Evidence map›Paper›PMID 9400742›Full record

ReviewEnvironmental health perspectives1997

The role of reactive oxygen and nitrogen species in the response of airway epithelium to particulates.

L D Martin, T M Krunkosky, J A Dye, B M Fischer, N F Jiang, L G Rochelle, N J Akley, K L Dreher, K B Adler

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% of its field
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  6. Polysaccharides From the Aerial Parts ofFrontiers in pharmacology · 2022
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  9. Exposure to PMLipids in health and disease · 2019
    Article
  10. Article
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  12. Effect of physicochemical character differences on the genotoxic potency of kaolin.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. In vitro effects of nanoparticles on renal cells.Particle and fibre toxicology · 2008
    Article
  18. Article
  19. Review
  20. 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

9 authors at 1 institution in 1 country.

L D MartinDepartment of Anatomy, North Carolina State University, College of Veterinary Medicine, Raleigh 27606, USA.
T M Krunkosky
J A Dye
B M Fischer
N F Jiang
L G Rochelle
N J Akley
K L Dreher
K B Adler
North Carolina State University · US

Funding

Mechanism of Oxidant-Induced Respiratory Mucin SecretionR37HL036982 · NHLBI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI ADLER, KENNETH BRUCE · 2004 to 2013
$4.0M
MECHANISM OF OXIDENT INDUCED RESPIRATORY MUCIN SECRETIONR01HL036982 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI ADLER, KENNETH BRUCE · 1986 to 2003
$1.2M
TNF ALPHA EFFECTS ON AIRWAY EPITHELIUMF32HL009063 · NHLBI · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI FISCHER, BERNARD M · 1994 to 1996
–
NHLBI NIH HHS HL 09063NHLBI NIH HHS HL 09512NHLBI NIH HHS HL 36982
6 · The paper itself

Abstract

Epidemiologic and occupational studies indicate adverse health effects due to inhalation of particulate air pollutants, but precise biologic mechanisms responsible have yet to be fully established. The tracheobronchial epithelium forms the body's first physiologic barrier to such airborne pollutants, where ciliary movement functions to remove the offending substances caught in the overlying mucus layer. Resident and infiltrating phagocytic cells also function in this removal process. In this paper, we examine the role of reactive oxygen and nitrogen species (ROS/RNS) in the response of airway epithelium to particulates. Some particulates themselves can generate ROS, as can the epithelial cells, in response to appropriate stimulation. In addition, resident macrophages in the airways and the alveolar spaces can release ROS/RNS after phagocytosis of inhaled particles. These macrophages also release large amounts of tumor necrosis factor alpha (TNF-alpha), a cytokine that can generate responses within the airway epithelium dependent upon intracellular generation of ROS/RNS. As a result, signal transduction pathways are set in motion that may contribute to inflammation and other pathobiology in the airway. Such effects include increased expression of intercellular adhesion molecule 1, interleukin-6, cytosolic and inducible nitric oxide synthase, manganese superoxide dismutase, cytosolic phospholipase A2, and hypersecretion of mucus. Ultimately, ROS/RNS may play a role in the global response of the airway epithelium to particulate pollutants via activation of kinases and transcription factors common to many response genes. Thus, defense mechanisms involved in responding to offending particulates may result in a complex cascade of events that can contribute to airway pathology.

Indexed as

Air PollutantsAnimalsEpitheliumHumansNitrogenReactive Oxygen SpeciesRespiratory SystemAir PollutantsNitrogenReactive Oxygen Species

Identifiers

PMID9400742
PMCPMC1470132
OpenAlexW2078915935

What OpenQuestion holds

Textmetadata
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.