Prevalence

Comparisons of COPD prevalence and mortality between countries and over time are important, because the disease is largely preventable. Studying global prevalence of COPD was previously difficult because of the lack of data representative of the world population and lack of consensus on case definitions. The initiation of multinational studies on COPD have improved the understanding of its global burden and shown variable disease prevalence among countries. An example of these studies is the Global Burden of Disease (GBD) study, which used a central database of registries, national surveys, and census data, among other sources, from more than 100 countries, stratified by sociodemographic index (SDI), a composite measure of income, education, and fertility. Using the fixed ratio diagnostic criteria, COPD affected an estimated 299 million people in 2015, which was an increase from 174 million or 44% since 1990.

In a 2015 systematic search of population-based studies across 52 countries, the highest COPD prevalence was estimated in the Americas (15% in 2010), and the lowest in Southeast Asia (10%). The study estimated a global prevalence of 12%, corresponding with 384 million cases in 2010, a number substantially higher than that estimated by the GBD study. The percentage increase in COPD cases between 1990 and 2010 was the highest in the eastern Mediterranean region (119%), followed by the African region (102%), whereas the European region recorded the lowest increase (23%). The COPD guidelines used across selected studies varied, but 92% of all retained studies used the fixed ratio diagnostic criteria.

Mortality

In 2015, more than 3 million people died of COPD worldwide, an increase of 12% compared with 1990. Disability-adjusted life years (DALYs), a summary measure of fatal and nonfatal disease outcomes, is defined as the total number of years lived with the disease plus the total number of years lost to the disease. In 2015, COPD represented about 64 million DALYs, ranking eighth among causes of global disease burden worldwide. Age-standardized DALY rates caused by COPD were highest (>2000 per 100,000 people) in Papua New Guinea, India, Lesotho, and Nepal ( Fig. 1 ). These rates were higher in countries between the low to middle range of the SDI, before reducing sharply from the middle to high range of the SDI. Other investigators have also reported that as much as 90% of COPD deaths worldwide occur in low-income and middle-income countries.

Age-standardized DALY rate per 100,000 people caused by COPD by country, both sexes, 2015. ATG, Antigua and Barbuda; FSM, Federated States of Micronesia; Isl, islands; LCA, Saint Lucia; TLS, Timor-Leste; TTO, Trinidad and Tobago; VCT, Saint Vincent and the Grenadines.

( Reprinted with permission from Elsevier; GBD 2015 Chronic Respiratory Disease Collaborators. Global, regional, and national deaths, prevalence, disability-adjusted life years, and years lived with disability for chronic obstructive pulmonary disease and asthma, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet Respir Med 2017; 5(9):691-706.)

Causes of Variation in Global Trends

The variations in trends between different world regions and countries are largely explained by the variations in smoking, secondhand smoke, and outdoor and household air pollution, including ozone, and occupational exposures. Together, these risks explain 73% of DALYs caused by COPD. Another important reason for global differences is the varying rates of COPD underdiagnosis in many jurisdictions.

Tobacco Smoke Exposure

Cigarette smoking is the most common risk factor for the development of COPD in the United States and high-income countries. However, it is the second most common risk factor worldwide after air pollution. Worldwide, more than 1 billion people smoked tobacco in 2015, but the rates of tobacco use are declining in most countries, except for the eastern Mediterranean and African regions. By 2015, the age-standardized global prevalence of daily smoking decreased to 15%, an overall 29% decrease since 1990. However, in 2015, 1 in every 4 men and 1 in every 20 women in the world continued to smoke daily. In 2017, active smoking contributed to 1.23 million COPD-related deaths and 28.28 million COPD-related DALYs ( Table 1 ).

To significantly and permanently bend the tobacco epidemic’s trajectory, a renewed and sustained focus is needed on comprehensive tobacco control policies and laws worldwide and in the United States. In 2003, the World Health Organization (WHO) adopted the Framework Convention on Tobacco Control to call on nations for stricter control of tobacco use. In addition, the WHO has drafted the 25 × 25 noncommunicable disease (NCD) targets, which include decreasing tobacco use by 30% between 2010 and 2025. Further reduction in cigarette smoking will help decrease the prevalence, morbidity, and mortality of COPD worldwide and in the United States.

