Evidence map›Paper›PMID 27092743›Full record

ArticleJournal of toxicology and environmental health. Part A2016

Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study.

Brandi N Snyder-Talkington, Chunlin Dong, Dale W Porter, Barbara Ducatman, Michael G Wolfarth, Michael Andrew, Lori Battelli, Rebecca Raese, Vincent Castranova, Nancy L Guo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of toxicology and environmental health. Part A, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.4field-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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  19. Engineered nanomaterial-induced lysosomal membrane permeabilization and anti-cathepsin agents.Journal of toxicology and environmental health. Part B, Critical reviews · 2017
    Review
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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

11 authors at 2 institutions in 1 country.

Brandi N Snyder-Talkingtona Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
Chunlin Dongb Mary Babb Randolph Cancer Center , West Virginia University , Morgantown , West Virginia , USA.
Dale W Portera Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
Barbara Ducatmanc Department of Pathology , West Virginia University , Morgantown , West Virginia , USA.
Michael G Wolfartha Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
Michael Andrewa Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
Lori Battellia Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
Rebecca Raeseb Mary Babb Randolph Cancer Center , West Virginia University , Morgantown , West Virginia , USA.
Vincent Castranovad Department of Pharmaceutical Sciences , School of Pharmacy, West Virginia University , Morgantown , West Virginia , USA.
Nancy L Guob Mary Babb Randolph Cancer Center , West Virginia University , Morgantown , West Virginia , USA.
Yong Qiana Pathology and Physiology Research Branch, Health Effects Laboratory Division , National Institute for Occupational Safety and Health , Morgantown , West Virginia , USA.
National Institute for Occupational Safety and Health · USWest Virginia University · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI JUDITH FEINBERG · 2012 to 2026
$81.0M
Systematic assessment of multi-walled carbon nanotubes in pulmonary diseaseR01ES021764 · NIEHS · WEST VIRGINIA UNIVERSITY · PI GUO, NANCY LAN · 2012 to 2016
$1.7M
A Novel Computational Framework for individualized clinical decision-makingR56LM009500 · NLM · WEST VIRGINIA UNIVERSITY · PI GUO, NANCY LAN · 2012 to 2013
$499k
NIEHS NIH HHS R01 ES021764NIGMS NIH HHS U54 GM104942NLM NIH HHS R56 LM009500
6 · The paper itself

Abstract

Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 μg MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-μg crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 μg MWCNT and in asbestos-exposed mice at 1 yr postexposure. To determine potential signaling pathways involved with MWCNT-associated pathological changes in comparison to asbestos, up- and down-regulated gene expression was determined in lung tissue at 1 yr postexposure. Exposure to MWCNT tended to favor those pathways involved in immune responses, specifically T-cell responses, whereas exposure to asbestos tended to favor pathways involved in oxygen species production, electron transport, and cancer. Data indicate that MWCNT are biopersistent in the lung and induce inflammatory and fibrotic pathological alterations similar to those of crocidolite asbestos, but may reach these endpoints by different mechanisms.

Indexed as

Inhalation ExposureAir PollutantsAnimalsAsbestos, CrocidoliteBronchoalveolar Lavage FluidDose-Response Relationship, DrugGene ExpressionInflammationL-Lactate DehydrogenaseLungMaleMiceMice, Inbred C57BLNanotubes, CarbonNeutrophil InfiltrationNeutrophilsAir PollutantsAsbestos, CrocidoliteL-Lactate DehydrogenaseNanotubes, Carbon

Identifiers

PMID27092743
PMCPMC4899319
OpenAlexW2337235773

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.