Evidence map›Paper›PMID 21660296›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2011

Lung injury after cigarette smoking is particle related.

Rahul G Sangani, Andrew J Ghio

Abstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Impact of fossil fuel emissions and particulate matter on pulmonary health.Proceedings (Baylor University. Medical Center) · 2019
    Article
  8. Smoking-induced iron dysregulation in the lung.Free radical biology & medicine · 2019
    Review
  9. Review
  10. Article
  11. Article
  12. Oxidative stress and skeletal muscle dysfunction are present in healthy smokers.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  13. Article
  14. Article
  15. COPD: balancing oxidants and antioxidants.International journal of chronic obstructive pulmonary disease · 2015
    Review
  16. Pleural plaques in smoking-associated fibrosis and pulmonary asbestosis.International journal of chronic obstructive pulmonary disease · 2015
    Article
  17. 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

2 authors.

Rahul G SanganiEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC 27599-7315, USA.
Andrew J Ghio

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2) the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 μg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis) after smoking cessation since the particle is retained in the lung and the exposure continues.

Indexed as

ApoptosisHumansInflammation MediatorsInhalation ExposureLungLung InjuryOxidative StressParticulate MatterReactive Oxygen SpeciesRisk AssessmentRisk FactorsSignal TransductionSmokeSmokingInflammation MediatorsParticulate MatterReactive Oxygen SpeciesSmokeair pollutionoxidantsoxidative stressparticulate mattersmoking

Identifiers

PMID21660296
PMCPMC3107695

What OpenQuestion holds

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Read underepoch 390

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.