Secondhand Smoke Exposure

The sidestream smoke from the burning of cigarettes is called secondhand smoke or environmental tobacco smoke. In a 2011 analysis, exposure to secondhand smoke was estimated to globally account for nearly 600,000 all-cause deaths and nearly 11 million DALYs annually. During 2011 to 2012, about 58 million nonsmokers in the United States, including 47% of African American nonsmokers, were exposed to secondhand smoke. During the same time frame, 2 out of every 5 children of ages 3 to 11 years, including 7 out of every 10 African American children, were exposed to secondhand smoke regularly.

Secondhand smoke exposure, particularly during childhood, is an important risk factor for COPD worldwide, including the United States. A cross-sectional population-based study from the United States involving 2113 adults between the ages of 55 and 75 years reported that the highest quartile of lifetime workplace exposure to secondhand smoke was associated with 36% greater odds of contracting COPD. The population-attributable fraction (PAF) for COPD was 11% for the highest quartile of home-based secondhand smoke exposure and 7% for work-based exposure. The respiratory health effects of secondhand smoke exposure provide a compelling rationale for legislation that mandates 100% smoke-free public places.

Ambient (Outdoor) Air Pollution

Industries, households, cars, and trucks emit complex mixtures of ambient air pollutants, many of which are harmful to health. Of all ambient air pollutants, fine particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) has the greatest effect on respiratory health. Although, in many Western countries, levels of ambient air pollution have been improving with the setting of upper limits and better urban planning, air pollution in developing countries, and particularly those with rapid industrialization, has become a major global problem.

Ambient air PM2.5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2.5 caused 4.2 million deaths and 103.1 million DALYs in 2015, representing 8% of total global deaths and 4% of global DALYs. Most deaths were in low-income and middle-income countries, particularly in east and south Asia. Deaths worldwide attributable to ambient PM2.5 increased from 3.5 million in 1990 to 4.2 million in 2015. In the contiguous United States, PM2.5 pollution in excess of the lowest observed concentration (2.8 μg/m ³ ) was responsible for an estimated 30,000 excess deaths during the time frame 1999 to 2015. The life expectancy loss caused by PM2.5 was largest around Los Angeles and in some southern states, such as Arkansas, Oklahoma, and Alabama.

Exposure to ambient air pollutants is associated with rapid decline in lung function in healthy populations ^, as well as a greater level of emphysema assessed quantitatively using computed tomography (CT) imaging, greater risk of acute exacerbations of COPD, and greater risk of death from chronic lower respiratory diseases. The pathologic effects in the lung are mediated via inflammatory pathways and involve oxidative stress similar to cigarette smoking. Reducing exposure to ambient air pollution has important health benefits but also reduces greenhouse gas emissions that contribute to climate change.

Household Air Pollution

Almost 3 billion people worldwide use solid fuel (eg, wood, charcoal, crop residues, animal dung) for cooking, with many more using solid fuels for heating homes. These so-called biomass fuels contribute to household air pollution. With inefficient combustion of these solid fuels, a complex mixture of carbon-based particles, inorganic particles, and irritant gases is generated indoors, which shares some characteristics with tobacco smoke.

The greatest proportions of the populations exposed to household air pollution are in countries of sub-Saharan Africa, India, China, and Central America. Although the exposure burden is highest in low-income countries, a significant number of households in high-income countries, including the United States, rely on solid fuel for heating homes. According to the GBD study, an estimated 2 million deaths and 60 million DALYs were attributable to household air pollution worldwide in 2017, almost all in low-income and middle-income countries, the published WHO estimates are even higher.

Observational studies show strong associations between household air pollution exposures and COPD, among other illnesses. The Global Alliance for Clean Cookstoves initiative hosted by the United Nations Foundation to enable the distribution of clean stoves and the initiatives of several governments to accelerate the progression away from biomass to clean fuels may help decrease the prevalence, morbidity, and mortality of COPD from household air pollution exposure.

