Evidence map›Paper›PMID 22486349›Full record

ReviewInhalation toxicology2012

Manufactured and airborne nanoparticle cardiopulmonary interactions: a review of mechanisms and the possible contribution of mast cells.

Jonathan H Shannahan, Urmila P Kodavanti, Jared M Brown

Open access · greenAbstract readReview
In one paragraph

Review in Inhalation toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. The size-dependent genotoxicity and oxidative stress of silica nanoparticles on endothelial cells.Environmental science and pollution research international · 2019
    Article
  7. Low-dose combined exposure of nanoparticles and heavy metal compared with PMEnvironmental science and pollution research international · 2017
    Article
  8. Review
  9. Article
  10. Lung function in asphalt pavers: a longitudinal study.International archives of occupational and environmental health · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Influence of physicochemical properties of silver nanoparticles on mast cell activation and degranulation.Toxicology in vitro : an international journal published in association with BIBRA · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. C₆₀ exposure augments cardiac ischemia/reperfusion injury and coronary artery contraction in Sprague Dawley rats.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    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

3 authors at 2 institutions in 1 country.

Jonathan H ShannahanDepartment of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA.
Urmila P Kodavanti
Jared M Brown
East Carolina University · USEnvironmental Protection Agency · US

Funding

Mechanisms of non-IgE Mast Cell Activation by Environmental ParticulatesR01ES019311 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI BROWN, JARED MICHAEL · 2010 to 2024
$7.0M
NIEHS NIH HHS R01 ES019311
6 · The paper itself

Abstract

Human inhalation exposures to manufactured nanoparticles (NP) and airborne ultrafine particles (UFP) continues to increase in both occupational and environmental settings. UFP exposures have been associated with increased cardiovascular mortality and morbidity, while ongoing research supports adverse systemic and cardiovascular health effects after NP exposures. Adverse cardiovascular health effects include alterations in heart rate variability, hypertension, thrombosis, arrhythmias, increased myocardial infarction, and atherosclerosis. Exactly how UFP and NP cause these negative cardiovascular effects is poorly understood, however a variety of mediators and mechanisms have been proposed. UFP and NP, as well as their soluble components, are known to systemically translocate from the lung. Translocated particles could mediate cardiovascular toxicity through direct interactions with the vasculature, blood, and heart. Recent study suggests that sensory nerve stimulation within the lung may also contribute to UFP- and NP-induced acute cardiovascular alterations. Activation of sensory nerves, such as C-fibers, within the lung may result in altered cardiac rhythm and function. Lastly, release of pulmonary-derived mediators into systemic circulation has been proposed to facilitate cardiovascular effects. In general, these proposed pulmonary-derived mediators include proinflammatory cytokines, oxidatively modified macromolecules, vasoactive proteins, and prothrombotic factors. These pulmonary-derived mediators have been postulated to contribute to the subsequent prothrombotic, atherogenic, and inflammatory effects after exposure. This review will evaluate the potential contribution of individual mediators and mechanisms in facilitating cardiopulmonary toxicity following inhalation of UFP and NP. Lastly, we will appraise the literature and propose a hypothesis regarding the possible role of mast cells in contributing to these systemic effects.

Indexed as

Air PollutantsAnimalsAutonomic Nervous SystemCardiovascular SystemHumansLungMast CellsNanoparticlesAir Pollutants

Identifiers

PMID22486349
PMCPMC3768266
OpenAlexW2090051810

What OpenQuestion holds

Textmetadata
LicenceTDM
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.