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(Chest. 2004;125:15-21.)
© 2004 American College of Chest Physicians

Smoking Patterns in African Americans and Whites With Advanced COPD*

Wissam M. Chatila, MD, FCCP; Walter A. Wynkoop, MD; Gwendolyn Vance, RN and Gerard J. Criner, MD, FCCP

* From the Department of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia, PA.

Correspondence to: Wissam Chatila, MD, Temple Lung Center, 763 PP, 3401 N Broad St, Philadelphia, PA 19140; e-mail: chatilw{at}tuhs.temple.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Background: The prevalence and mortality associated with COPD increases with age, with higher rates observed in whites than African Americans. Causes and explanations for smoking-related racial differences on the respiratory system have not been determined.

Objective: To investigate racial differences in smoking patterns and lung function in patients with advanced COPD.

Design: Retrospective record review of patients with advanced COPD.

Setting: Outpatient pulmonary clinic in a tertiary-care urban hospital.

Patients: One hundred sixty patients with advanced COPD (80 African Americans and 80 whites) referred for either lung volume reduction surgery or transplantation evaluation.

Data collection: Demographics, smoking profile, pulmonary function testing, arterial blood gases, and exercise stress tests were compared between African-American and white patients.

Results: Despite comparable pulmonary function, African Americans were younger at presentation and had lower overall pack-years of smoking than whites (58 ± 10 years vs 62 ± 8 years, and 44 ± 23 pack-years vs 66 ± 31 pack-years, respectively; p < 0.05 [mean ± SD]). Additionally, African Americans started smoking later in life than whites (18 ± 5 years vs 16 ± 4 years). Similarly, women presented at a younger age and smoked less compared to men (58 ± 9 years vs 62 ± 9 years, and 49 ± 28 pack-years vs 61 ± 29 pack-years, respectively; p < 0.05), without showing any difference in lung function or exercise performance.

Conclusion: Among susceptible patients with advanced COPD, African Americans and women seem more prone to the effects of tobacco smoke than their counterparts.

Key Words: chronic bronchitis • emphysema • ethnicity • smoking


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Despite narrowing differences in smoking patterns between races and genders,1 2 the prevalence of COPD remains higher in whites than in African Americans, and in men than women.3 In addition, whites and men continue to have higher mortality rates than African Americans and women; however, both latter groups appear to be catching up to their counterparts.3 In 1962, Murphy and colleagues4 were the first to suggest that COPD is a disease of the "white male." Since then, many large epidemiologic surveys3 5 have confirmed that the prevalence and attributable mortality in COPD is greater in whites and men. Despite these observations, population-based studies have not shown a difference in the rates of decline in FEV1 between African Americans and whites when adjusted for pack-years of smoking.6 A limitation of these population-based studies is the observation that only 10 to 15% of regular smokers acquire COPD. To our knowledge, no studies have examined racial differences in cigarette smoking exposure in a group of susceptible smokers.

Possible explanations for smoking-related racial differences on the respiratory system are currently obscure. Previously published epidemiologic studies3 6 do not discriminate whether the observed differences are due to genetic differences in susceptibility to smoking, or other confounding factors such as differences in smoking behavior (debut, amount, duration), environmental exposure, or physiologic differences (eg, smaller lung volumes). More importantly, selection and survivor effects could bias estimated COPD racial prevalences. Smaller numbers of African Americans in studies,7 which in part may be due to their greater attrition from the increased smoking-related cardiovascular/cancer mortality, might have lead to an underestimation of the prevalence of COPD and, thus, to the observed wider racial gap.

