About

Dr. Ilona Jaspers is a pediatric microbiologist and immunologist specializing in the effects of environmental oxidants on human immune responses. She holds multiple leadership roles at the University of North Carolina at Chapel Hill, including Director of the Center for Environmental Medicine, Asthma and Lung Biology, Director of the Curriculum in Toxicology at the UNC School of Medicine, and Associate Director of Scientific Development at the Children's Research Institute. She is also a Professor of Pediatrics and Microbiology & Immunology, as well as a Professor of Environmental Sciences and Engineering at the Gillings School of Global Public Health. Dr. Jaspers has developed several human in vitro and clinical in vivo models to investigate the adverse health effects caused by pollutant exposures. Her research focuses on modifiers of disease and environmental disease, particularly examining exposures to diesel exhaust, ozone, and tobacco smoke through e-cigarettes. She employs basic and translational research models to study how factors such as nutrition, pre-existing diseases, and co-exposures to environmental agents influence mucosal host defense responses. Her work includes the development of experimental models to explore how exposure to environmental pollutants alters immune responses, utilizing human organotypic epithelial cell culture models in vitro, mouse lung models in vivo, and human studies in vivo. Dr. Jaspers collaborates extensively with investigators from UNC and the U.S. Environmental Protection Agency to conduct translational studies related to the health effects of air pollution.

Research topics

• Medicine
• Environmental health
• Biology
• Pathology
• Internal medicine
• Toxicology
• Immunology
• Intensive care medicine
• Computer Science
• Psychiatry
• Risk analysis (engineering)
• Pediatrics
• Business
• Ecology
• Virology
• Genetics
• Biochemical engineering
• Engineering
• Biotechnology
• Environmental science
• Biochemistry
• Cell biology

Selected publications

• Dysbiosis of the nasal microbiome is associated with prospective acute exacerbation of COPD

  Microbiome · 2026-03-16

  articleOpen access

  BACKGROUND: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is often associated with respiratory viral infection and the need for increased medical intervention. The nasal mucosa plays a critical role in infection susceptibility and severity, with the nasal microbiome shaping mucosal immunity. This study investigated the association between the bacterial nasal microbiome and AECOPD. Participants included 41 individuals with COPD and 15 healthy non-COPD controls. Nasal microbiome composition was assessed from nasal epithelial lining fluid and compared at baseline between healthy participants and individuals with COPD, stratified by AECOPD history. COPD subjects who experienced one or more AECOPD in the year prior to enrollment were categorized as Ever AECOPD. COPD participants without a history of AECOPD in the prior year were categorized as Never AECOPD. Prospective exacerbation data were collected and used in a case-control analysis to identify clinical and microbiological markers predictive of future AECOPD in COPD-diagnosed subjects. RESULTS: We found two distinct nasal microbiome architectures with enrichment of protective taxa (healthy signature) or pathobionts (pathogenic signature). Nasal microbiome analysis demonstrated significant differences in nasal bacterial composition between COPD-diagnosed individuals with prior AECOPD (Ever AECOPD) compared to healthy controls. For COPD individuals with no prior AECOPD (Never AECOPD), we identified two underlying community structures; Cluster 1 subjects harbored a nasal microbiome significantly similar to healthy controls (healthy signature) and Cluster 2 subjects were significantly similar to the Ever AECOPD cohort (pathogenic signature). We evaluated the baseline microbiome of COPD-diagnosed participants based on the occurrence of at least one AECOPD 1-year after baseline sample collection (prospective AECOPD) and found that the nasal microbiome was associated with the occurrence of future AECOPD events. Prospective exacerbation was associated with reduced relative abundance of Dolosigranulum pigrum. Further analysis by qPCR showed that decreased D. pigrum abundance was associated with lower lung function and higher risk of future AECOPD. CONCLUSIONS: Our data indicates that the nasal microbiome is associated with AECOPD phenotypes. Moreover, participants with decreased nasal Dolosigranulum pigrum abundance had lower lung function and a higher risk of future exacerbations. These findings suggest that D. pigrum may serve as a biomarker for AECOPD risk; however, validation of these findings in a larger multicenter cohort is needed. Video Abstract.

  PublisherDOI

• Interpretable Machine Learning to Understand Wildfire Toxicity: Bridging Chemicals, Omics, and Toxicological Outcomes via Symbolic Regression with Novel Feature Scoring.

