Han Woo1, Emily P Brigham1, Kassandra Allbright1, Chinedu Ejike1, Panagis Galiatsatos1, Miranda R Jones2, Gabriela R Oates3, Jerry A Krishnan4, Christopher B Cooper5,6, Richard E Kanner7, Russell P Bowler8, Eric A Hoffman9, Alejandro P Comellas9, Gerard Criner10, R Graham Barr11, Fernando J Martinez12, MeiLan Han13, Victor E Ortega14, Trisha M Parekh15, Stephanie Christenson16, Daniel Belz1, Sarath Raju1, Amanda Gassett17,18,19, Laura M Paulin20, Nirupama Putcha1, Joel D Kaufman17,18,19, Nadia N Hansel1. 1. Division of Pulmonary and Critical Care Medicine and. 2. Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland. 3. Division of Pediatric Pulmonary and Sleep Medicine and. 4. Division of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois, Chicago, Illinois. 5. Department of Medicine and. 6. Department of Physiology, School of Medicine, University of California, Los Angeles, Los Angeles, California. 7. Division of Pulmonary and Critical Care, School of Medicine, University of Utah, Salt Lake City, Utah. 8. Division of Pulmonary and Critical Care, National Jewish Health, Denver, Colorado. 9. Department of Radiology, Medicine and Biomedical Engineering, University of Iowa, Iowa City, Iowa. 10. Division of Pulmonary and Critical Care, Temple University Hospital, Philadelphia, Pennsylvania. 11. Division of Pulmonary and Critical Care Presbyterian Hospital, Columbia University Medical Center, New York, New York. 12. Department of Internal Medicine, Weill Cornell Medical College, New York, New York. 13. Division of Pulmonary and Critical Care, University of Michigan Health System, Ann Arbor, Michigan. 14. Center for Genomics and Personalized Medicine Research, Wake Forest University, Winston-Salem, North Carolina. 15. Division of Pulmonary and Critical Care, University of Alabama at Birmingham, Birmingham, Alabama. 16. Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, San Francisco, California. 17. Department of Environmental and Occupational Health Sciences. 18. Department of Medicine, and. 19. Department of Epidemiology, University of Washington, Seattle, Washington; and. 20. Section of Pulmonary and Critical Care, Dartmouth-Hitchcock Medical Center, Geisel School of Medicine, Hanover, New Hampshire.
Abstract
Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established. Objectives: To investigate whether racial residential segregation is associated with COPD morbidity among urban Black adults with or at risk of COPD. Methods: Racial residential segregation was assessed using isolation index, based on 2010 decennial census and baseline address, for Black former and current smokers in the multicenter SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), a study of adults with or at risk for COPD. We tested the association between isolation index and respiratory symptoms, physiologic outcomes, imaging parameters, and exacerbation risk among urban Black residents, adjusting for established COPD risk factors, including smoking. Additional mediation analyses were conducted for factors that could lie on the pathway between segregation and COPD outcomes, including individual and neighborhood socioeconomic status, comorbidity burden, depression/anxiety, and ambient pollution.Measurements and Main Results: Among 515 Black participants, those residing in segregated neighborhoods (i.e., isolation index ⩾0.6) had worse COPD Assessment Test score (β = 2.4; 95% confidence interval [CI], 0.7 to 4.0), dyspnea (modified Medical Research Council scale; β = 0.29; 95% CI, 0.10 to 0.47), quality of life (St. George's Respiratory Questionnaire; β = 6.1; 95% CI, 2.3 to 9.9), and cough and sputum (β = 0.8; 95% CI, 0.1 to 1.5); lower FEV1% predicted (β = -7.3; 95% CI, -10.9 to -3.6); higher rate of any and severe exacerbations; and higher percentage emphysema (β = 2.3; 95% CI, 0.7 to 3.9) and air trapping (β = 3.8; 95% CI, 0.6 to 7.1). Adverse associations attenuated with adjustment for potential mediators but remained robust for several outcomes, including dyspnea, FEV1% predicted, percentage emphysema, and air trapping.Conclusions: Racial residential segregation was adversely associated with COPD morbidity among urban Black participants and supports the hypothesis that racial segregation plays a role in explaining health inequities affecting Black communities.
Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established. Objectives: To investigate whether racial residential segregation is associated with COPD morbidity among urban Black adults with or at risk of COPD. Methods: Racial residential segregation was assessed using isolation index, based on 2010 decennial census and baseline address, for Black former and current smokers in the multicenter SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), a study of adults with or at risk for COPD. We tested the association between isolation index and respiratory symptoms, physiologic outcomes, imaging parameters, and exacerbation risk among urban Black residents, adjusting for established COPD risk factors, including smoking. Additional mediation analyses were conducted for factors that could lie on the pathway between segregation and COPD outcomes, including individual and neighborhood socioeconomic status, comorbidity burden, depression/anxiety, and ambient pollution.Measurements and Main Results: Among 515 Black participants, those residing in segregated neighborhoods (i.e., isolation index ⩾0.6) had worse COPD Assessment Test score (β = 2.4; 95% confidence interval [CI], 0.7 to 4.0), dyspnea (modified Medical Research Council scale; β = 0.29; 95% CI, 0.10 to 0.47), quality of life (St. George's Respiratory Questionnaire; β = 6.1; 95% CI, 2.3 to 9.9), and cough and sputum (β = 0.8; 95% CI, 0.1 to 1.5); lower FEV1% predicted (β = -7.3; 95% CI, -10.9 to -3.6); higher rate of any and severe exacerbations; and higher percentage emphysema (β = 2.3; 95% CI, 0.7 to 3.9) and air trapping (β = 3.8; 95% CI, 0.6 to 7.1). Adverse associations attenuated with adjustment for potential mediators but remained robust for several outcomes, including dyspnea, FEV1% predicted, percentage emphysema, and air trapping.Conclusions: Racial residential segregation was adversely associated with COPD morbidity among urban Black participants and supports the hypothesis that racial segregation plays a role in explaining health inequities affecting Black communities.
Entities:
Keywords:
COPD; health disparities; neighborhood; racial segregation; residential segregation
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