If the higher COPD prevalence rates found in whites compared to African Americans are secondary to whites being more susceptible to the adverse effects of cigarette smoking, then one would expect whites to have more severe COPD. At our center, however, which treats a relatively large number of African-American patients with COPD, our experience indicates that African Americans present with as severe manifestations of COPD as their white counterparts. Accordingly, we performed a retrospective review of medical records of patients with advanced COPD referred to our urban teaching hospital with the aim to investigate racial differences in smoking patterns and lung function.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patient Selection
A retrospective review of medical records was performed of all African-American patients with COPD who presented to our lung center for evaluation of lung volume reduction surgery or lung transplantation during the period January 1994 to January 2001. Patients likely to have at least moderate COPD were identified. Patients were excluded if they were found to have interstitial lung disease or other restrictive physiology, a history of congestive heart failure, or only mild airflow obstruction. COPD was diagnosed and staged according to the Global Initiative for Chronic Obstructive Lung Disease criteria.8 Patients had a >= 15 pack-year history of smoking and moderate-to-severe airflow limitation by pulmonary function testing, ie, FEV1 < 50%. A pack-year of smoking was defined as the average number of cigarette packs smoked per day multiplied by the number of years the patient smoked.

After identifying all African-American patients, we matched them by gender with white patients with COPD. We selected white patients from the same database using similar criteria, ie, FEV1 < 50% and >= 15 pack-years of smoking. A person naïve to the hypothesis of the study followed the alphabetic order of the whites’ surnames to pick one or two patients from each letter. Patients were referred by primary care physicians, pulmonary specialists, or self-referred for evaluation of lung volume reduction surgery or transplantation.

Demographics and Smoking Pattern
Patient age and body mass index (BMI) were obtained at the initial visit. Smoking habits were gleaned from medical records and included the age when the patient started smoking (debut), pack-years smoked, and current smoking status. Smoking profile was obtained in the lung center by pulmonary specialists at the initial visit.

Pulmonary Function and Exercise Testing
All patients underwent repeat pulmonary function studies following American Thoracic Society guidelines.9 Pulmonary function data after use of a bronchodilator are reported as the percentage of reference predicted values using the prediction equations from Crapo and colleagues10 for whites. We multiplied the predicted values of Crapo et al by 0.88 for African Americans to correct for their smaller lung volumes,11 a race adjustment factor used in the National Emphysema Treatment Trial.12 Thoracic gas volumes were measured by body plethysmography, and diffusion capacity of the lung for carbon monoxide (DLCO) was measured by the single-breath technique. In addition, arterial blood gas levels and maximal oxygen consumption (O2max) on cardiopulmonary exercise tests were recorded when available. Exercise testing was performed using the incremental maximum treadmill exercise to symptom-limited maximum (SensorMedics 2900; SensorMedics; Yorba Linda, CA) following American Heart Association guidelines.13

Statistical Analysis
Statistical analysis was performed by stratifying data by race and sex. Comparisons among variables were made using Student t test with Bonferroni correction for multiple comparisons for subgroup analysis (eg, African-American men vs white men, African-American men vs African-American women, etc). Statistical computations were done on Sigmastat Version 2.0 (SPSS; San Rafael, CA). Data are presented as mean ± SD; p < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Records of 160 patients were included in the final analysis. From an original group of 94 African-American patients, we identified 40 African-American men and 40 African-American women with moderate-to-severe COPD. Fourteen patients were excluded because of coexistent restrictive defects or concomitant heart disease. A random sample of 40 white men and 40 white women, all fitting our selection criteria, from a database of 430 white patients was then compared to the African-American patients.

Racial Differences
Patient characteristics at time of referral are shown in Table 1 . When compared to whites, African-American patients were younger at time of referral, started smoking later in life, and had fewer total pack-years of smoking (Fig 1 ). No differences were noted in BMI, severity of the airflow limitation, maximal exercise performance, and measurement of gas exchange.


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  		Table 1. Patient Characteristics*

 


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  		Figure 1. Race, smoking, and gas exchange. *African Americans were significantly younger at presentation than white patients (p = 0.002). {dagger}African Americans smoked significantly less than white patients (p < 0.001). {ddagger}African Americans started smoking later in life than white patients (p = 0.047). PY = pack-years.

