Evidence map›Paper›PMID 20634362›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2010

Small particles disrupt postnatal airway development.

DongYoub Lee, Chris Wallis, Anthony S Wexler, Edward S Schelegle, Laura S Van Winkle, Charles G Plopper, Michelle V Fanucchi, Ben Kumfer, Ian M Kennedy, Jackie K W Chan

Abstract readComparative Study
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Air pollution and lung function in children.The Journal of allergy and clinical immunology · 2021
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Perinatal factors in neonatal and pediatric lung diseases.Expert review of respiratory medicine · 2013
    Article
  11. Article
  12. Article
  13. Review
  14. Age-specific effects on rat lung glutathione and antioxidant enzymes after inhaling ultrafine soot.American journal of respiratory cell and molecular biology · 2013
    Article
  15. Article
  16. Susceptibility to inhaled flame-generated ultrafine soot in neonatal and adult rat lungs.Toxicological sciences : an official journal of the Society of Toxicology · 2011
    Article
  17. Article
  18. 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

10 authors at 4 institutions in 3 countries.

DongYoub LeeDepartment of Mechanical and Aerospace Engineering, Univ. of California, Davis, CA 95616, USA.
Chris Wallis
Anthony S Wexler
Edward S Schelegle
Laura S Van Winkle
Charles G Plopper
Michelle V Fanucchi
Ben Kumfer
Ian M Kennedy
Jackie K W Chan
Institute of Cell Biology and Neurobiology · ITQuality Research · USThuyloi University · VNUniversity of Alabama · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI VASYLIEVA, NATALIA · 1987 to 2021
$50.1M
NIEHS NIH HHS P42 ES004699
6 · The paper itself

Abstract

Increasing numbers of epidemiologic studies associate air pollution exposure in children with decreased lung function development. The objective of this study was to examine the effects of exposure to combustion-generated fine [230 and 212 nm number mean aerodynamic particle diameter (NMAD)] to ultrafine (73 nm NMAD) particles differing in elemental (EC) and organic (OC) carbon content on postnatal airway development in rats. Neonatal Sprague-Dawley rats were exposed from postnatal day 7 through 25, and lung function and airway architecture were evaluated 81 days of age. In a separate group of rats, cell proliferation was examined after a single particle exposure at 7 days of age. Early life exposure to 73 nm high OC/EC particles altered distal airway architecture and resulted in subtle changes in lung mechanics. Early life exposure to 212 nm high OC/EC particles did not alter lung architecture but did alter lung mechanics in a manner suggestive of central airway changes. In contrast, early life exposure to 230 nm low OC/EC particles did not alter lung architecture or mechanics. A single 6-h exposure to 73 nm high OC/EC particle decreased airway cell proliferation, whereas 212 nm high OC/EC particles increased it and 230 nm low OC/EC particles did not. The early life exposure to ultrafine, high OC/EC particles results in persistent alterations in distal airway architecture that is characterized by an initial decrease in airway cell proliferation.

Indexed as

Age FactorsAnimalsAnimals, NewbornBronchial Provocation TestsBronchoconstrictionCarbonCell ProliferationImmunohistochemistryInhalation ExposureLungParticle SizeParticulate MatterProliferating Cell Nuclear AntigenRatsRats, Sprague-DawleyRespiratory MechanicsCarbonParticulate MatterProliferating Cell Nuclear Antigen

Identifiers

PMID20634362
PMCPMC4182294
OpenAlexW2112960127

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.