Evidence map›Paper›PMID 33602020›Full record

ArticleInhalation toxicology2021

Lung toxicity and gene expression changes in response to whole-body inhalation exposure to cellulose nanocrystal in rats.

Pius Joseph, Christina M Umbright, Jenny R Roberts, Jared L Cumpston, Marlene S Orandle, Walter G McKinney, Tina M Sager

Open access · greenAbstract read
In one paragraph

Article in Inhalation toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 44% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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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

7 authors at 1 institution in 1 country.

Pius JosephHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Christina M UmbrightHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Jenny R RobertsHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Jared L CumpstonHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Marlene S OrandleHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Walter G McKinneyHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Tina M SagerHealth Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
National Institute for Occupational Safety and Health · US

Funding

Intramural CDC HHS CC999999
6 · The paper itself

Abstract

objectiveHuman exposure to cellulose nanocrystal (CNC) is possible during the production and/or use of products containing CNC. The objectives of the current study were to determine the lung toxicity of CNC and the underlying molecular mechanisms of the toxicity.

methodsRats were exposed to air or CNC (20 mg/m

resultsSignificant increases in lactate dehydrogenase activity, pro-inflammatory cytokine levels, phagocyte oxidant production, and macrophage and neutrophil counts were detected in the bronchoalveolar lavage cells or fluid from the CNC exposed rats. Mild lung histological changes, such as the accumulation of macrophages and neutrophils, were detected in the CNC exposed rats. Gene expression profiling by next generation sequencing identified 531 genes whose expressions were significantly different in the lungs of the CNC exposed rats, compared with the controls. Bioinformatic analysis of the lung gene expression data identified significant enrichment in several biological functions and canonical pathways including those related to inflammation (cellular movement, immune cell trafficking, inflammatory diseases and response, respiratory disease, complement system, acute phase response, leukocyte extravasation signaling, granulocyte and agranulocyte adhesion and diapedesis, IL-10 signaling, and phagosome formation and maturation) and oxidative stress (NRF2-mediated oxidative stress response, production of nitric oxide and reactive oxygen species in macrophages, and free radical scavenging).

conclusionOur data demonstrated that inhalation exposure of rats to CNC resulted in lung toxicity mediated mainly through the induction of inflammation and oxidative stress.

Indexed as

AnimalsBody WeightBronchoalveolar Lavage FluidCelluloseComputational BiologyCytokinesGene Expression RegulationInhalation ExposureLungLung InjuryMaleNanoparticlesOxidantsRatsRats, Inbred F344TranscriptomeCelluloseCytokinesOxidantsCellulose nanocrystal (CNC)gene expressioninflammationlung toxicitymechanismsoxidative stressrat

Identifiers

PMID33602020
PMCPMC10442725
OpenAlexW3132803476

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.