 
Gender Differences
When the identical genders of each race were combined, differences in smoking between male and female patients were noted. Female patients were younger at the time of referral, smoked less, and tended to start smoking at an older age (17.6 ± 4.7 years vs 16.7 ± 4.4 years, p = 0.12; Fig 2 ). However, despite similar lung function (FEV1 29 ± 10% predicted vs 28 ± 10% predicted, p = 0.43) and exercise capacity (O2max 41 ± 13% predicted vs 44 ± 14% predicted, p = 0.23), women were more hypercapnic compared to men (PaCO2 49.0 ± 10.5 mm Hg vs 45.2 ± 7.3 mm Hg, p = 0.03). There was no difference in BMI between male and female patients (24.1 ± 4.7 vs 25.1 ± 4.7, respectively; p = 0.64)



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  		Figure 2. Gender, smoking, and gas exchange. *Women presented at an earlier age compared to men (58 ± 9 years vs 62 ± 8 years, p = 0.04). {dagger}Women smoked less than their male counterparts (49 ± 28 pack-years vs 61 ± 29 pack-years, p = 0.007). {ddagger}Women were more hypercapnic than men (p = 0.03). There was a trend for women to start smoking at a later age than men (17.6 ± 4.7 years vs 16.7 ± 4.4 years, p = 0.12). See Figure 1 legend for expansion of abbreviation.

 
Race/Gender Subgroup Analysis
Intraracial Gender Comparisons:
There were 40 patients in each race/gender subgroup. Gender differences in the two racial groups were not similar. White men smoked more than white women (74 ± 30 pack-years vs 57 ± 30 pack-years, p = 0.03), and men tended to start smoking at a younger age (15.6 ± 3.8 years vs 17.6 ± 4.1 years, p = 0.13; Fig 3 ). White patients, regardless of gender, presented at the same age (Fig 3) and had comparable lung function (Fig 4 ), gas exchange, and exercise performance (Fig 5 ). However, no differences were noted between African-American men and women in smoking pattern (Fig 3) , pulmonary function (Fig 4) , and maximal O2 during exercise (Fig 5) .



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  		Figure 3. Race, gender, and smoking. *There was a trend for white men to be older at presentation compared to African-American men (p = 0.06). {dagger}White men smoked more than white women and African Americans (p = 0.03 and < 0.001, respectively). {ddagger}White men tended to start smoking earlier compared to African-American men (p = 0.08).

 


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  		Figure 4. Race, gender, and pulmonary function tests. No differences were noted between all subgroups. Fem = female patients; TLC = total lung capacity; RV = residual volume.

 


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  		Figure 5. Race, gender, gas exchange, and exercise. No differences were noted between all subgroups. For blood gas analysis, n = 40 per subgroup. VO2 = O2 at maximal exercise.

 
Interracial Gender Comparisons:
White men and women smoked more than their African-American counterparts (74 ± 30 pack-years vs 47 ± 22 pack-years for men [p < 0.001] and 57 ± 30 pack-years vs 42 ± 25 pack-years for women [p = 0.03]). African-American women tended to present at an earlier age compared to white women (56 ± 10 years vs 60 ± 9 years, p = 0.17). There was also a trend for African-American men to present at a younger age and to start smoking at a later age than white men (59 ± 9 years vs 64 ± 7 years [p = 0.06] and 18.0 ± 4.8 years vs 15.6 ± 3.8 years [p = 0.08], respectively). Further subgroup analysis between African-American men and white men found no racial/gender differences in pulmonary function, gas exchange, and exercise performance.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In this study, we found that African-American patients with COPD started smoking later in life, smoked fewer total pack-years, and yet presented to our clinic with similar disease severity at an earlier age compared to white patients. Reasons for these differences may be biological (dissimilar proteases and inflammatory responses), physiologic (lower lung volumes in African Americans), and/or due to environmental factors (urban air pollution, exposure to second-hand smoke and occupational dusts), smoking behaviors, differences in referral patterns and health-care access, as well as mortality from other smoking-related diseases.

