used in primary care practice in the United States. Additionally, data suggests that using spirometry for case finding in a manner consistent with guideline recommendations is vastly underutilized.^{30, 53} This underutilization may be due to a number of causes, including but not limited to low diagnostic yield and complexity of the testing.^{38, 54–60} In the NHANES III, 63.3 percent of adults who were found to have airflow obstruction reported never having received a previous diagnosis of COPD.²¹ In one US study, COPD Genetic Epidemiology (COPDGene), Black adults had a higher odds of not having a prior COPD diagnosis regardless of severity of airflow obstruction compared to White adults (44 percent versus 29 percent undiagnosed, respectively).⁶¹ And women were more than three times as likely than men to have severe disease at the time of diagnosis.⁶²

Previous USPSTF Recommendation

In 2016 the USPSTF issued a D Recommendation against screening for COPD in asymptomatic adults (defined as individuals who do not recognize or report respiratory symptoms).² Previously the USPSTF did not find direct evidence that screening for COPD in asymptomatic persons improved health-related quality of life (HRQoL), morbidity, or mortality. Although they found that screening for COPD could accurately identify persons with COPD, they determined that, based on the included evidence, early detection of COPD did not alter the course of the disease or improve patient outcomes. The previous systematic review found no treatment studies conducted in patients with screen-detected COPD and relatively few in patients with mild COPD.¹ Overall, the included treatment evidence was largely limited to subgroup analyses, almost exclusively among individuals with moderate COPD, and primarily the more severe end of moderate COPD (e.g., FEV₁ 60 percent predicted). Even among these groups, the only consistent benefit observed was reduced COPD exacerbations with no consistent benefits in mortality, dyspnea, or HRQoL. The USPSTF did not judge this evidence to be widely applicable to persons with COPD identified through screening.

This review also found limited evidence that did not support screening as a means to improve smoking cessation rates or the uptake of other recommended preventive services.¹ In addition, the USPSTF also judged that the amount of time and effort required to screen for COPD in asymptomatic persons (using screening spirometry with or without prescreening questionnaires) was not trivial. Therefore, based on the moderate certainty of no net benefit and opportunity cost of screening asymptomatic adults, the USPSTF renewed their 2008 D recommendation. However, in this recommendation statement, the USPSTF included language encouraging clinicians to offer smoking cessation interventions to all patients who currently smoke and to pursue case finding for COPD in patients with risk factors (e.g., exposure to cigarette smoke or heating fuels, occupational exposure to dusts or chemicals, family history of α1-antitrypsin deficiency).