Abstract
Rationale
In predominantly White populations, early chronic obstructive pulmonary disease (COPD) (i.e., COPD in people aged <50 yr) has been linked to higher hospitalization rates and mortality; however, the prevalence, risk factors, and population attributable risk (PAR) of early COPD remain to be determined in non-White populations.
Objectives
We aimed to examine the prevalence, risk factors, and PARs of early COPD among Hispanic/Latino individuals, the largest U.S. minority group.
Methods
We used baseline data from the Hispanic Community Health Study/Study of Latinos, a population-based probability sample of 16,415 Hispanic/Latino individuals aged 18–74 years. Participants aged <50 years were included (N = 7,323). Early COPD was defined as a forced expiratory volume in 1 second to forced vital capacity ratio less than the lower limit of normal. We used survey logistic regression analysis to identify risk factors and estimate the prevalence of early COPD. PARs of the risk factors identified were estimated.
Results
A total of 524 participants met the criteria for early COPD, yielding a sex- and age-adjusted prevalence of 7.6% (95% confidence interval [CI], 6.8–8.6). Asthma (odds ratio [OR], 3.37; 95% CI, 2.57–4.41), smoking status (ever vs. never; OR, 1.65; 95% CI, 1.24–2.20), and chronic sinusitis (OR, 1.71; 95% CI, 1.09–2.66) were associated with increased odds of early COPD. Immigrants versus U.S.-born individuals have lower odds of early COPD (age at immigration <15 yr and living in the United States <10 yr; OR, 0.94; 95% CI, 0.39–2.27; age at immigration <15 yr and living in the United States ⩾10 yr; OR, 0.55; 95% CI, 0.37–0.84; age at immigration ⩾15 yr and living in the United States <10 yr; OR, 0.86; 95% CI, 0.57–1.30; and age at immigration ⩾15 yr and living in the United States ⩾10 yr; OR, 0.63; 95% CI, 0.42–0.95). Among smokers, pack-years was not associated with early COPD (5–9.9 vs. <5 pack-years; OR, 1.04; 95% CI, 0.59–1.82; ⩾10 vs. <5 pack-years; OR, 1.20; 95% CI, 0.74–1.94). The mean PAR for asthma, smoking status, and chronic sinusitis was 26.3% (95% CI, 22.1–30.3), 22.4% (95% CI, 17.4–27.1), and 6.9% (95% CI, 4.3–9.4), respectively.
Conclusions
Among U.S. Hispanic/Latino individuals, asthma is one of the most important risk factors for early COPD, followed by smoking and chronic sinusitis. Immigrants appear to have a lower risk of early COPD than U.S.-born Hispanic/Latino individuals.
Keywords: COPD, asthma, smoking, chronic sinusitis, Hispanic/Latino
Chronic obstructive pulmonary disease (COPD) affects more than 29 million people and is the fourth leading cause of death in the United States (1, 2). The disease develops slowly over many years and is typically diagnosed when patients are >60 years of age and have substantial airflow obstruction, making therapies less effective (3, 4). Because of this, experts have proposed to shift the focus on younger individuals (5–7). In a predominantly White population, early COPD (i.e., COPD in those <50 yr) has been linked to higher hospitalization rates and mortality (8).
Identifying risk factors will inform preventive strategies and interventions targeted to treat early COPD and halt its progression. Several studies in predominantly White older populations have identified various risk factors for COPD, including smoking and asthma (9, 10). However, early COPD studies focusing on other populations are lacking. Hispanic/Latino individuals are the largest and youngest minority group in the United States—in 2018, more than 60 million or 18% of the population, median age 30 years, 48% 18–49 years (11). Thus, identifying risk factors and estimating population attributable risk (PAR) of early COPD in this minority group is of public health and clinical relevance.
Prior studies demonstrated that compared with non–U.S.-born Hispanic/Latino individuals, U.S.-born Hispanic/Latino individuals have a higher risk of asthma and chronic bronchitis, suggesting that place of birth and immigration to a new country might be linked to disease risk (12–14). Hispanic/Latino ethnicity encompasses several heritage backgrounds, including Mexicans, Cubans, and Puerto Ricans (15). The prevalence of known COPD risk factors, such as smoking and asthma, varies by heritage and sex. Smoking rates and pack-years are the highest among Cubans and Puerto Ricans and higher in men than women of any heritage (16). The prevalence of asthma is the highest in Puerto Ricans and is higher in Hispanic/Latino women than their male counterparts (12). In addition, a less known potential risk factor for COPD, chronic sinusitis, has not been examined in this population. Chronic sinusitis and COPD are considered chronic inflammatory processes, and paranasal sinus opacities were found to be associated with COPD (17), suggesting a link between these two conditions. Therefore, we aimed to determine the prevalence, risk factors, and PARs for early COPD in U.S. Hispanic/Latino individuals in this cross-sectional study.
Methods
We used the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), described elsewhere (18, 19), to conduct this analysis. Details about this study are in the online supplement. Briefly, this is a population-based study in four U.S. communities that enrolled self-identified Hispanic/Latino men and women aged 18–74 years from households selected in a random, multistage fashion. In this analysis, we included participants aged 18–49 years enrolled at baseline (between 2008 and 2011) who completed the respiratory questionnaire and performed valid spirometry (Figure 1) (12). Informed consent was obtained from all study participants, and each site’s institutional review board approved HCHS/SOL. The current study was approved by the Partners Human Research Committee (2017P001688/PHS).
Figure 1.