Our findings paint a different impression, although not totally at odds, with the current knowledge of COPD epidemiology. Whereas this study demonstrates identical disease severity in both racial groups, data from US health and vital statistics have long established the higher prevalence rates and attributable mortality of COPD in whites compared to African Americans.3 5 7 Our observation is not genuinely in conflict with population-based longitudinal studies that examined changes in lung function. In the National Health and Nutrition Examination Survey, the age-specific rates of airflow limitation are similar between the two races.5 In addition, the meta-analysis performed by Vollmer and colleagues6 in gender/race strata of eight large population-based studies failed to demonstrate a difference in smoking-related declines in lung function between African Americans and whites (excess FEV1 decline attributed to smoking [> 10 cigarettes per day], - 7 ± 1.2 mL/yr vs - 10 ± 1.0 mL/yr, p > 0.05). Large surveys as well as our study do not offer explanations for the observed racial prevalence gap. Nevertheless, the greater prevalence of COPD in whites cannot be attributed to rates of smoking, presence of airway hyperresponsiveness, or low socioeconomic status, because these risk factors are more prevalent in African Americans.1 2 14 The aforementioned factors along with a possible earlier life exposure to smoke and pollutants impairing lung maturation15 16 and/or greater exacerbation rates could have contributed to greater COPD progression in susceptible African Americans.

Most significant in this study is the fact that African-American patients have acquired COPD as severe as white patients earlier in life despite a lesser smoking burden. This observation questions the clinical COPD phenotype (is it progressive severe asthma, small airways disease/chronic bronchitis, or the alveolar destruction of emphysema?) and biological racial differences. By virtue of the retrospective nature of our study, and its limitations, we could not address these questions. Potential confounding factors of COPD, such as smoking behavior (cigarette brand and depth of inhalation), environmental and occupational exposure, dietary intake (vitamin supplements and polyunsaturated fatty acids), and history of lower respiratory illnesses, were not examined nor adjusted for; this was not the goal of our study. The study aimed to preliminarily characterize and compare COPD in susceptible patients within the two racial groups.

In regards to environmental exposure, we attempted to examine the role of urbanization by performing analysis on subgroups of patients based on zip codes. The majority of African Americans were indigenous to Philadelphia, and whites were from suburban zip codes. The subanalysis of urban vs suburban patients did not reveal any independent effect on COPD severity. Only a prospective study that adjusts for the above confounding demographic factors, and further investigates specific biological risks such as airway hyperresponsiveness and inflammatory mediators would help to delineate differences in airway and alveolar injury between the racial groups.

Selection and referral bias may be important factors contributing to the younger age of African Americans in our clinic. Referral bias by families or physicians familiar with our lung center, along with oversampling more African Americans of the total COPD clinic population might have accentuated the age difference between the two racial groups. In spite of this limitation, certain observations suggest that the age difference is not purely artifactual. Firstly, urban minorities have historically less access to medical care. If true, this could lead to delay in diagnosis and referral, thus they should be older rather than younger at time of referral. Secondly, higher mortality in African Americans from other smoking-related diseases, such as cancer, heart, and cerebrovascular diseases,7 could result in differences in the mean age of the survivors, with whites living longer and having more COPD later in life. Thirdly, 4 decades ago, Massaro and colleagues17 also reported that African-American patients with chronic bronchitis were 2 to 6 years younger compared to white patients across all strata of smoking burden.

Racial differences in COPD prevalence have been noted for almost half a century. COPD in African Americans has not been previously well characterized despite its staggering health and economic burden. There is an increasing trend in COPD hospitalizations, emergency department visits, and mortality of African Americans.3 The rates of COPD hospitalizations and emergency department visits are now higher in African Americans, and their mortality rates compared with whites < 55 years old are even greater.3 7 So far, no clues have been followed to elucidate reasons for these differences. The rate of decline in lung function and prevalence of COPD in population-based surveys may not tell the whole story. Our study raises the possibility that some African Americans are highly susceptible to cigarette smoking and acquire severe obstructive lung disease despite less exposure to smoking than susceptible whites. These findings need to be confirmed in future broad-based studies that adjust for confounding factors and focus on basic physiologic as well as biological measurements.