  UNC Libraries · 2026-04-09

  articleOpen access

  Wildfire smoke exposures are increasingly common, consisting of complex mixtures of gases and particulates known to cause diverse pulmonary health effects. While health outcomes are regularly studied, quantitative links between smoke chemical composition and toxicological outcomes remain poorly defined, limiting interpretation of wildfire smoke health risks. This study explores symbolic regression (SR) as an interpretable artificial intelligence/machine learning method to generate closed-form mathematical models linking chemical exposure to biological responses relevant to wildfire smoke. Prior to application on wildfire-relevant data sets, we benchmarked three Python-based SR packages on simulated data, assessing performance across varying noise levels and operator complexities. Insights from these simulation tests, such as the importance of including necessary operators, were incorporated when applying SR to lab-generated wildland fire exposure-toxicity data. This data set included chemical characterizations of biomass smoke exposures and corresponding pulmonary responses in female CD-1 mice (<em>n</em> = 60). Specifically, we evaluated the ability to predict a lung injury marker using (1) targeted measures of over 80 chemicals measured in smoke (RMSE = 17.57 mg/mL) and (2) lung tissue measures of hundreds of transcripts (RMSE = 15.12 mg/mL). Resulting error metrics were comparable to Random Forest and XGBoost models. To aid model interpretation, we developed directional ensemble contribution scores (DECS), a novel feature importance scoring method that quantifies the direction and magnitude of predictor contributions across top-performing models. Expert toxicologists also contributed to model prioritization, integrating a "biologists-in-the-loop" approach. Results highlighted polycyclic aromatic hydrocarbons as drivers of lung injury and methoxyphenols as suppressors. Transcriptomic analyses highlighted a small set of genes, which have roles in metabolism, cell proliferation, immune regulation, and oncogenic processes, with MYC proto-oncogene (<em>Myc</em>) showing the strongest association. Overall, this study demonstrates SR and associated DECS as practical, interpretable tools for modeling environmental mixtures, such as wildfire smoke, and their toxicological effects.

  PublisherDOI

• Interpretable Machine Learning to Understand Wildfire Toxicity: Bridging Chemicals, Omics, and Toxicological Outcomes via Symbolic Regression with Novel Feature Scoring

  Chemical Research in Toxicology · 2026-04-03

  articleOpen access

  Wildfire smoke exposures are increasingly common, consisting of complex mixtures of gases and particulates known to cause diverse pulmonary health effects. While health outcomes are regularly studied, quantitative links between smoke chemical composition and toxicological outcomes remain poorly defined, limiting interpretation of wildfire smoke health risks. This study explores symbolic regression (SR) as an interpretable artificial intelligence/machine learning method to generate closed-form mathematical models linking chemical exposure to biological responses relevant to wildfire smoke. Prior to application on wildfire-relevant data sets, we benchmarked three Python-based SR packages on simulated data, assessing performance across varying noise levels and operator complexities. Insights from these simulation tests, such as the importance of including necessary operators, were incorporated when applying SR to lab-generated wildland fire exposure-toxicity data. This data set included chemical characterizations of biomass smoke exposures and corresponding pulmonary responses in female CD-1 mice (n = 60). Specifically, we evaluated the ability to predict a lung injury marker using (1) targeted measures of over 80 chemicals measured in smoke (RMSE = 17.57 mg/mL) and (2) lung tissue measures of hundreds of transcripts (RMSE = 15.12 mg/mL). Resulting error metrics were comparable to Random Forest and XGBoost models. To aid model interpretation, we developed directional ensemble contribution scores (DECS), a novel feature importance scoring method that quantifies the direction and magnitude of predictor contributions across top-performing models. Expert toxicologists also contributed to model prioritization, integrating a “biologists-in-the-loop” approach. Results highlighted polycyclic aromatic hydrocarbons as drivers of lung injury and methoxyphenols as suppressors. Transcriptomic analyses highlighted a small set of genes, which have roles in metabolism, cell proliferation, immune regulation, and oncogenic processes, with MYC proto-oncogene (Myc) showing the strongest association. Overall, this study demonstrates SR and associated DECS as practical, interpretable tools for modeling environmental mixtures, such as wildfire smoke, and their toxicological effects.