Flow chart of HCHS/SOL participants’ selection. HCHS/SOL = Hispanic Community Health Study/Study of Latinos.
Outcome
The outcome was early COPD, defined as age <50 years, and prebronchodilator forced expiratory volume in 1 second (FEV1) to forced vital capacity ratio less than the lower limit of normal. Although the proposed definition of early COPD included 10 or more pack-years of cigarettes smoked as a criterion (5), we included never-smoking participants because a prior study showed that they contributed 23.4% to the burden of airflow obstruction in the U.S. population (20).
Covariates
Standardized questionnaires were used to obtain information on age, sex, heritage background, country of birth, years living in the United States, age at immigration, education level, health insurance, smoking history, maternal smoking, number of smokers at home, tuberculosis, chronic sinusitis, childhood pneumonia, asthma, nasal/eye symptoms to allergen exposures, and occupational exposures (available at http://www.cscc.unc.edu/hchs). Details on those covariates are in the online supplement. Age was categorized into three groups (18–29 yr, 30–39 yr, and 40–49 yr). Country of birth, age at immigration, and the number of years living in the United States were collapsed into a five-category variable termed immigration history as follows: U.S.-born (nonimmigrant); age at immigration <15 years and living in the United States <10 years; age at immigration <15 years and living in the United States ⩾10 years; age at immigration ⩾15 years and living in the United States <10 years; and age at immigration ⩾15 years and living in the United States ⩾10 years. We used this approach based on prior studies (12, 13) and reflected the variation of Hispanic/Latino immigration history. Heritage backgrounds included Mexican, Cuban, Dominican, Puerto Rican, Central American, South American, and other/mixed heritage. Education level was classified as high school or General Education Diploma (GED) and greater than high school or GED. Health insurance was dichotomized as yes/no (12). Smoking status was categorized as never and ever. Never smoking was defined as smoking fewer than 100 cigarettes ever. Pack-years of smoking were categorized as <5, 5–9.9, and ⩾10 pack-years (16). Maternal smoking was considered present if the participant had a female caregiver who smokes in his/her home. The number of smokers at home was dichotomized as 0 versus ⩾1. A history of tuberculosis, chronic sinusitis, childhood pneumonia, asthma, and nasal/eye allergy was based on the respiratory questionnaire (12). Occupational exposure to cleaning and disinfecting solutions and vapors, gas, dust, or fumes was extracted from the occupational questionnaire (14). Tuberculosis, chronic sinusitis, childhood pneumonia, asthma, nasal/eye allergy, and occupational exposures were treated as binary variables. The body mass index was calculated using weight and height measurements performed in a standardized manner.
Spirometry
Spirometry was performed following the American Thoracic Society/European Respiratory Society guidelines using a dry rolling sealed spirometer with automated quality checks (Occupational Marketing) with overreading by one investigator (12, 21). All participants, except those with recent cardiovascular events or surgery, were asked to perform prebronchodilator spirometry. Prediction equations for the general U.S. population were used to calculate predicted values (22).
Statistical Analysis
To account for the sampling design, stratification, and clustering, means and prevalence rates were weighted (18, 19). Models for early COPD were built using survey logistic regression analysis (14). Modeling for early COPD was guided by the directed acyclical graph approach (Figure 2) (23). First, we selected all the following 17 factors based on clinical knowledge and prior studies (9, 10, 13, 17, 19, 24): sex, age, immigration history (control, U.S.-born), heritage background, education level, health insurance, smoking status (ever vs. never), pack-years smoked, maternal smoking, number of smokers at home, tuberculosis, chronic sinusitis, childhood pneumonia, asthma, nasal/eye allergy, occupational exposure to cleaning and disinfecting solutions, and occupational exposure to vapors, gas, dust, or fumes. We then considered the following variables as main exposures: smoking status, pack-years smoked (among smokers only), asthma, chronic sinusitis, and immigration history. The rest of the variables above were considered confounders of the relationships between the main exposures and early COPD (Figure 2). We also conducted a smoking status-stratified analyses (ever- vs. never-smoking) to estimate the association between the pack-year categories and early COPD among ever-smoking participants.
Figure 2.
The directed acyclic graph (DAG) was the basis to inform the survey logistic regression models used in this cross-sectional study to assess relationships of main exposures (purple circles) and early chronic obstructive pulmonary disease (COPD). Yellow circles represent ancestors of main exposures and the outcome (confounders). Black arrows and blue arrows represent paths between confounders and main exposures and between confounders and early COPD, respectively. Green arrows represent paths between main exposures and early COPD. This DAG is intended to depict a simple framework for early COPD used in this analysis. It does not reflect the complex relationships that exist or potentially exist between all the variables shown. For visual clarity, blue arrows are shortened. *Pack-years was used among ever-smoking participants only.
The prevalence of early COPD was estimated using logistic-regression conditional marginal analysis. In this analysis, the estimated mean is the expected outcome for an individual conditional on belonging to a specific group (e.g., Hispanic background) and having covariate values equal to the weighted average covariates (14). We report the prevalence of early COPD for all the main exposures used in the overall analysis and by sex, age categories, and heritage background. These estimates are of clinical and epidemiological interest. Finally, we calculated the PAR, which is the excess prevalence of early COPD attributable to risk factors (24). We estimated PARs using the following two equations: 1) Population Attributable Fraction, PAF = Pe(RR − 1)/RR, where Pe is the proportion of cases exposed to the risk factor and RR is the relative risk; and 2) PAR = PAF × Pd, where Pd is the prevalence of early COPD (24). We report PAR estimates for the entire population and stratified by sex. A sex-stratified analysis was conducted because of sex differences in the prevalence of risk factors for COPD, such as smoking and asthma, in Hispanic/Latino individuals. PAR estimation was performed using the STDRATE procedure of SAS 9.4 (SAS Institute). Analyses were performed by a statistician (W.W.).