   Footnotes
 
Abbreviations: BMI = body mass index; DLCO = diffusion capacity of the lung for carbon monoxide; O2max = maximal oxygen consumption

Received for publication April 30, 2003. Accepted for publication July 30, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. U. S. Department of Health and Human Services. Tobacco use among U. S. racial/ethnic minority groups: a report of the Surgeon General. Atlanta, GA: U. S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1998. Available at: http://www.cdc.gov/ tobacco/sgr/sgr_1998/sgr-min-pdf/exec-sum.pdf. Accessed December 8, 2003
  2. American Lung Association. Trends in tobacco use: best practice and program services; Epidemiology and Statistics Unit, June 2001. Available at: http://www.lungusa.org/data/smoke/SMK2.pdf. Accessed February 26, 2003
  3. Mannino, DM, Homa, DM, Akinbami, LJ, et al Chronic obstructive pulmonary disease surveillance–United States, 1971–2000. MMWR Surveill Summ 2002;51,SS-S6
  4. Murphy, RE, Katz, S, Massaro, DJ, et al Is emphysema a disease predominantly of the white male? JAMA 1962;181,140-141
  5. Mannino, DM, Gagnon, RC, Petty, TL, et al Obstructive lung disease and low lung function in adults in the United States: data from the National Health and Nutrition Examination Survey, 1988–1994. Arch Intern Med 2000;160,1683-1689[Abstract/Free Full Text]
  6. Vollmer, WM, Enright, PL, Kathryn, LP, et al Race and gender differences in the effects of smoking on lung function. Chest 2000;117,764-772[Abstract/Free Full Text]
  7. National Center for Health Statistics. National vital statistics report 2002, Vol 50, No. 16. Available at: http://www.cdc.gov/nchs/data/nvsr/nvsr50/nvsr50_16.pdf. Accessed February 26, 2003
  8. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO workshop report. 2001 National Institutes of Health. Bethesda, MD:
  9. American Thoracic Society. Lung function testing: selection of reference values and interpretive strategies. Am Rev Respir Dis 1991;144,1202-1218[ISI][Medline]
  10. Crapo, RO, Morris, AH, Gardner, RM Reference spirometric values using techniques and equipment that meet ATS recommendations. Am Rev Respir Dis 1981;123,659-664[ISI][Medline]
  11. 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[Abstract/Free Full Text]
  12. Geddes, D, Davies, M, Koyama, H, et al Effect of lung volume reduction surgery in patients with severe emphysema. N Engl J Med 2000;343,239-245[Abstract/Free Full Text]
  13. Pina, IL, Balady, GJ, Hanson, P, et al AHA committee guidelines for clinical exercise testing laboratories. Circulation 1995;91,912-921[Free Full Text]
  14. Hardie, GE, Janson, S, Gold, WM, et al Ethnic differences: word descriptors used by African-American and white asthma patients during induced bronchoconstriction. Chest 2000;117,935-943[Abstract/Free Full Text]
  15. Gold, DR, Wang, X, Wypij, D, et al Effects of cigarette smoking on lung function in adolescent boys and girls. N Engl J Med 1996;335,931-937[Abstract/Free Full Text]
  16. Apostol, GC, Jacobs, DR, Tsai, AW, et al Early life factors contribute to the decrease in lung function between ages 18 and 40. Am J Respir Crit Care Med 2002;166,166-172[Abstract/Free Full Text]
  17. Massaro, D, Cusick, A, Katz, S Racial differences in incidence of chronic bronchitis. Am Rev Respir Dis 1965;92,94-101[ISI][Medline]



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