About

Dr. David B. Peden is the Senior Associate Dean for Translational Research at the UNC School of Medicine and the Medical Director of the Center for Environmental Medicine, Asthma and Lung Biology. He holds the distinguished title of Harry S. Andrews Distinguished Professor of Pediatrics. Dr. Peden is a pediatric allergist and immunologist with a particular interest in inflammation, inflammatory disorders, and environmental exposures. His primary research focuses on the impact of environmental agents and pollutants on respiratory and systemic inflammation and physiology, which affect airway diseases such as asthma, COPD, inhalational injury, airway infections, and can trigger cardiovascular events. His laboratory's efforts have led to the identification of personal mitigation strategies, including chemoprevention and personal monitoring, for pollutant-induced diseases. Additionally, his work has provided scientific support for regulatory approaches aimed at mitigating pollutant-induced diseases at both state and national levels. Dr. Peden's research has also identified and examined genetic, biological, behavioral, and societal risk factors that increase susceptibility to pollutant-induced diseases. Dr. Peden's secondary research focus involves examining inflammatory processes and mechanisms in the respiratory tract and translating basic scientific findings to human studies. This includes developing and conducting innovative and high-quality pre-clinical and clinical investigations of novel treatments for lung and allergic diseases. His research broadly centers on the biology of airway and systemic inflammation and lung function in humans, with an emphasis on asthma, allergic disease, and immunological processes in the lung. He employs translational, clinical, and epidemiological methods to explore these questions through four interrelated areas of interest. Furthermore, Dr. Peden has developed several model airway challenge protocols using ozone, endotoxin, particulate matter, and allergen. These protocols facilitate the screening of potential interventions, testing of sensor devices, and identification or confirmation of genetic or physiological risk factors for pollutant-induced and airway diseases.

Research topics

• Environmental health
• Medicine
• Immunology
• Demography
• Pharmacology
• Internal medicine
• Surgery
• Pediatrics
• Intensive care medicine

Selected publications

• Lung function and inflammation in healthy young adults after 6.6 hours of 0.07 ppm ozone exposure

  Environmental Research · 2026-04-01

  article
  PublisherDOI

• Inhaled endotoxin induces a systemic neutrophil response without affecting cardiovascular measures in a randomized cross-over exposure study

  UNC Libraries · 2026-04-21

  articleOpen access

  OBJECTIVE: The gram-negative bacterial cell wall component endotoxin (lipopolysaccharide, LPS) is a key component of particulate matter (PM). PM exposure is associated with cardiovascular morbidity and mortality. However, the contribution of individual components of PM to acute and chronic cardiovascular measures is not clear. This study examines whether systemic inflammation induced by LPS inhalation causes acute changes in cardiovascular physiology measures. MATERIALS AND METHODS: In this double blinded, placebo-controlled crossover study, fifteen adult volunteers underwent inhalation exposure to 20,000 EU Clinical Center Reference Endotoxin (CCRE). Peripheral blood and induced sputum neutrophils were obtained at baseline and six hours post-exposure. Blood pressure, measures of left ventricular function (ejection fraction (LVEF) and global longitudinal strain (LVGLS)), and indices of endothelial function (flow mediated dilation (FMD) and velocity time integral during hyperemia (VTIhyp)) were measured before and after treatment. Wilcoxon sign-rank tests and linear mixed models were used for statistical analysis. RESULTS: In comparison with normal saline, LPS inhalation resulted in significant increases in peripheral blood and sputum neutrophils but was not associated with significant alterations in blood pressure, LVGLS, LVEF, FMD, or VTIhyp. DISCUSSION AND CONCLUSIONS: In healthy adults, systemic inflammation after LPS inhalation was not associated with acute changes in cardiovascular physiology. Larger studies are needed to investigate the effects of other PM components on inflammation induced cardiovascular dysfunction.

  PublisherDOI

• Acute and durable effect of inhaled hypertonic saline on mucociliary clearance in adult asthma

  UNC Libraries · 2025-07-31

  articleOpen access

  BACKGROUND: Impaired mucus clearance and airway mucus plugging have been shown to occur in moderate-severe asthma, especially during acute exacerbations. In cystic fibrosis, where airway mucus is dehydrated, it has been shown that inhaled hypertonic saline (HS) produces both acute and sustained enhancement of mucociliary clearance (MCC). The current study was designed to assess the acute and sustained effect of inhaled 7% HS on MCC in adult asthma. METHODS: Well-controlled, moderate-severe female asthmatic patients (n=8) were screened with a single test dose of albuterol (four puffs by metered-dose inhaler) followed by HS (7% sodium chloride, 4 mL using PARI LC Star nebuliser). Spirometry was measured pre-treatment and 5 and 30 min post-treatment for safety. MCC was measured using &gamma;-scintigraphy on three separate visits: at baseline, during inhalation and 4 h after a single dose of HS. RESULTS: MCC was acutely enhanced during HS treatment; mean&plusmn;sd clearance over 60 min of dynamic imaging (Ave60Clr) was 8.9&plusmn;7.9% (baseline) <em>versus</em> 23.4&plusmn;7.6% (acute HS) (p&lt;0.005). However, this enhancement was not maintained over a 4-h period where post-HS treatment Ave60Clr was 9.3&plusmn;8.2%. In this small cohort we found no decrements in lung function up to 30 min post-treatment (forced expiratory volume in 1 s 97.4&plusmn;10.0% predicted pre-treatment and 98.9&plusmn;10.7% predicted 30 min post-treatment). CONCLUSION: While MCC was rapidly enhanced during 7% HS treatment there was no effect on MCC at 4 h post-treatment. While these findings may not support aerosolised HS use for maintenance therapy, they do suggest a benefit of treating acute exacerbations in patients with moderate-severe asthma.

