Evidence map›Paper›PMID 35189914›Full record

ArticleParticle and fibre toxicology2022

The pro-inflammatory effects of combined exposure to diesel exhaust particles and mineral particles in human bronchial epithelial cells.

Vegard Sæter Grytting, Prem Chand, Marit Låg, Johan Øvrevik, Magne Refsnes

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  3. Cyclic Strain and Macrophage-Mediated Transport Govern Micron-Sized PMAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. 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

5 authors at 1 institution in 1 country.

Vegard Sæter GryttingSection of Air Quality and Noise, Department of Environmental Health, Norwegian Institute of Public Health, PO box 4404, 0403, Nydalen, Oslo, Norway. vegard.saeter.grytting@fhi.no.ORCID 0000-0003-0801-4223
Prem ChandSection of Air Quality and Noise, Department of Environmental Health, Norwegian Institute of Public Health, PO box 4404, 0403, Nydalen, Oslo, Norway.
Marit LågSection of Air Quality and Noise, Department of Environmental Health, Norwegian Institute of Public Health, PO box 4404, 0403, Nydalen, Oslo, Norway. marit.lag@fhi.no.
Johan ØvrevikSection of Air Quality and Noise, Department of Environmental Health, Norwegian Institute of Public Health, PO box 4404, 0403, Nydalen, Oslo, Norway.
Magne RefsnesSection of Air Quality and Noise, Department of Environmental Health, Norwegian Institute of Public Health, PO box 4404, 0403, Nydalen, Oslo, Norway.
Norwegian Institute of Public Health · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPeople are exposed to ambient particulate matter (PM) from multiple sources simultaneously in both environmental and occupational settings. However, combinatory effects of particles from different sources have received little attention in experimental studies. In the present study, the pro-inflammatory effects of combined exposure to diesel exhaust particles (DEP) and mineral particles, two common PM constituents, were explored in human lung epithelial cells.

methodsParticle-induced secretion of pro-inflammatory cytokines (CXCL8 and IL-1β) and changes in expression of genes related to inflammation (CXCL8, IL-1α, IL-1β and COX-2), redox responses (HO-1) and xenobiotic metabolism (CYP1A1 and CYP1B1) were assessed in human bronchial epithelial cells (HBEC3-KT) after combined exposure to different samples of DEP and mineral particles. Combined exposure was also conducted using lipophilic organic extracts of DEP to assess the contribution of soluble organic chemicals. Moreover, the role of the aryl hydrocarbon receptor (AhR) pathway was assessed using an AhR-specific inhibitor (CH223191).

resultsCombined exposure to DEP and mineral particles induced increases in pro-inflammatory cytokines and expression of genes related to inflammation and redox responses in HBEC3-KT cells that were greater than either particle sample alone. Moreover, robust increases in the expression of CYP1A1 and CYP1B1 were observed. The effects were most pronounced after combined exposure to α-quartz and DEP from an older fossil diesel, but enhanced responses were also observed using DEP generated from a modern biodiesel blend and several stone particle samples of mixed mineral composition. Moreover, the effect of combined exposure on cytokine secretion could also be induced by lipophilic organic extracts of DEP. Pre-incubation with an AhR-specific inhibitor reduced the particle-induced cytokine responses, suggesting that the effects were at least partially dependent on AhR.

conclusionsExposure to DEP and mineral particles in combination induces enhanced pro-inflammatory responses in human bronchial epithelial cells compared with exposure to the individual particle samples. The effects are partly mediated through an AhR-dependent pathway and lipophilic organic chemicals in DEP appear to play a central role. These possible combinatory effects between different sources and components of PM warrant further attention and should also be considered when assessing measures to reduce PM-induced health effects.

Indexed as

Cytochrome P-450 CYP1A1Vehicle EmissionsCytokinesEpithelial CellsHumansInflammationMineralsParticulate MatterCytochrome P-450 CYP1A1CytokinesMineralsParticulate MatterVehicle EmissionsAir pollutionCombustion particlesCytokinesEpitheliumInflammationMineralsParticulate matterPulmonaryQuartzStone particles

Identifiers

PMID35189914
PMCPMC8862321
OpenAlexW4213166269

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.