Results
Participants’ Characteristics
Out of 16,415 HCHS/SOL participants, 7,980 were aged 18–49 years, and 657 out of those 7,980 had missing data, leaving a final sample with complete data of 7,323 (Figure 1). A comparison between participants with and without valid spirometry was reported (12). Briefly, compared with participants with valid spirometry, those without valid spirometry were older, females, and had lower education attained, higher health insurance rate, and higher pack-years. The characteristics of the participants by early COPD status are in Table 1. Compared with those without early COPD, participants with early COPD were more often males, U.S.-born, and of Puerto Rican heritage and had lower education level and health insurance rate. Early COPD participants were more often ever-smokers and fell in the category of ⩾10 pack-years than those without early COPD. These participants had a higher prevalence of maternal smoking exposure, ⩾1 smoker at home, tuberculosis, chronic sinusitis, childhood pneumonia, asthma, and nasal/eye allergy. Early COPD participants also had a higher prevalence of respiratory symptoms and a substantial lung function impairment with a lower mean FEV1% predicted (82.7% vs. 95.9%) and a higher proportion of participants with <80% (42.6% vs. 8.7%).
Table 1.
Characteristics of U.S. Hispanic/Latino participants aged 18–49 years by early COPD status and overall
| Variable | Non-COPD (n = 6,799) | Early COPD (n = 524) | Overall (n = 7,323) |
|---|---|---|---|
| Age, median (IQR), yr | 32.7 (24.5–41.0) | 31.9 (23.1–41.6) | 32.7 (24.4–41.0) |
| Age category, % (SE) | |||
| 18–29 | 38.3 (1.0) | 40.6 (3.3) | 38.4 (1.0) |
| 30–39 | 30.3 (0.9) | 25.7 (3.0) | 29.9 (0.9) |
| 40–49 | 31.5 (0.9) | 33.7 (2.9) | 31.6 (0.8) |
| Male sex, % (SE) | 49.4 (0.8) | 55.6 (3.0) | 49.9 (0.8) |
| BMI, median (IQR), kg/m2 | 28.3 (24.8–32.6) | 27.6 (24.6–32.7) | 28.3 (24.8–32.6) |
| Heritage background, % (SE) | |||
| Dominican | 10.0 (0.9) | 9.4 (1.9) | 9.9 (0.8) |
| Central American | 8.1 (0.7) | 4.9 (1.0) | 7.9 (0.7) |
| Cuban | 18.2 (1.6) | 17.9 (3.1) | 18.2 (1.6) |
| Mexican | 39.9 (1.7) | 37.6 (3.4) | 39.7 (1.7) |
| Puerto Rican | 13.6 (0.8) | 21.5 (2.9) | 14.2 (0.8) |
| South American | 4.9 (0.4) | 3.9 (0.9) | 4.9 (0.4) |
| Mixed/other | 5.3 (0.5) | 4.7 (1.1) | 5.2 (0.4) |
| Immigration history, % (SE) | |||
| U.S. born (no immigrant) | 29.1 (1.1) | 40.1 (3.5) | 29.9 (1.1) |
| Age at immigration <15 yr and living in the United States <10 yr | 1.9 (0.2) | 2.1 (0.8) | 1.9 (0.2) |
| Age at immigration <15 yr and living in the United States ⩾10 yr | 14.5 (0.6) | 10.5 (1.7) | 14.2 (0.6) |
| Age at immigration ⩾15 yr and living in the United States <10 yr | 28.9 (1.1) | 27.6 (3.0) | 28.8 (1.1) |
| Age at immigration ⩾15 yr and living in the United States ⩾10 yr | 25.7 (0.7) | 19.7 (2.3) | 25.2 (0.7) |
| Education level, % (SE) | |||
| High school/GED or less | 26.0 (0.9) | 29.6 (2.8) | 26.3 (0.9) |
| More than high school/GED | 74.0 (0.9) | 70.4 (2.8) | 73.7 (0.9) |
| Health insurance, % (SE) | 45.2 (1.1) | 46.3 (3.1) | 45.3 (1.1) |
| Smoking status, % (SE) | |||
| Never | 65.5 (0.9) | 49.9 (3.2) | 64.3 (0.8) |
| Ever | 34.5 (0.9) | 50.1 (3.2) | 35.7 (0.8) |
| Pack-years smoked, median (IQR) | 3.8 (1.2–10.1) | 4.1 (1.9–13.0) | 3.9 (1.3–10.4) |
| Pack-years smoked category*, % (SE) | |||
| <5 | 58.2 (1.6) | 51.9 (5.1) | 57.5 (1.5) |
| 5–9.9 | 15.5 (1.0) | 16.8 (4.3) | 15.6 (1.0) |
| ⩾10 | 26.3 (1.3) | 31.3 (3.8) | 26.9 (1.3) |
| Maternal smoking, % (SE) | 23.2 (0.9) | 30.6 (2.8) | 23.8 (0.8) |
| ⩾1 smokers at home, % (SE) | 22.7 (0.9) | 26.1 (2.5) | 23.0 (0.8) |
| Tuberculosis, % (SE) | 2.6 (0.3) | 4.1 (1.2) | 2.8 (0.3) |
| Chronic sinusitis, % (SE) | 6.3 (0.4) | 13.2 (2.5) | 6.8 (0.4) |
| Childhood pneumonia, % (SE) | 3.3 (0.3) | 5.6 (2.0) | 3.5 (0.3) |
| Asthma, % (SE) | 14.7 (0.6) | 38.5 (2.7) | 16.5 (0.6) |
| Nasal/eye allergy, % (SE) | 38.3 (0.9) | 47.0 (3.2) | 38.9 (0.9) |
| Exposure to cleaning and disinfecting solutions, % (SE) | 22.5 (0.8) | 20.7 (2.3) | 22.4 (0.8) |
| Exposure to vapors, gas, dust, or fumes, % (SE) | 25.2 (0.8) | 25.3 (2.5) | 25.2 (0.8) |
| Respiratory symptoms, % (SE) | |||
| Cough | 5.5 (0.4) | 9.8 (2.1) | 5.8 (0.4) |
| Phlegm | 7.6 (0.5) | 11.5 (2.1) | 7.9 (0.5) |
| Shortness of breath | 25.0 (0.8) | 36.2 (2.9) | 25.8 (0.8) |
| FEV1% predicted, median (IQR) | 95.9 (88.0–103.6) | 82.7 (73.1–90.5) | 95.1 (86.9–102.9) |
