Evidence map›Paper›PMID 42562292›Full record

ArticleChemico-biological interactions2026

Transcriptomic signature comparisons identify conserved key events and respiratory disease signatures most similar to wildfire-relevant exposure.

Sarah L Miller, Jessie R Chappel, Elise Hickman, Lauren Koval, Mark Heise, Meghan E Rebuli, Ilona Jaspers, Cynthia Rider, David Reif, Julia E Rager

Abstract read
In one paragraph

Article in Chemico-biological interactions, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Sarah L MillerCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA.
Jessie R ChappelCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA; Department of Environmental Sciences & Engineering, University of North Carolina, Chapel Hill, NC, USA.
Elise HickmanCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA; Department of Environmental Sciences & Engineering, University of North Carolina, Chapel Hill, NC, USA; Center for Environmental Medicine, Asthma & Lung Biology, University of North Carolina, Chapel Hill, NC, USA.
Lauren KovalDepartment of Environmental Sciences & Engineering, University of North Carolina, Chapel Hill, NC, USA.
Mark HeiseDepartment of Genetics, University of North Carolina, Chapel Hill, NC, USA.
Meghan E RebuliCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA; Center for Environmental Medicine, Asthma & Lung Biology, University of North Carolina, Chapel Hill, NC, USA; Institute for Environmental Health Solutions, University of North Carolina, Chapel Hill, NC, USA.
Ilona JaspersCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA; Institute for Environmental Health Solutions, University of North Carolina, Chapel Hill, NC, USA; Marsico Lung Institute, University of North Carolina, Chapel Hill, NC, USA.
Cynthia RiderDivision of Translational Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
David ReifDivision of Translational Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Julia E RagerCurriculum in Toxicology & Environmental Medicine, University of North Carolina, Chapel Hill, NC, USA; Department of Environmental Sciences & Engineering, University of North Carolina, Chapel Hill, NC, USA; Center for Environmental Medicine, Asthma & Lung Biology, University of North Carolina, Chapel Hill, NC, USA; Institute for Environmental Health Solutions, University of North Carolina, Chapel Hill, NC, USA. Electronic address: jrager@unc.edu.

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
Wildland Urban Interface Exposure Toxicity in Cells, Animals, and HumansR01ES035878 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Julia Rager · 2024 to 2026
$2.2M
NIEHS NIH HHS R01 ES035878NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Wildfire events pose increasing threats to public health, especially concerning the respiratory system. The chemistries of emission mixtures vary widely based on factors including fuel source, burn temperature, and atmospheric and photochemical processes. Because of these varying exposure conditions, differing biological responses may occur, making it difficult to identify common mediators of wildfire smoke-induced disease with which to base health and risk assessments upon. To address this difficulty, this study set out to identify genes and modes of action highly shared across biological responses to wildfire-relevant exposures and respiratory disease outcomes. Specifically, we mined the Molecular Signatures Database and Computational Toxicogenomics Database for human consensus gene expression signatures of respiratory diseases and infections putatively linked to wildfire smoke exposures. These gene signatures were then compared to transcriptomic signatures measured in the lung of mice exposed to condensates derived from variable controlled biomass burn conditions. Data cleaning followed by similarity scoring, clustering, data reduction, and pathway enrichment methods were used to identify patterns amongst exposure and disease profiles. Fifty-three genes were identified as highly shared across signatures of both exposure and disease. Jaccard-based similarity scoring analyses of these top shared genes revealed asthma as the respiratory disease most similar across the majority of biomass conditions under evaluation. Pathway enrichment of these top shared genes identified interleukin signaling, oxidative stress response, and estrogen signaling as mechanisms of action likely linking exposure-to-disease outcomes across these variable smoke exposure conditions. Altogether, these results highlight consistent mediators to use in future health risk-based evaluations of wildfire smoke emissions.

Indexed as

Respiratory Tract DiseasesSmokeTranscriptomeWildfiresAnimalsGene Expression ProfilingHumansLungMiceSmokeAsthmaEstrogen signalingInterleukinsOxidative stressRespiratory diseaseTranscriptomicsWildfire smoke

Identifiers

PMID42562292
PMCPMC13501526

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.