Occupational Exposures

A 2019 ATS statement concluded that pooled estimates of the PAF are 14% for the occupational contribution to the burden of COPD and 13% for chronic bronchitis. Moreover, a higher occupational PAF for COPD among never smokers (31%) suggests that occupational exposures contribute more substantially to the burden of COPD in nonsmokers. This finding means that, as the prevalence of cigarette smoking in the general population decreases, other COPD-related risk factors may become more prominent. Cigarette smoking and occupation act as additive risks for COPD, which is plausible given that each of these exposures subsumes a heterogeneous mix of toxic materials.

Occupational exposures to vapors, gas, dust, or fumes (VGDF) are associated with COPD. Causal associations with coal dust, silica, construction dust, cotton dust, asbestos, and grain dust are well documented in the literature. The Faces of Black Lung series by the National Institute of Occupational Safety and Health (NIOSH) provides useful information on the impact of coal mine dust and other work-related exposures on patients with COPD Video 1: Available at: https://youtu.be/H2U9Onrxepg and Video 2: Available at: https://youtu.be/X-agtyN4py4 . However, there are multiple other at-risk occupations that are not well studied. For example, a recent study indicated that the highest COPD prevalence in industries or occupations was noted among workers in the information industry (including publishing, telecommunications, broadcasting, and data processing workers) and office and administrative support occupations (including secretaries, administrative and dental assistants, and clerks). Often overlooked, workers in these industries are exposed to organic and inorganic dusts, isocyanates, irritant gases, paper dust, fumes from photocopiers, chemicals, oil-based ink, paints, glues, toxic metals, and solvents, all of which are known respiratory irritants associated with COPD.

Prevention of occupational COPD relies on worker education; governmental regulation for appropriately protective work setting and effective enforcement of the same ; continued surveillance; early identification of COPD; and reduction or elimination of COPD-associated risk factors, such as VGDF, chemicals, and exposure to indoor and outdoor air pollutants.

Prevalence

Information on rural-urban disparities in the prevalence of self-diagnosed COPD comes from 3 national surveys in the United States: the Behavioral Risk Factor Surveillance System (BRFSS), the National Health Interview Survey (NHIS), and NHANES, and the results are remarkably similar.

BRFSS uses the random digit dialing system to collect self-reported population-based data on exposures and diseases. A 2015 analysis of the BRFSS data identified an age-adjusted national prevalence of 6% of self-reported COPD. The prevalence in noncore rural areas (8%) was much higher than in large metropolitan centers (5%). Similarly, a review of the NHIS data from 2012 to 2015 on self-reported COPD reported an estimated overall prevalence of 8%. The prevalence of 16% in rural poor regions was more than twice that in the urban nonpoor region (6%). Even when adjusted for confounders such as smoking, sex, age, race, wealth, and education, rural residence was associated with 23% greater odds for COPD than urban residence. Raju and colleagues reviewed the NHANES data from 2007 to 2012 and showed that rural residence was associated with 106% greater odds for COPD than urban residence. Despite the variation in the absolute prevalence rates reported, these surveys consistently show that rural populations are at high risk for COPD.

Mortality

Based on data from the National Vital Statistics, chronic lower respiratory disease, consisting primarily of COPD, was the third leading cause of death in the United States in 2015 and the fourth leading cause of death from 2016 through 2018. The year-on-year nationwide COPD mortality decreased by about 2% in 2018, to 40 per 100,000. The year-on-year nationwide mortality increased in 2017 but decreased in 2016. Despite these sinusoidal fluctuations, the overall mortality trend for COPD within the United States has decreased since 2002.

Causes of Rural-Urban Disparity

The basis for rural-urban disparity in COPD is likely multifactorial. Rural populations may have higher COPD risk because these populations have a greater proportion with a history of smoking, and more secondhand smoke exposure but less access to smoking cessation programs. Occupational exposures to VGDF is a risk factor for COPD, and rural residents are more likely than urban residents to work in dusty jobs such as crop farming and coal mining. ^, Environmental exposures to wood smoke and coal smoke also place rural residents at risk for COPD. The 2015 cross-sectional analysis of the BRFSS data showed that rural residents had the highest Medicare hospitalizations and death rates from COPD.