| FEV1% predicted <80, % (SE) | 8.7 (0.5) | 42.6 (3.1) | 11.3 (0.5) |
| FVC % predicted, median (IQR) | 95.9 (87.6–103.4) | 98.4 (87.2–107.5) | 96.0 (87.6–103.8) |
| FEV1/FVC ratio, median (IQR) | 83.6 (80.5–87.0) | 70.4 (67.1–73.3) | 83.1 (79.5–86.6) |
Definition of abbreviations: BMI = body mass index; COPD = chronic obstructive pulmonary disease; FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity; GED = General Education Diploma; IQR = interquartile range; SE = standard error.
Data are presented as median (IQR) for continuous variables and percentage (SE) for categorical variables. Estimates are weighted to account for the Hispanic Community Health Study/Study of Latinos design, stratification, and clustering.
Computed only among ever-smoking participants.
Factors Associated with Early COPD
Overall, in the adjusted multivariable model, asthma (odds ratio [OR], 3.37; 95% confidence interval [CI], 2.57–4.41), ever-smoking status (OR, 1.65; 95% CI, 1.24–2.20), and chronic sinusitis (OR, 1.71; 95% CI, 1.09–2.66) were significantly associated with increased odds of early COPD. Compared with U.S.-born Latino/Hispanic individuals, the odds of early COPD were lower for all four immigration history groups, with the estimates being statistically significant (i.e., CIs do not cross 1) in two groups (Figure 3). The ORs for the four immigration groups versus U.S.-born were as follows: age at immigration <15 years and living in the United States <10 years; OR, 0.94; 95% CI, 0.39–2.27; age at immigration <15 years and living in the United States ⩾10 years; OR, 0.55; 95% CI, 0.37–0.84; age at immigration ⩾15 years and living in the United States <10 years; OR, 0.86; 95% CI, 0.57–1.30; and age at immigration ⩾15 years and living in the United States ⩾10 years; OR, 0.63; 95% CI, 0.42–0.95. Full model results for the overall study participants are shown in Table E1 in the online supplement.
Figure 3.
Association between main exposures and early chronic obstructive pulmonary disease (COPD) in the overall Hispanic/Latino cohort and never-smoking and ever-smoking participants. Odds ratios (ORs) and 95% CI estimates are from a survey logistic regression multivariable model. Asthma and chronic sinusitis are binary (yes/no) variables. Referent for ever-smoking, pack-years smoked, and immigration history was never-smoking, <5 pack-years, and U.S.-born (nonimmigrant), respectively. The model was adjusted for heritage background, sex, age category, education level, maternal smoking, ⩾1 smokers at home, nasal/eye allergy, health insurance, childhood pneumonia, tuberculosis, exposure to cleaning and disinfecting solutions, and exposure to vapors, gas, dust, or fumes. The estimates are weighted to account for Hispanic Community Health Study/Study of Latinos sampling design, stratification, and clustering. Supplementary Table E1 shows estimates for all the variables. *Smoking status was used in the overall participants’ analysis only. †Pack-years were used in the ever-smoking participants’ analysis only. ‡OR for the group age at immigration <15 years and living in the United States <10 years was not estimated in ever-smoking participants because there are no individuals in one of the outcome categories. CI = confidence interval.
The estimates of the association between main exposures and early COPD from the smoking status–stratified analysis are shown in Figure 3. Among never-smoking participants, asthma and immigration history but not chronic sinusitis were associated with early COPD. Among ever-smoking participants, asthma and chronic sinusitis were associated with early COPD, whereas pack-years smoked and immigration history were not. Additional results among participants without asthma are in Table E2.
Prevalence of Early COPD
The overall age- and sex-adjusted prevalence of early COPD was 7.6% (95% CI, 6.8 – 8.6). The prevalence of early COPD estimated from the final multivariable model above was significantly higher in ever-smoking participants, those with asthma, and those with chronic sinusitis than never-smoking participants, those without asthma, and those without chronic sinusitis. Compared with U.S.-born Hispanic/Latino individuals, the prevalence of early COPD was lower in all four immigration history groups, with a varied magnitude of the differences and precision of estimates (Figure 4). Table E3 shows the prevalence of early COPD by sex, age category, and heritage.
Figure 4.