  PublisherDOI

• Seasonal PM 2.5 exposures induce differential responses to influenza A virus infection in primary human airway epithelial cells

  Research Square · 2025-07-10

  preprintOpen accessSenior author
  PublisherOA PDFDOI

• Cannabinoid Vaping Products: Regulation, Composition, Toxicological Effects, and Emerging Research

  Chemical Research in Toxicology · 2025-11-11

  articleOpen accessSenior authorCorresponding

  The 2018 U.S. Farm Bill inadvertently paved the way for a market of unregulated, hemp-derived cannabinoid vaping products, including cannabidiol (CBD) and Δ8-tetrahydrocannabinol (Δ8-THC). These products contain extremely high cannabinoid concentrations, contaminants, and potentially harmful byproducts from heating, raising concerns about respiratory toxicity. This review examines the regulatory landscape, manufacturing practices, composition, and toxicological mechanisms associated with hemp-derived cannabinoid vaping products. While vaping-related lung injuries, such as E-cigarette or Vaping, Product use-Associated Lung Injury (EVALI), have been linked to vitamin E acetate (VEA), a definitive mechanism of injury has not been established, and cases continue to be reported. Studies reveal multiple mechanisms of lung toxicity associated with cannabinoid vaping, including inflammatory responses, oxidative stress, and damage from contaminants like heavy metals and flavoring agents. Emerging evidence also highlights the formation of reactive cannabinoid quinones (e.g., CBDQ) during vaping, which form covalent adducts with protein cysteine residues, potentially altering their function, and also have the potential to drive oxidative damage through redox cycling. These electrophilic quinones may act as pleiotropic modifiers of cellular function and represent an important, yet understudied, contributor to cannabinoid vaping toxicity. This review identifies key research gaps, including the need for studies on chronic exposure models, mechanisms of lung injury, and the interplay between VEA, cannabinoid quinones, and other harmful byproducts. Additionally, given the potential for both therapeutic benefits and toxic effects, research should investigate optimal temperatures and formulations that balance efficacy and safety over potential toxicity caused by thermal oxidation. Overall, a comprehensive understanding of the toxicological mechanisms of cannabinoid vaping products is essential to guide public health decisions, inform regulatory frameworks, and support the development of safer products.

  PublisherOA PDFDOI

• Prothrombotic Biomarkers Are Not Altered by Wood Smoke: A Pilot Controlled Exposure Study

  UNC Libraries · 2025-07-25

  articleOpen access

  Inhalation of wood smoke (WS) has been associated with increased risk of cardiovascular events, including heart attacks and strokes, both of which are caused in part by the thrombotic occlusion of blood vessels. To characterize the effects of WS on levels of established, circulating prothrombotic biomarkers, healthy human subjects at rest were exposed to WS (500&thinsp;&mu;g/m3) or filtered air for 2&thinsp;h. Plasma samples were then used to assess markers of endogenous procoagulant activity: cellular activation (tissue factor-positive extracellular vesicles, TF&thinsp;+&thinsp;EVs), thrombin-antithrombin complexes (TAT), fibrin formation/breakdown (D-dimer), and thrombin generation potential. No significant differences in TF&thinsp;+&thinsp;EVs, TATs, D-dimer, or thrombin generation parameters were detected between WS- or filtered air-exposed individuals. Although females had significantly higher TATs and D-dimers, and slightly but non-significantly shorter thrombin generation lag times than males, there were no significant differences between WS- or air-exposed males or females in any measurements. These data suggest that acute WS exposure does not increase prothrombotic biomarkers in plasma.

  PublisherDOI

• Propylene Glycol and Vegetable Glycerin E-cigarette Aerosols Disrupt Mucociliary Function and Cause Cytotoxicity in Human Airway Epithelium

  Research Square · 2025-09-25 · 1 citations

  preprintOpen access
  PublisherOA PDFDOI

• Simulated burn pit smoke condensates cause sustained impact on human airway epithelial cells

  UNC Libraries · 2025-12-20

  articleOpen access

  Inhalation of smoke from burn pits during military deployment is associated with several adverse pulmonary outcomes. We exposed human airway epithelial cells to smoke condensates from burn pit waste materials. Single and repeated exposure of condensates triggered unique and common responses in terms of gene expression, that sustained through the recovery phase. Source material and combustion condition influenced the outcome. Intensified response in female donor cells indicated a determining role of biological sex. The observations indicate a lasting impact of burn pit smoke exposure on epithelial gene expression, potentially contributing to disease pathogenesis.