The WHO defines social determinants of health as “the conditions in which people are born, grow, live, work, and age. These circumstances are shaped by the distribution of money, power, and resources at global, national and local levels.” Relevant social determinants of health for rural residents include low socioeconomic status (SES), inadequate access to health care, lack of healthy lifestyles, and low levels of education and income. Low SES is a risk factor for COPD in the United States and other parts of the world. Inadequate access to health care for rural residents is related to the lower rates of those insured, unavailability of clinical expertise, long travel distance, and unavailability of transportation. Despite higher rates of COPD-related hospitalizations, rural residents are less likely to receive and complete outpatient pulmonary rehabilitation. As the disease progresses, patients require specialist management from a pulmonologist. Only about 30% of rural residents have access to pulmonologist services within a 16-km (10-mile) radius, compared with more than 90% of urban residents. Because of the shortage of pulmonologists, COPD management in rural areas is provided by primary care providers (PCPs), often without access to quality spirometry. COPD care by PCPs may not be consistent and may differ from guideline practices.

Prevalence

The estimated age-adjusted prevalence of self-reported COPD in 2017 in the United States, based on the BRFSS data, varied by race/ethnicity: American Indian/Alaska Native 11.9%, white 6.7%, black 6.6%, Hispanic 3.6%, Asian 1.7%, and Native Hawaiian/Pacific Islander 3.3%. By using the definition of self-reported physician diagnosis of COPD, BRFSS data may underestimate true disease prevalence. This underestimation may occur because of recall and social desirability biases, differing likelihoods of COPD diagnosis by physicians in states with high smoking rates and rurality, and exclusion of institutionalized adults who live in long-term care facilities or prisons. Using postbronchodilator spirometry as the gold standard, a study found that as much as 81% of spirometrically defined COPD cases were underdiagnosed, with greater probability of underdiagnosis associated with male sex, younger age, never and current smoking, lower education, no previous spirometry, and less severe airflow limitation.

Racial/ethnic disparities in COPD may be confounded by the presence of similar disparities in smoking behavior, which, despite recent decline, remains the biggest risk factor for the development of COPD in the United States. Thus, American Indian/Alaska Native populations are the racial/ethnic category with the highest prevalence of self-reported current cigarette smoking at 32%, whereas Hispanic and Asian populations have the lowest rates of 11% and 9%, and white people and African Americans have intermediate rates of 17% and 17% respectively. By limiting comparisons to never-smokers, the confounding effect of smoking can be excluded. Using data from the self-reported never-smokers, the comparison of prevalence of self-reported COPD among racial/ethnic groups reveals an interesting trend. American Indians/Alaska Natives and African Americans have the highest prevalence rates of COPD at 5.7% and 4.1% respectively, Hispanic and white people have intermediate prevalence rates at 2.3% and 2.7% respectively, and the lowest prevalence is noted among Asian people and Native Hawaiian/Pacific Islanders at 1.2% and 0.9% respectively. When examining the population of employed never-smokers from 2013 to 2017, the prevalence of self-reported physician diagnosis of COPD was lower among Hispanic people at 1.7% compared with non-Hispanic white people at 2.5% and non-Hispanic African Americans at 2.6%, with greater differences noted among women than among men.

Racial/ethnic disparities are confirmed with studies using objective COPD outcomes rather than self-report. Multiple studies, using spirometric end points, indicate that Hispanic people have a lower prevalence of self-reported COPD than non-Hispanic white people. In a national study using the NHANES III data, an obstructive pattern was less common in Mexican Americans (8%) than non-Hispanic white people (15%). Several studies, many from New Mexico, have shown reduced prevalence of COPD, higher baseline lung function, and lower decline in lung function in Hispanic groups, compared with non-Hispanic white people.

Although national studies report high prevalence rates of COPD in American Indians, there are remarkable differences among American Indian groups in different parts of the country. For instance, some investigators have shown a protective effect of an American Indian ancestry component in racially admixed populations in New Mexico and Costa Rica ^, on the spirometric prevalence of COPD and lung function decline.