Prevalence of early chronic obstructive pulmonary disease (COPD) in U.S. Hispanic/Latino individuals aged 18–49 years. The estimates (%) and confidence intervals for the prevalence of early COPD by smoking status (red, ever vs. never), asthma (peach), chronic sinusitis (purple), and immigration history (blue) are from a multivariable model described in the Statistical Analysis section. For immigration history, P values versus U.S.-born (nonimmigrant) category.
Population Attributable Risk
The estimates of early COPD risk attributable to three factors identified in this analysis are shown in Table 2. The most important risk factor for early COPD was asthma (PAR, 26.3%), followed by smoking status (PAR, 22.4%) and chronic sinusitis (PAR, 6.9%). The PARs differed by sex in that compared with men, women had higher PAR for asthma (35.6% vs. 19.4%) and lower for ever-smoking status (18.2% vs. 24.2%) and chronic sinusitis (5.2% vs. 8.4%).
Table 2.
PAR for early COPD by risk factor and sex among U.S. Hispanic/Latino individuals aged 18–49 years
| Risk Factor | Overall [PAR (95% CI)] (%) | Women [PAR (95% CI)] (%) | Men [PAR (95% CI)] (%) |
|---|---|---|---|
| Asthma | 26.3 (22.1–30.3) | 35.6 (29.0–41.7) | 19.4 (14.1–24.4) |
| Smoking status (ever vs. never) | 22.4 (17.4–27.1) | 18.2 (11.3–24.6) | 24.2 (16.9–30.9) |
| Chronic sinusitis | 6.9 (4.3–9.4) | 5.2 (1.3–8.9) | 8.4 (4.8–11.8) |
Definition of abbreviations: CI = confidence interval; COPD = chronic obstructive pulmonary disease; PAR = population attributable risk.
PAR is the percentage of the population aged <50 years with early COPD attributable to the identified risk factor. For details about PAR estimation, see the Statistical Analysis section. The estimates are weighted to account for the Hispanic Community Health Study/Study of Latinos sampling design, stratification, and clustering.
Discussion
In this population-based study of more than 7,300 U.S. Hispanic/Latino individuals younger than 50 years, we found that the prevalence of early COPD was 7.6% and identified asthma, ever-smoking status, and chronic sinusitis as risk factors of early COPD. Hispanic/Latino immigrants appear to have a lower risk of early COPD. We also determined that the PAR of early COPD for asthma was the highest, followed by smoking and chronic sinusitis.
This study is one of the largest studies exploring risk factors of early COPD in Hispanic/Latino individuals, an understudied U.S. population. We found that the prevalence of early COPD was 7.6%, which is lower than that of 15% reported in a recent European study (8), a discrepancy that population differences might explain. The European study only included heavy smokers—10 or more pack-years—and older participants (mean age, 45.9 yr). However, our figure is similar to the prevalence of COPD of 8.2% in HCHS/SOL participants aged 45 years or older (12), suggesting that younger Hispanic/Latino individuals seem to be similarly susceptible to the disease and supporting the notion of comprehensibly understanding the disease in younger people.
We also found that asthma was the strongest risk factor associated with early COPD in this minority population and that the association remained the strongest in both smoking and never-smoking participants, strengthening the relevance of this factor. This finding is in line with two recent studies in predominantly White populations showing that the prevalence of asthma was higher in early COPD defined with 10 or more pack-years of smoking (8, 25). The relevance of asthma for early COPD in Hispanic/Latino individuals may be due to a couple of reasons. A decreasing trend in smoking rates from 42% to 16% in the U.S. general population in the last five decades has been noted, and that this ethnicity has a lower smoking rate than non-Hispanic White individuals (26). The prevalence of asthma in HCHS/SOL was 15.3% (12), almost twofold higher than the average of 8.0% among U.S. adults in 2019 (27).
Although this study cannot tease out the complex interplay between asthma and early COPD, it is known that poorly controlled asthma can lead to fixed airflow obstruction, and asthma has been proposed as a risk factor for COPD. Explanations for the latter include the following: first, a prevalence of asthma up to 26% in mild to moderate smoking COPD (28); second, longitudinal studies have demonstrated a rapid decline in lung function in adult smokers with asthma and asthma was associated with a greater risk for developing COPD (9, 29); and third, in smokers with childhood-onset asthma, smaller airways are associated with lower lung function and a higher risk of COPD (30). Collectively, our and prior findings support the notion that asthma might be a risk factor for early COPD, a finding that deserves further research.
In this study, chronic sinusitis was associated with early COPD, a factor that has not been widely explored in COPD. The association we observed is in line with prior studies showing that participants with chronic rhinosinusitis have higher rates of adult-onset asthma and that sinus opacities on magnetic resonance imaging were associated with COPD (17, 31). Note that the cross-sectional nature of this study does not allow us to establish the directionality of the relationship between chronic sinusitis and early COPD or claim causality. We believe that one reason to support the plausibility of the observed association is inflammatory changes in the upper and lower airways. Studies have demonstrated elevated nasal interleukin 8 in stable COPD and upper airway inflammation in those with COPD exacerbations (32). Thus, our finding warrants further investigation in other populations.
Our study also confirmed that ever-smoking is a risk factor for early COPD in Hispanic/Latino individuals. This finding is in line with other early smoking COPD studies conducted in predominantly White participants in which the smoking intensity was higher (16.5–31.6 pack-years) than that seen in our study, suggesting differential susceptibility to tobacco smoke (8, 25). Our finding that 5.3% of never-smokers (Figure 4) had early COPD supports the belief that future investigations of early COPD should include never-smokers and people with a range of smoking histories (33).