  PublisherDOI

• Human Sputum Microbiome Composition and Sputum Inflammatory Cell Profiles Are Altered with Controlled Wood Smoke Exposure as a Model for Wildfire Smoke

  American Journal of Respiratory and Critical Care Medicine · 2025-06-13 · 3 citations

  articleOpen access

  Abstract Rationale Wood smoke exposure is increasing worldwide because of the increase in wildfire events. Various studies have associated exposure to wildfire-derived smoke with adverse respiratory conditions. However, the mechanism by which this occurs is unknown. Previous studies using wood smoke as a model of wildfire smoke have focused on the respiratory immune response and have reported increased neutrophil percentage and cytokine production in airway samples. The effect of wood smoke on the respiratory microbiome, however, has not been examined. Objectives The objective of this study was to evaluate whether inhaled wood smoke exposure can alter the respiratory microbiome in humans. Methods Healthy volunteers (N = 54) were subjected to controlled wood smoke exposure (500 μg/m3) for 2 hours, and induced sputum samples were collected and processed for microbiome analysis, immune mediators, and cell differentials at baseline and at 6 hours and 24 hours after exposure. A negative binomial mixed model analysis examined associations between microbiome components and inflammatory cells in sputum. Measurements and Main Results After wood smoke exposure, although sputum microbiome diversity remained unchanged, the microbiome composition was altered, particularly the abundance of several low-abundance bacteria, including Fretibacterium and Selenomonas, indicating that this inhalational exposure can alter the composition of the sputum microbiome. In addition, a significant decrease in macrophage cells was observed at 24 hours without a significant change in neutrophils. We further found small but significant associations between different taxa and macrophages (per milligram of sputum), including a negative association with Fretibacterium. Conclusions Together, these findings demonstrate that inhalational wood smoke exposure can modify several low-abundance bacteria within the respiratory microbiome and that these changes are associated with sputum inflammatory cell alterations, providing insights for future studies to focus on respiratory innate immune host–microbiome crosstalk in the context of environmental exposures.

  PublisherOA PDFDOI

• WAO - ARIA consensus on chronic cough: Executive summary

  World Allergy Organization Journal · 2025-02-24 · 8 citations

  reviewOpen access

  Acute cough is a highly prevalent symptom in clinical practice. Chronic cough is a complex disease with significant impact on quality of life. The mechanistic pathways of chronic cough in cough-comorbid clinical phenotypes are elusive. Mounting evidence suggests presence of a hypersensitive cough reflex and implication of transient receptor potential channels and P2X receptors in cough neuronal pathways. Previously, the World Allergy Organization (WAO)/Allergic Rhinitis and its Impact on Asthma (ARIA) Joint Committee on Chronic Cough published updated experimental and clinical data on chronic cough, in addition to a multidisciplinary care pathway approach to its management. The goal of this manuscript is to provide clinicians with a succinct summary of chronic cough pathophysiology, clinical phenotypes, and management strategies in both primary and cough specialty care. This executive summary is a primer for clinicians on chronic cough. Increasing awareness on the topic among primary care physicians will improve the outcome of management of patients with chronic cough.

  PublisherOA PDFDOI

• COVID-19, asthma, and biological therapies: What we need to know

  El Repositorio Academico Digital de la UANL (Universidad Autónoma de Nuevo León) · 2025-06-26

  articleOpen access
  OA PDFDOI

• Treating asthma in the time of COVID

  UNC Libraries · 2025-04-29

  articleOpen access
  PublisherDOI

• Acute asthma management during SARS-CoV2-pandemic 2020

  UNC Libraries · 2025-06-28

  articleOpen access
  PublisherDOI

• Predictive Modelling for Allergic Rhinitis: A Real-World Study on the Association Between Level of Allergens and Symptoms Occurrence &amp; Severity

  Journal of Allergy and Clinical Immunology · 2025-02-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Low-level ozone has both respiratory and systemic effects in African American adolescents with asthma despite asthma controller therapy

  UNC Libraries · 2025-09-05

  articleOpen access
  PublisherDOI

Recent grants

• NIH Grant U19AI077437

  NIH · $13.5M · 2014

• NIH Grant R01HL062624

  NIH · $1.9M · 2006

• NIH Grant M01RR000046

  NIH · $3.5M · 2008

• NIH Grant R01HL066559

  NIH · $1.3M · 2006

• NIH Grant RC1ES018417

  NIH · $977k · 2012

Frequent coauthors

• Neil E. Alexis

  University of North Carolina at Chapel Hill

  110 shared

• Michelle L. Hernandez

  Cohort (United Kingdom)

  60 shared

• John C. Lay

  University of North Carolina at Chapel Hill

  44 shared

• Robert B. Devlin

  Environmental Protection Agency

  36 shared

• David Díaz-Sánchez

  Environmental Protection Agency

  31 shared

• Haibo Zhou

  University of North Carolina at Chapel Hill

  31 shared

• Martha Almond

  University of North Carolina at Chapel Hill

  31 shared

• Philip A. Bromberg

  University of North Carolina at Chapel Hill

  28 shared

Education

• Ph.D., Toxicology

  University of North Carolina at Chapel Hill

  1990

• M.S., Toxicology

  University of North Carolina at Chapel Hill

  1986

• B.S., Toxicology

  University of North Carolina at Chapel Hill

  1984