Evidence map›Paper›PMID 24304303›Full record

ArticleInhalation toxicology2013

Comparison of how ambient PMc and PM2.5 influence the inflammatory potential.

Matthew D Ferguson, Chris Migliaccio, Tony Ward

Abstract readComparative Study
In one paragraph

Article in Inhalation toxicology, 2013. 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
–field-weighted citation impact
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.

  1. Trial
  2. Ambient PMEnvironmental research · 2024
    Article
  3. Article
  4. Article
  5. Inflammatory effects of particulate matter air pollution.Environmental science and pollution research international · 2020
    Review
  6. Article
  7. Air Pollutants Are Associated With Obstructive Sleep Apnea Severity in Non-Rapid Eye Movement Sleep.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2019
    Article
  8. Article
  9. A review on recent progress in observations, sources, classification and regulations of PMEnvironmental science and pollution research international · 2016
    Review
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.

Matthew D FergusonCenter for Environmental Health Sciences, University of Montana , Missoula, MT , USA.
Chris Migliaccio
Tony Ward

Funding

THE ROLE OF PULMONARY SUBPOPULATIONS AND TH2 IMMUNITY IN BALB/C SILICOSIS MODELP20RR017670 · NCRR · UNIVERSITY OF MONTANA · PI SHEPHERD, DAVID C · 2002 to 2011
$22.0M
Molecular Histology and Fluorescent ImagingP30GM103338 · NIGMS · UNIVERSITY OF MONTANA · PI MORANDI, MARIA T. · 2013 to 2017
$5.6M
NCRR NIH HHS P20 RR017670NCRR NIH HHS P20RR017670NIGMS NIH HHS P30 GM103338
6 · The paper itself

Abstract

Airborne particulate matter (PM) is one of the six criteria air pollutants currently regulated by the U.S. Environmental Protection Agency (EPA), with existing ambient standards for PM2.5 and PM10. Currently there are no health-based regulations for the size fraction between 2.5 and 10 µm, commonly known as the coarse fraction (PMc). The present study investigates current gaps in knowledge for PMc including exposure toxicity and PM ratios (PMc:PM2.5) in PM10. Throughout the world, all the three PM size fractions have been shown to be associated with adverse impacts. Recent studies have shown that PMc can be more detrimental to susceptible populations when directly compared to PM2.5, and that the PMc fraction in PM10 can account for the majority of the inflammatory response from PM10 exposure. In our studies we utilized a bone marrow-derived mouse macrophage in vitro system to compare the inflammatory potential of PMc, PM2.5 and mixtures of the two. The result was a linear increase in interleukin(IL) -1β with increasing levels of exposure to winter and summer PMc, as compared to PM2.5, which exhibited logarithmic growth. Also, exposure to PM10 as a function of PM2.5 and PMc mass ratios showed that IL-1β and TNF-α levels increased synergistically with a greater burden of PMc. Endotoxin content in the PM did not correlate with these results, suggesting that other activators in PMc are likely responsible for activating the NF-κB pathway and the inflammasome.

Indexed as

Air PollutantsAnimalsBone Marrow CellsEndotoxinsEnvironmental MonitoringInflammationInterleukin-1betaMacrophagesMiceMice, Inbred BALB CMontanaParticle SizeParticulate MatterSeasonsTumor Necrosis Factor-alphaAir PollutantsEndotoxinsInterleukin-1betaParticulate MatterTumor Necrosis Factor-alpha

Identifiers

PMID24304303
PMCPMC3906723

What OpenQuestion holds

Textmetadata
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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.