학술논문

Black carbon content in airway macrophages is associated with increased severe exacerbations and worse COPD morbidity in SPIROMICS.
Document Type
Academic Journal
Author
Tejwani V; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA. tejwanv@ccf.org.; Respiratory Institute, Cleveland Clinic, 9500 Euclid Avenue, A90, 44195, Cleveland, OH, USA. tejwanv@ccf.org.; Woo H; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA.; Liu C; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA.; Tillery AK; Center for Environmental Medicine, Asthma, and Lung Biology, Division of Allergy and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.; Gassett AJ; Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, WA, USA.; Kanner RE; Division of Respiratory, Critical Care and Occupational Medicine, University of Utah, Salt Lake City, UT, USA.; Hoffman EA; Department of Radiology, Medicine and Biomedical Engineering, University of Iowa, Iowa City, IA, USA.; Martinez FJ; Division of Pulmonology and Critical Care Medicine, Weill-Cornell Medical Center, Cornell University, New York, NY, USA.; Woodruff PG; Division of Pulmonary, Critical Care and Sleep Medicine, University of California San Francisco, San Francisco, CA, USA.; Barr RG; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA.; Fawzy A; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA.; Koehler K; Environmental Health and Engineering, Johns Hopkins University, Baltimore, MD, USA.; Curtis JL; Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI, USA.; Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, MI, USA.; Freeman CM; Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI, USA.; Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, MI, USA.; Cooper CB; Division of Pulmonary and Critical Care Medicine, University of California Los Angeles Medical Center, Los Angeles, CA, USA.; Comellas AP; Division of Pulmonary, Critical Care, and Occupational Medicine, College of Medicine, University of Iowa, Iowa City, IA, USA.; Pirozzi C; University of Utah Hospital, Salt Lake City, UT, USA.; Paine R; University of Utah Hospital, Salt Lake City, UT, USA.; Tashkin D; Division of Pulmonary and Critical Care Medicine, University of California Los Angeles Medical Center, Los Angeles, CA, USA.; Krishnan JA; Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA.; Sack C; Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, WA, USA.; Putcha N; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA.; Paulin LM; Pulmonary/Critical Care, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.; Zusman M; Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, WA, USA.; Kaufman JD; Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, WA, USA.; Alexis NE; Center for Environmental Medicine, Asthma, and Lung Biology, Division of Allergy and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.; Hansel NN; Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA.
Source
Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 101090633 Publication Model: Electronic Cited Medium: Internet ISSN: 1465-993X (Electronic) Linking ISSN: 14659921 NLM ISO Abbreviation: Respir Res Subsets: MEDLINE
Subject
Language
English
Abstract
Background: Airway macrophages (AM), crucial for the immune response in chronic obstructive pulmonary disease (COPD), are exposed to environmental particulate matter (PM), which they retain in their cytoplasm as black carbon (BC). However, whether AM BC accurately reflects environmental PM 2.5 exposure, and can serve as a biomarker of COPD outcomes, is unknown.
Methods: We analyzed induced sputum from participants at 7 of 12 sites SPIROMICS sites for AM BC content, which we related to exposures and to lung function and respiratory outcomes. Models were adjusted for batch (first vs. second), age, race (white vs. non-white), income (<$35,000, $35,000~$74,999, ≥$75,000, decline to answer), BMI, and use of long-acting beta-agonist/long-acting muscarinic antagonists, with sensitivity analysis performed with inclusion of urinary cotinine and lung function as covariates.
Results: Of 324 participants, 143 were current smokers and 201 had spirometric-confirmed COPD. Modeled indoor fine (< 2.5 μm in aerodynamic diameter) particulate matter (PM 2.5 ) and urinary cotinine were associated with higher AM BC. Other assessed indoor and ambient pollutant exposures were not associated with higher AM BC. Higher AM BC was associated with worse lung function and odds of severe exacerbation, as well as worse functional status, respiratory symptoms and quality of life.
Conclusion: Indoor PM 2.5 and cigarette smoke exposure may lead to increased AM BC deposition. Black carbon content in AMs is associated with worse COPD morbidity in current and former smokers, which remained after sensitivity analysis adjusting for cigarette smoke burden. Airway macrophage BC, which may alter macrophage function, could serve as a predictor of experiencing worse respiratory symptoms and impaired lung function.
(© 2022. The Author(s).)