Evidence map›Paper›PMID 23985773›Full record

ReviewInternational journal of environmental research and public health2013

Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms.

Athanasios Valavanidis, Thomais Vlachogianni, Konstantinos Fiotakis, Spyridon Loridas

Open access · goldAbstract readReview
In one paragraph

Review in International journal of environmental research and public health, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 311 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
311citing papers in PubMed, 4 pooled it
23.8field-weighted citation impact, top 1% 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

311 citing papers in PubMed, 4 syntheses or guidelines pooled it, 897 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Effect of Fine Particulate Matter Exposure on Liver Enzymes: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2023
    Pooled it
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Article
  15. The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

251 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Athanasios ValavanidisDepartment of Chemistry, University of Athens, University Campus Zografou, Athens 15784, Greece. valavanidis@chem.uoa.gr
Thomais Vlachogianni
Konstantinos Fiotakis
Spyridon Loridas
National and Kapodistrian University of Athens · GRNational Technical University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM₁₀ and PM₂.₅) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.

Indexed as

Air PollutantsAnimalsDNA DamageHumansLungLung NeoplasmsOxidative StressOzoneParticulate MatterPneumoniaReactive Oxygen SpeciesAir PollutantsOzoneParticulate MatterReactive Oxygen Species

Identifiers

PMID23985773
PMCPMC3799517
OpenAlexW2036942985

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.