We found that Hispanic/Latino immigrants had lower odds of early COPD, a finding replicated among never-smoking participants only (Figure 3). This finding aligns with prior studies demonstrating that U.S.-born Hispanic/Latino individuals had a higher risk of asthma and chronic bronchitis than their non–U.S.-born counterparts (13, 14). In contrast, a prior study did not find such differences in COPD risk among older U.S. Hispanic/Latino individuals (12). A reason for this discrepancy between the current study and that prior study might rely on differences in disease susceptibility between younger and older immigrants. Explanations for the lower odds of early COPD in U.S.-born Hispanic/Latino individuals, particularly among nonsmokers, include differences in exposures to environmental respiratory hazards and health status. For instance, 80% of U.S. Hispanic/Latino individuals reside in areas that do not meet one Environmental Protection Agency standard of clean air, and 28.3% reside near a major highway (15, 34). It is conceivable that Hispanic/Latino individuals born in the United States might have been exposed longer and during a more critical period of lung development than those coming from abroad. In addition, immigrants tend to be healthier than the home-country population, likely decreasing their risk for chronic respiratory diseases (15). Further investigation is warranted to study the interaction between immigration, environmental exposures, and lung disease risk.
We have estimated PARs of early COPD in Hispanic/Latino individuals, which is a novel addition to understand the proportion of the disease in this minority group exposed to identified risk factors. Those PARs indicate the burden of early COPD that would be eliminated if the exposures were eliminated. Smoking is a known modifiable cause of COPD, and eliminating tobacco exposure would benefit 22.4% of the HCHS/SOL participants under 50 years of age. Our findings may inform public health policies toward smoking cessation programs in the Hispanic/Latino population. The Burden of Obstructive Lung Disease study, an international effort for studying COPD, also showed that PARs for other factors, such as poor education, were more relevant than smoking in certain countries (24). In this study, we found that asthma was the most important factor, followed by smoking and chronic sinusitis. We also observed sex differences in PARs. Because the prevalence of early COPD did not differ significantly between sexes, some PARs differences might be due to sex disparities in the prevalence of the risk factors (for asthma: women 18.0%; 95% CI, 16.3–19.7 vs. men 15.0%; 95% CI, 13.4–16.7; for ever-smoking status: women 26.4%; 95% CI, 24.3–28.7 vs. men 44.5%; 95% CI, 42.1–47.0). We believe that assessing PARs across populations and countries may be an important tool to understand the public health impact of early COPD and inform policies to reduce its burden.
This study has several strengths and limitations. We analyzed a large, representative population-based cohort of Hispanic/Latino individuals, including several of its heritage backgrounds. HCHS/SOL used standardized procedures to collect data, including the respiratory questionnaire and spirometric testing. However, some limitations should be noted. First, we used participants who may not have reached their lung function peak (e.g., those aged 18–30 yr) and those who did. However, we found that the prevalence of COPD did not differ by age categories. Second, we used prebronchodilator spirometric data. Compared with post-bronchodilator spirometric values, prebronchodilator values may overestimate the prevalence of COPD, but there does not appear to be a discrepancy in diagnostic discrimination for COPD between them (35). Furthermore, two recent early COPD studies have used prebronchodilator data, which is an acceptable approach for epidemiological studies (8, 36). Third, participants with restrictive lung physiology were not excluded, which may bias the OR estimates toward the null. Fourth, although an array of risk factors was used in the models, they were collected by questionnaires, which have inherent biases, such as recall bias. Also, other factors, including air pollution and childhood crowding, were not available. Despite this limitation, we identified plausible risk factors, all of which have already been linked to COPD (9, 10, 17). Fifth, the cross-sectional nature of this observational study does not allow us to make inferences about causality. Sixth, we deliberately included never-smoking participants, a diversion of the proposed definition of early COPD (5). By doing so, we could determine the prevalence of early COPD in never-smoking participants, supporting the arguments to include that population in the proposed definition (33). Seventh, we also caution that PARs estimates are based on the assumption of causality. Whereas an assumption of causality is supported for smoking (10), there is an ongoing debate for asthma and chronic sinusitis. Eighth, HCHS/SOL has no chest imaging data available, so we could not account for structural changes of the lung, which can occur even before the spirometric criterion for early COPD is met.
In summary, we have demonstrated that the prevalence of early COPD in Hispanic/Latino individuals is 7.6% and is higher in ever-smoking participants and those with asthma and chronic sinusitis. The population risk attributable to asthma was the highest, followed by smoking and chronic sinusitis. Latino/Hispanic immigrants appear to have a lower risk of early COPD than their U.S.-born counterparts.
Acknowledgments
Acknowledgment
The authors thank the staff and participants of HCHS/SOL for their essential contributions. A complete list of staff and investigators has been published previously (19) and is also available on the study website (http://www.cscc.unc.edu/hchs/). Statistical analyses were performed at the Brigham and Women’s Hospital following HCHS/SOL documentation directions. The authors also thank the National Heart, Lung, and Blood Institute BioLINCC staff for making the data available for this analysis.
Footnotes
Supported by National Heart, Lung, and Blood Institute grants R01-HL133137 and R01-HL149861 and the Brigham and Women’s Hospital Minority Faculty Career Development Award (A.A.D.). The funding agency had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.
