Evidence map›Paper›PMID 38706568›Full record

ArticleFrontiers in toxicology2024

Assessing susceptibility for polycyclic aromatic hydrocarbon toxicity in an

Reese M Valdez, Brianna N Rivera, Yvonne Chang, Jamie M Pennington, Kay A Fischer, Christiane V Löhr, Susan C Tilton

Abstract read
In one paragraph

Article in Frontiers in toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
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

7 authors.

Reese M ValdezEnvironmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.
Brianna N RiveraEnvironmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.
Yvonne ChangEnvironmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.
Jamie M PenningtonEnvironmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.
Kay A FischerOregon Veterinary Diagnostic Laboratory, College of Veterinary Medicine, Oregon State University, Corvallis, OR, United States.
Christiane V LöhrOregon Veterinary Diagnostic Laboratory, College of Veterinary Medicine, Oregon State University, Corvallis, OR, United States.
Susan C TiltonEnvironmental and Molecular Toxicology Department, Oregon State University, Corvallis, OR, United States.

Funding

Research Experience and Training Coordination CoreP42ES016465 · NIEHS · OREGON STATE UNIVERSITY · PI Robyn L Tanguay · 2009 to 2026
$52.5M
MODE OF ACTION OF ENVIRONMENTAL TOXICANTST32ES007060 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt, Siva Kumar Kolluri · 1985 to 2026
$11.6M
Zebrafish Biomedical Research Facility CoreP30ES030287 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt · 2020 to 2026
$9.8M
NIEHS NIH HHS P30 ES030287NIEHS NIH HHS P42 ES016465NIEHS NIH HHS T32 ES007060
6 · The paper itself

Abstract

There is increased emphasis on understanding cumulative risk from the combined effects of chemical and non-chemical stressors as it relates to public health. Recent animal studies have identified pulmonary inflammation as a possible modifier and risk factor for chemical toxicity in the lung after exposure to inhaled pollutants; however, little is known about specific interactions and potential mechanisms of action. In this study, primary human bronchial epithelial cells (HBEC) cultured in 3D at the air-liquid interface (ALI) are utilized as a physiologically relevant model to evaluate the effects of inflammation on toxicity of polycyclic aromatic hydrocarbons (PAHs), a class of contaminants generated from incomplete combustion of fossil fuels. Normal HBEC were differentiated in the presence of IL-13 for 14 days to induce a profibrotic phenotype similar to asthma. Fully differentiated normal and IL-13 phenotype HBEC were treated with benzo[a]pyrene (BAP; 1-40 μg/mL) or 1% DMSO/PBS vehicle at the ALI for 48 h. Cells were evaluated for cytotoxicity, barrier integrity, and transcriptional biomarkers of chemical metabolism and inflammation by quantitative PCR. Cells with the IL-13 phenotype treated with BAP result in significantly (

Indexed as

3D in vitro modelasthmabenzo[a]pyrenelung cellspolycyclic aromatic hydrocarbons

Identifiers

PMID38706568
PMCPMC11066177

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.