  PublisherDOI

• Prothrombotic Biomarkers Are Not Altered by Wood Smoke: A Pilot Controlled Exposure Study

  FASEB BioAdvances · 2025-07-01

  articleOpen accessSenior authorCorresponding

  ABSTRACT Inhalation of wood smoke (WS) has been associated with increased risk of cardiovascular events, including heart attacks and strokes, both of which are caused in part by the thrombotic occlusion of blood vessels. To characterize the effects of WS on levels of established, circulating prothrombotic biomarkers, healthy human subjects at rest were exposed to WS (500 μg/m 3 ) or filtered air for 2 h. Plasma samples were then used to assess markers of endogenous procoagulant activity: cellular activation (tissue factor‐positive extracellular vesicles, TF + EVs), thrombin‐antithrombin complexes (TAT), fibrin formation/breakdown (D‐dimer), and thrombin generation potential. No significant differences in TF + EVs, TATs, D‐dimer, or thrombin generation parameters were detected between WS‐ or filtered air‐exposed individuals. Although females had significantly higher TATs and D‐dimers, and slightly but non‐significantly shorter thrombin generation lag times than males, there were no significant differences between WS‐ or air‐exposed males or females in any measurements. These data suggest that acute WS exposure does not increase prothrombotic biomarkers in plasma.

  PublisherOA PDFDOI

• E-Cigarette Use, Cigarette Smoking, and Sex Are Associated With Nasal Microbiome Dysbiosis

  UNC Libraries · 2025-07-18

  articleOpen access

  INTRODUCTION: Previous research suggests that e-cigarettes can alter immune function, including in the nasal mucosa, in unique ways. The respiratory microbiome plays a key role in respiratory host defense, but the effects of e-cigarettes on the respiratory or nasal microbiome, are not well understood. METHODS: Using 16S rRNA gene sequencing on nasal samples from adult e-cigarette users, smokers, and nonsmokers, we determined that e-cigarette use and cigarette smoking are associated with differential respiratory microbiome dysbiosis and substantial sex-dependent differences in the nasal microbiome, particularly in e-cigarette users. RESULTS: Staphylococcus aureus, a common respiratory pathogen, was more abundant in both e-cigarette users and smokers in comparison with nonsmokers, while Lactobacillus iners, often consider a protective species, was more abundant in smokers but less abundant in e-cigarette users in comparison with nonsmokers. In addition, we identified significant dysbiosis of the nasal microbiome between e-cigarette users and smokers with high versus low serum cotinine levels, an indicator of tobacco product use and toxicant exposure. We also analyzed nasal lavage fluid for immune mediators associated with host-microbiota interactions. CONCLUSIONS: Our analysis identified disruption of immune mediators in the nose of e-cigarette users and smokers, which is indicative of disrupted respiratory mucosal immune responses. Taken together, our data identified unique, sex-dependent host immune dysfunction associated with e-cigarette use in the nasal mucosa. More broadly, our data highlight the need for continued inclusion and careful consideration of sex as an important variable in the context of toxicant exposures. IMPLICATIONS: This is the first study investigating the effects of e-cigarette use and sex on the nasal microbiome, which is considered an important gatekeeper for protecting the lower respiratory tract from pathogens. We found significant sex, exposure group, and serum cotinine level associated differences in the composition of the nasal microbiome, demonstrating the importance of considering sex in future nasal microbiome studies and warranting further investigation of the mechanisms by which e-cigarette use dysregulates nasal immune homeostasis.

  PublisherDOI

Recent grants

• Core B: Sample Acquisition and Repository Core

  NIH · $33.0M · 2020

• Ozone, lipid-protein adducts, and biological effects

  NIH · $437k · 2015–2017

• The Role of Nasal Mucosal Immunity and Microbiome on the Frequent Exacerbation Phenotype of COPD

  NIH · $3.0M · 2021–2026

• Fate, transport, and toxicity of engineered nanoparticles in the atmosphere

  NSF · $470k · 2010–2015

• NIH Grant R01ES013611

  NIH · $3.7M · 2017

Frequent coauthors

• Meghan E. Rebuli

  University of North Carolina at Chapel Hill

  87 shared

• Luisa E. Brighton

  University of North Carolina at Chapel Hill

  45 shared

• Terry L. Noah

  University of North Carolina at Chapel Hill

  42 shared

• Andrew J. Ghio

  Environmental Protection Agency

  39 shared

• Kenneth G. Sexton

  35 shared

• Carole Robinette

  University of North Carolina at Chapel Hill

  34 shared

• Julia E. Rager

  University of North Carolina at Chapel Hill

  32 shared

• James M. Samet

  Environmental Protection Agency

  32 shared

Labs

• Curriculum in Toxicology & Environmental MedicinePI

Education

• Ph.D., Toxicology

  University of North Carolina at Chapel Hill

  2000

• M.S., Toxicology

  University of North Carolina at Chapel Hill

  1996

• B.S., Toxicology

  University of North Carolina at Chapel Hill

  1994