Author Contributions: Concept and design; acquisition, analysis, or interpretation of data; and critical revision of the manuscript for important intellectual content: all authors. Drafting of the manuscript: F.K., D.M., and A.A.D. Statistical analysis: W.W. Supervision and obtained funding: F.K., W.W., and A.A.D. A.A.D. had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
This article has an online supplement, which is accessible from this issue’s table of contents at www.atsjournals.org.
Author disclosures are available with the text of this article at www.atsjournals.org.
References
- 1. Ford ES, Mannino DM, Wheaton AG, Giles WH, Presley-Cantrell L, Croft JB. Trends in the prevalence of obstructive and restrictive lung function among adults in the United States: findings from the National Health and Nutrition Examination surveys from 1988-1994 to 2007-2010. Chest . 2013;143:1395–1406. doi: 10.1378/chest.12-1135. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Ma J, Ward EM, Siegel RL, Jemal A. Temporal trends in mortality in the United States, 1969-2013. JAMA . 2015;314:1731–1739. doi: 10.1001/jama.2015.12319. [DOI] [PubMed] [Google Scholar]
- 3. Vogelmeier CF, Criner GJ, Martinez FJ, Anzueto A, Barnes PJ, Bourbeau J, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2017 Report. GOLD Executive Summary. Am J Respir Crit Care Med . 2017;195:557–582. doi: 10.1164/rccm.201701-0218PP. [DOI] [PubMed] [Google Scholar]
- 4. Lowe KE, Regan EA, Anzueto A, Austin E, Austin JHM, Beaty TH, et al. COPDGene® 2019: redefining the diagnosis of chronic obstructive pulmonary disease Chronic Obstr Pulm Dis 2019. 6 384 399 31710793 [Google Scholar]
- 5. Martinez FJ, Han MK, Allinson JP, Barr RG, Boucher RC, Calverley PMA, et al. At the root: defining and halting progression of early chronic obstructive pulmonary disease. Am J Respir Crit Care Med . 2018;197:1540–1551. doi: 10.1164/rccm.201710-2028PP. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6. Rennard SI, Drummond MB. Early chronic obstructive pulmonary disease: definition, assessment, and prevention. Lancet . 2015;385:1778–1788. doi: 10.1016/S0140-6736(15)60647-X. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Soriano JB, Polverino F, Cosio BG. What is early COPD and why is it important? Eur Respir J . 2018;52:1801448. doi: 10.1183/13993003.01448-2018. [DOI] [PubMed] [Google Scholar]
- 8. Çolak Y, Afzal S, Nordestgaard BG, Vestbo J, Lange P. Prevalence, characteristics, and prognosis of early chronic obstructive pulmonary disease. The Copenhagen General Population Study. Am J Respir Crit Care Med . 2020;201:671–680. doi: 10.1164/rccm.201908-1644OC. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9. Tai A, Tran H, Roberts M, Clarke N, Wilson J, Robertson CF. The association between childhood asthma and adult chronic obstructive pulmonary disease. Thorax . 2014;69:805–810. doi: 10.1136/thoraxjnl-2013-204815. [DOI] [PubMed] [Google Scholar]
- 10. Eisner MD, Anthonisen N, Coultas D, Kuenzli N, Perez-Padilla R, Postma D, et al. Committee on Nonsmoking COPD, Environmental and Occupational Health Assembly An official American Thoracic Society public policy statement: novel risk factors and the global burden of chronic obstructive pulmonary disease. Am J Respir Crit Care Med . 2010;182:693–718. doi: 10.1164/rccm.200811-1757ST. [DOI] [PubMed] [Google Scholar]
- 11.United States Census Bureau 2020https://www.census.gov/quickfacts/fact/table/US/PST045219.
- 12. Barr RG, Avilés-Santa L, Davis SM, Aldrich TK, Gonzalez F, II, Henderson AG, et al. Pulmonary disease and age at immigration among Hispanics. Results from the Hispanic Community Health Study/Study of Latinos. Am J Respir Crit Care Med . 2016;193:386–395. doi: 10.1164/rccm.201506-1211OC. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13. Holguin F, Mannino DM, Antó J, Mott J, Ford ES, Teague WG, et al. Country of birth as a risk factor for asthma among Mexican Americans. Am J Respir Crit Care Med . 2005;171:103–108. doi: 10.1164/rccm.200402-143OC. [DOI] [PubMed] [Google Scholar]
- 14. Kim V, Wang W, Mannino D, Diaz A. Association of birthplace and occupational exposures with chronic bronchitis in US Hispanics/Latinos, 2008-2011. Occup Environ Med . 2020;77:344–350. doi: 10.1136/oemed-2019-106081. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Díaz AA, Celli B, Celedón JC. Chronic obstructive pulmonary disease in Hispanics. A 9-year update. Am J Respir Crit Care Med . 2018;197:15–21. doi: 10.1164/rccm.201708-1615PP. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16. Kaplan RC, Bangdiwala SI, Barnhart JM, Castañeda SF, Gellman MD, Lee DJ, et al. Smoking among U.S. Hispanic/Latino adults: the Hispanic community health study/study of Latinos. Am J Prev Med . 2014;46:496–506. doi: 10.1016/j.amepre.2014.01.014. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17. Hansen AG, Helvik AS, Thorstensen WM, Nordgård S, Langhammer A, Bugten V, et al. Paranasal sinus opacification at MRI in lower airway disease (the HUNT study-MRI) Eur Arch Otorhinolaryngol . 2016;273:1761–1768. doi: 10.1007/s00405-015-3790-7. [DOI] [PubMed] [Google Scholar]