In addition to the higher prevalence of COPD in African American than white never-smokers in the Wheaton and colleagues study, several reports have shown that African Americans develop COPD with less intense cumulative smoking and at a younger age, possibly because of differences in nicotine metabolism. Among patients with severe COPD, African Americans were disproportionately represented among those with early-onset disease (occurring before the age of 55 years) compared with those with late-onset disease. African genetic ancestry has been associated with reduced FEV ₁ and faster decline in lung function.

Mortality

The 2016 data from the National Vital Statistics System showed the following age-adjusted death rates per 100,000 standard US population for chronic lower respiratory disease (mostly COPD) by race: white 46, American Indian/Alaska Native 41, black 30, Hispanic 17, and Asian 12, with overall estimated death rate of 41. Although mortality is lower among African Americans than among white people, some reports indicate that COPD mortalities may be increasing faster among African Americans than among white Americans. Although national studies report high mortalities of COPD in American Indians, there are remarkable differences among American Indian groups in different parts of the country. For instance, county-level mortalities from COPD in American Indian communities of New Mexico are generally low.

Although many studies show that Hispanic people have disproportionately low COPD mortalities, 1 study suggested that the risk of death was similar to that of white people and African Americans. Kinney and colleagues showed that the protective effect of Hispanic ethnicity on COPD mortality was not explained away by their lower cumulative exposure to tobacco smoke. In 2013, the age-adjusted death rates (per 100,000 people) from COPD among US Hispanic people were highest in Cubans and Puerto Ricans and lowest in Mexican Americans, showing significant variability within Hispanic ethnic subgroups.

Causes for Racial/Ethnic Disparities

Health disparities in racial/ethnic groups are largely affected by social determinants of health indices. These indices include low SES, lack of health care access, lack of insurance, health literacy, cultural beliefs, social and family situations, governmental structure or laws that do not protect vulnerable individuals, individual preferences, availability of quality health care providers, and racial and ethnic discrimination. Racial/ethnic minority groups are more likely to live in cities with poorer air quality and, therefore, experience a disparately larger impact on chronic lung disease. Household air pollution from smoky cooking or heating fires is more common in racial/ethnic minority households, particularly among American Indian communities.

Possible causes for the disproportionately high prevalence of COPD in African American never-smokers include increased likelihood of exposure to secondhand smoke (especially caused by living conditions and poverty), smaller/lower lung function that increases the likelihood of development of COPD with very little irritant exposure, and higher contribution of occupational exposures. In addition, African Americans report worse dyspnea and health-related quality of life than white people, after adjustment for lung function. One possible explanation may be their use of fewer respiratory medications, lower use of medical care, and poorer access to care. ^, Another possible explanation is that African Americans are twice as likely than non-Hispanic white people to report a history of asthma. Patients with COPD with concomitant asthma experience poor quality of life and greater dyspnea. The presence of comorbidities such as gastroesophageal reflux has a greater negative impact on dyspnea on African Americans than on non-Hispanic white people, which may also help explain their greater report of dyspnea.

The so-called Hispanic paradox refers to the fact that, despite their lower social determinants of health indices, Hispanic people have a lower all-cause mortality than non-Hispanic white people. Although some investigators have attributed the paradox to the lower cumulative exposure to tobacco smoke, others show a protective effect of an American Indian ancestry component in racially admixed Hispanic populations of New Mexico and Costa Rica. ^, Furthermore, disparities in COPD prevalence across US Hispanic subgroups are seen, and may be partly explained by differences in racial ancestry. For example, Puerto Ricans have a greater proportion of African ancestry but a lower proportion of Native American ancestry than New Mexican Hispanic people. Studies have also identified unique genetic loci that may play a role in COPD pathogenesis in Hispanic populations. Despite the lower prevalence and mortality of COPD, Hispanic smokers report greater dyspnea than non-Hispanic white smokers, which is consistent with their lower health-related quality of life and is not explained by differences in either lung function or CT measure of lung structure. It is possible that social determinants of health may explain the difference in dyspnea and health-related quality of life among Hispanic people.