Evidence map›Paper›PMID 27206323›Full record

ArticleInhalation toxicology2016

Differential expression of pro-inflammatory and oxidative stress mediators induced by nitrogen dioxide and ozone in primary human bronchial epithelial cells.

Jaime E Mirowsky, Lisa A Dailey, Robert B Devlin

Abstract read
In one paragraph

Article in Inhalation toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 3 pooled it
–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

31 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Effects of prenatal exposure to NOEnvironmental science and pollution research international · 2020
    Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Article
  8. The Impact of NOJournal of applied toxicology : JAT · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Short-term association of CO and NOFrontiers in public health · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

3 authors.

Jaime E Mirowskya Curriculum in Toxicology, University of North Carolina School of Medicine , Chapel Hill , NC , USA .
Lisa A Daileyc Environmental Public Health Division, National Health and Environmental Effects Laboratory, US Environmental Protection Agency , Chapel Hill , NC , USA.
Robert B Devlinc Environmental Public Health Division, National Health and Environmental Effects Laboratory, US Environmental Protection Agency , Chapel Hill , NC , USA.

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

contextNO2 and O3 are ubiquitous air toxicants capable of inducing lung damage to the respiratory epithelium. Due to their oxidizing capabilities, these pollutants have been proposed to target specific biological pathways, but few publications have compared the pathways activated.

objectiveThis work will test the premise that NO2 and O3 induce toxicity by activating similar cellular pathways.

methodsPrimary human bronchial epithelial cells (HBECs, n = 3 donors) were exposed for 2 h at an air-liquid interface to 3 ppm NO2, 0.75 ppm O3, or filtered air and harvested 1 h post-exposure. To give an overview of pathways that may be influenced by each exposure, gene expression was measured using PCR arrays for toxicity and oxidative stress. Based on the results, genes were selected to quantify whether expression changes were changed in a dose- and time-response manner using NO2 (1, 2, 3, or 5 ppm), O3 (0.25, 0.50, 0.75, or 1.00 ppm), or filtered air and harvesting 0, 1, 4 and 24 h post-exposure.

resultsUsing the arrays, genes related to oxidative stress were highly induced with NO2 while expression of pro-inflammatory and vascular function genes was found subsequent to O3. NO2 elicited the greatest HMOX1 response, whereas O3 more greatly induced IL-6, IL-8 and PTGS2 expression. Additionally, O3 elicited a greater response 1 h post-exposure and NO2 produced a maximal response after 4 h.

conclusionWe have demonstrated that these two oxidant gases stimulate differing mechanistic responses in vitro and these responses occur at dissimilar times.

Indexed as

AdultAir PollutantsBronchiCells, CulturedEpithelial CellsHumansNitrogen DioxideOxidative StressOzoneRNA, MessengerTranscriptomeAir PollutantsNitrogen DioxideOzoneRNA, MessengerinflammationIn vitronitrogen dioxideoxidantoxidative stressozone

Identifiers

PMID27206323
PMCPMC4967931

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.