Long-term air pollution exposure and the risk of primary graft dysfunction after lung transplantation.

acute lung injury air pollution lung transplantation primary graft dysfunction

Journal

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703

Informations de publication

Date de publication:
15 Jul 2024
Historique:
received: 11 10 2023
revised: 02 07 2024
accepted: 08 07 2024
medline: 18 7 2024
pubmed: 18 7 2024
entrez: 17 7 2024
Statut: aheadofprint

Résumé

Primary graft dysfunction (PGD) contributes substantially to both short and long-term mortality after lung transplantation but the mechanisms that lead to PGD are not well understood. Exposure to ambient air pollutants is associated with adverse events during waitlisting for lung transplantation, and chronic lung allograft dysfunction but its association with PGD has not been studied. We hypothesized that long-term exposure of the lung donor and recipient to high levels of ambient air pollutants would increase the risk of PGD in lung transplant recipients. Using data from 1428 lung transplant recipients and their donors enrolled in the Lung Transplant Outcomes Group (LTOG) observational cohort study, we evaluated the association between the development of PGD and zip-code based estimates of long-term exposure to six major air pollutants (ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, PM2.5 and PM10) in both the lung donor and the lung recipient. Exposure estimates used daily EPA air pollutant monitoring data and were based on the geographic centroid of the each subject's residential zip code. Associations were tested in both univariable and multivariable models controlling for known PGD risk factors. We did not find strong associations between air pollutant exposures in either the donor or the recipient and PGD. Exposure to ambient air pollutants, at the levels observed in this study, may not be sufficiently harmful to prime the donor lung or the recipient to develop PGD particularly when considering the robust associations with other established PGD risk factors.

Sections du résumé

BACKGROUND BACKGROUND
Primary graft dysfunction (PGD) contributes substantially to both short and long-term mortality after lung transplantation but the mechanisms that lead to PGD are not well understood. Exposure to ambient air pollutants is associated with adverse events during waitlisting for lung transplantation, and chronic lung allograft dysfunction but its association with PGD has not been studied. We hypothesized that long-term exposure of the lung donor and recipient to high levels of ambient air pollutants would increase the risk of PGD in lung transplant recipients.
METHODS METHODS
Using data from 1428 lung transplant recipients and their donors enrolled in the Lung Transplant Outcomes Group (LTOG) observational cohort study, we evaluated the association between the development of PGD and zip-code based estimates of long-term exposure to six major air pollutants (ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, PM2.5 and PM10) in both the lung donor and the lung recipient. Exposure estimates used daily EPA air pollutant monitoring data and were based on the geographic centroid of the each subject's residential zip code. Associations were tested in both univariable and multivariable models controlling for known PGD risk factors.
RESULTS RESULTS
We did not find strong associations between air pollutant exposures in either the donor or the recipient and PGD.
CONCLUSIONS CONCLUSIONS
Exposure to ambient air pollutants, at the levels observed in this study, may not be sufficiently harmful to prime the donor lung or the recipient to develop PGD particularly when considering the robust associations with other established PGD risk factors.

Identifiants

pubmed: 39019353
pii: S1053-2498(24)01737-6
doi: 10.1016/j.healun.2024.07.003
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflict of Interest Statement This study was funded by National Institutes of Health grants HL140026, HL155821, HL126176, HL087115, HL115354, HL145435, and HL163303. Dr. Koyama and Mr. Zhao report no conflicts of interest. Dr. Balmes reports grants from the National Institute of Environmental Health Sciences and the United States Environmental Protection Agency and service as a physician member of the California Air Resources Board. Dr. Calfee reports grants from the National Institutes of Health, research contracts from Roche-Genentech and Quantum Leap Healthcare Collaborative, and consulting fees from Cellenkos, Vasomune, NGMBio, Gen1e Life Sciences, Arrowhead Pharmaceuticals and Calcimedica. Dr. Matthay reports grants from the National Institutes of Health, the Department of Defense, and the California Institute of Regenerative Medicine, research contracts with Roche Genentech and Quantum Health, and consulting fees from Gilead Pharmaceuticals, LifeEScience, Novartis, Johnson and Johnson, Pliant Therapeutics and Citius Pharmaceuticals. Dr. Reilly reports grants from the National Institutes of Health and the Department of Defense. Dr. Porteous Dr. Diamond reports royalties from UpToDate and consulting fees from CSL Behring. Dr. Christie reports grants from the National Institutes of Health and the Cystic Fibrosis Foundation. Dr. Cantu reports grants from the National Institutes of Health, research contracts from XVIVO Inc., CareDx, and Pulmocide. And consulting fees from CSL Behring, United Therapeutics and Pulmocide. Dr. Ware reports grant support from the National Institutes of Health, research contracts with Genentech and Boehringer Ingelheim, consulting fees from Arrowhead, Akebia, Santhera and Global Blood Therapeutics and stock ownership in Virtuoso Surgical.

Auteurs

Tatsuki Koyama (T)

Department of Biostatistics, Vanderbilt University Medical Center.

Zhiguo Zhao (Z)

Department of Biostatistics, Vanderbilt University Medical Center.

John R Balmes (JR)

Department of Medicine, University of California, San Francisco.

Carolyn S Calfee (CS)

Department of Medicine, University of California, San Francisco; Department of Anesthesia and Cardiovascular Research Institute, University of California, San Francisco.

Michael A Matthay (MA)

Department of Medicine, University of California, San Francisco; Department of Anesthesia and Cardiovascular Research Institute, University of California, San Francisco.

John P Reilly (JP)

Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania.

Mary K Porteous (MK)

Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania.

Joshua M Diamond (JM)

Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania.

Jason D Christie (JD)

Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania; Center for Translational Lung Biology, Perelman School of Medicine, University of Pennsylvania; Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania.

Edward Cantu (E)

Division of Cardiovascular Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.

Lorraine B Ware (LB)

Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center. Electronic address: Lorraine.ware@vumc.org.

Classifications MeSH