- 18. Lavange LM, Kalsbeek WD, Sorlie PD, Avilés-Santa LM, Kaplan RC, Barnhart J, et al. Sample design and cohort selection in the Hispanic Community Health Study/Study of Latinos. Ann Epidemiol . 2010;20:642–649. doi: 10.1016/j.annepidem.2010.05.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19. Sorlie PD, Avilés-Santa LM, Wassertheil-Smoller S, Kaplan RC, Daviglus ML, Giachello AL, et al. Design and implementation of the Hispanic Community Health Study/Study of Latinos. Ann Epidemiol . 2010;20:629–641. doi: 10.1016/j.annepidem.2010.03.015. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20. Celli BR, Halbert RJ, Nordyke RJ, Schau B. Airway obstruction in never smokers: results from the Third National Health and Nutrition Examination Survey. Am J Med . 2005;118:1364–1372. doi: 10.1016/j.amjmed.2005.06.041. [DOI] [PubMed] [Google Scholar]
- 21. Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R, et al. Interpretative strategies for lung function tests. Eur Respir J . 2005;26:948–968. doi: 10.1183/09031936.05.00035205. [DOI] [PubMed] [Google Scholar]
- 22. Hankinson JL, Odencrantz JR, Fedan KB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med . 1999;159:179–187. doi: 10.1164/ajrccm.159.1.9712108. [DOI] [PubMed] [Google Scholar]
- 23.Lederer DJ, Bell SC, Branson RD, Chalmers JD, Marshall R, Maslove DM, et al. Control of confounding and reporting of results in causal inference studies. Guidance for authors from editors of respiratory, sleep, and critical care journals. Ann Am Thorac Soc. 2019;16:22–28. doi: 10.1513/AnnalsATS.201808-564PS. [DOI] [PubMed] [Google Scholar]
- 24. Burney P, Patel J, Minelli C, Gnatiuc L, Amaral AFS, Kocabaş A, et al. Prevalence and population attributable risk for chronic airflow obstruction in a large multinational study. Am J Respir Crit Care Med . 2020;203:1353–1365. doi: 10.1164/rccm.202005-1990OC. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25. Cosío BG, Pascual-Guardia S, Borras-Santos A, Peces-Barba G, Santos S, Vigil L, et al. Phenotypic characterisation of early COPD: a prospective case-control study. ERJ Open Res . 2020;6:00047-2020. doi: 10.1183/23120541.00047-2020. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26. Oelsner EC, Balte PP, Bhatt SP, Cassano PA, Couper D, Folsom AR, et al. Lung function decline in former smokers and low-intensity current smokers: a secondary data analysis of the NHLBI Pooled Cohorts Study. Lancet Respir Med . 2020;8:34–44. doi: 10.1016/S2213-2600(19)30276-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Center for Disease Control and Prevention. 2019. https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm
- 28. Woodruff PG, Barr RG, Bleecker E, Christenson SA, Couper D, Curtis JL, et al. SPIROMICS Research Group Clinical significance of symptoms in smokers with preserved pulmonary function. N Engl J Med . 2016;374:1811–1821. doi: 10.1056/NEJMoa1505971. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29. Lange P, Parner J, Vestbo J, Schnohr P, Jensen G. A 15-year follow-up study of ventilatory function in adults with asthma. N Engl J Med . 1998;339:1194–1200. doi: 10.1056/NEJM199810223391703. [DOI] [PubMed] [Google Scholar]
- 30. Diaz AA, Hardin ME, Come CE, San José Estépar R, Ross JC, Kurugol S, et al. COPDGene Investigators Childhood-onset asthma in smokers. association between CT measures of airway size, lung function, and chronic airflow obstruction. Ann Am Thorac Soc . 2014;11:1371–1378. doi: 10.1513/AnnalsATS.201403-095OC. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31. Jarvis D, Newson R, Lotvall J, Hastan D, Tomassen P, Keil T, et al. Asthma in adults and its association with chronic rhinosinusitis: the GA2LEN survey in Europe. Allergy . 2012;67:91–98. doi: 10.1111/j.1398-9995.2011.02709.x. [DOI] [PubMed] [Google Scholar]
- 32. Hurst JR, Wilkinson TM, Perera WR, Donaldson GC, Wedzicha JA. Relationships among bacteria, upper airway, lower airway, and systemic inflammation in COPD. Chest . 2005;127:1219–1226. doi: 10.1378/chest.127.4.1219. [DOI] [PubMed] [Google Scholar]
- 33. Agusti A, Faner R. How to define early chronic obstructive pulmonary disease. Am J Respir Crit Care Med . 2018;198:973. doi: 10.1164/rccm.201805-0880LE. [DOI] [PubMed] [Google Scholar]
- 34. Wernette DR, Nieves LA. Breathing polluted air: minorities are disproportionately exposed. EPA J . 1992;18:16–17. [Google Scholar]
- 35. Mohamed Hoesein FA, Zanen P, Sachs AP, Verheij TJ, Lammers JW, Broekhuizen BD. Spirometric thresholds for diagnosing COPD: 0.70 or LLN, pre- or post-dilator values? COPD . 2012;9:338–343. doi: 10.3109/15412555.2012.667851. [DOI] [PubMed] [Google Scholar]
- 36. Çolak Y, Afzal S, Nordestgaard BG, Lange P, Vestbo J. Importance of early COPD in young adults for development of clinical COPD: findings from the Copenhagen General Population Study. Am J Respir Crit Care Med . 2021;203:1245–1256. doi: 10.1164/rccm.202003-0532OC. [DOI] [PMC free article] [PubMed] [Google Scholar]