Evidence map›Paper›PMID 31740036›Full record

ArticleEnvironmental research2020

The effect of dust storm particles on single human lung cancer cells.

Karin Ardon-Dryer, Caroline Mock, Jose Reyes, Galit Lahav

Open access · greenAbstract read
In one paragraph

Article in Environmental research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

9 citing papers in PubMed, 60 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Karin Ardon-DryerDepartment of System Biology Harvard Medical School Harvard University, 200 Longwood Avenue Warren Alpert Building, Harvard Medical School, Boston, MA, 02115, USA; Department of Geosciences, Atmospheric Science Group, Texas Tech University, 3003 15th Street Department of Geosciences, Atmospheric Science Group, Texas Tech University, Lubbock, TX, 79409, USA. Electronic address: Karin.ardon-dryer@ttu.edu.
Caroline MockDepartment of System Biology Harvard Medical School Harvard University, 200 Longwood Avenue Warren Alpert Building, Harvard Medical School, Boston, MA, 02115, USA.
Jose ReyesDepartment of System Biology Harvard Medical School Harvard University, 200 Longwood Avenue Warren Alpert Building, Harvard Medical School, Boston, MA, 02115, USA.
Galit LahavDepartment of System Biology Harvard Medical School Harvard University, 200 Longwood Avenue Warren Alpert Building, Harvard Medical School, Boston, MA, 02115, USA.
Harvard University · USTexas Tech University · US

Funding

Dynamics of Signaling Pathways: Mechanism and FunctionR01GM083303 · NIGMS · HARVARD MEDICAL SCHOOL · PI LAHAV, GALIT · 2008 to 2020
$5.2M
Dynamics of Cellular Senescence in Single CellsR01GM116864 · NIGMS · HARVARD MEDICAL SCHOOL · PI LAHAV, GALIT · 2017 to 2020
$1.6M
NIGMS NIH HHS R01 GM083303NIGMS NIH HHS R01 GM116864
6 · The paper itself

Abstract

Exposure to dust particles during dust storms can lead to respiratory problems, diseases, and even death. The effect of dust particles at the cellular level is poorly understood. In this study, we investigated the impact that dust storm particles (Montmorillonite) have on human lung epithelial cells (A549) at the single cell level. Using live-cell imaging, we continuously followed individual cells after exposure to a wide range of concentrations of dust particles. We monitored the growth trajectory of each cell including number and timing of divisions, interaction with the dust particles, as well as time and mechanism of cell death. We found that individual cells show different cellular fates (survival or death) even in response to the same dust concentration. Cells that died interacted with dust particles for longer times, and engulfed more dust particles, compared with surviving cells. While higher dust concentrations reduced viability in a dose-dependent manner, the effect on cell death was non-monotonic, with intermediate dust concentration leading to a larger fraction of dying cells compared to lower and higher concentrations. This non-monotonic relationship was explained by our findings that high dust concentrations inhibit cell proliferation. Using cellular morphological features, supported by immunoblots and proinflammatory cytokines, we determined that apoptosis is the dominant death mechanism at low dust concentrations, while higher dust concentrations activate necrosis. Similar single cell approaches can serve as a baseline for evaluating other aerosol types that will improve our understanding of the health-related consequences of exposure to dust storms.

Indexed as

DustLung NeoplasmsAerosolsHumansLungParticle SizeAerosolsDustCell deathCell divisionDust storm particlesEngulfingSingle cell analysis

Identifiers

PMID31740036
PMCPMC6982605
OpenAlexW2985066207

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.