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

John P Reilly, Edward Cantu, Jason D Christie, Michael A Matthay, Joshua M Diamond, Lorraine B Ware, John R Balmes, Carolyn S Calfee, Tatsuki Koyama, Zhiguo Zhao, Mary K Porteous

Journal: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation 2024;44(1):64-74

PMID: 39019353

Abstract

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

Using data from 1428 lung transplant recipients and their donors enrolled in the Lung Transplant Outcomes Group observational cohort study, we evaluated the association between the development of PGD and zip-code-based estimates of long-term exposure to 6 major air pollutants (ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, particulate matter 2.5, and particulate matter 10) 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 each subject's residential zip code. Associations were tested in both univariable and multivariable models controlling for known PGD risk factors.

RESULTS

We did not find strong associations between air pollutant exposures in either the donor or the recipient and PGD.

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.

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Address: Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.; Department of Medicine, University of California, San Francisco, California.; Department of Medicine, University of California, San Francisco, California; Department of Anesthesia and Cardiovascular Research Institute, University of California, San Francisco, California.; Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.; Division of Pulmonary, Allergy, and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Center for Translational Lung Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.; Division of Cardiovascular Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: [email protected].
Bant logo

© Copyright 2026, Nutrition Evidence

NED wishes to thank the following organisations for their support:

We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.