Evidence map›Paper›PMID 42395944›Full record

ArticleACS omega2026

Differential Impacts of Components of Particulate Matter on Epithelial Cell Toxicity and Immune Responses.

George Adams, Oliver Wagstaff, Dave Topping, David Brough, Gloria Lopez-Castejon, Riccardo D'Elia, Sheena M Cruickshank

Abstract read
In one paragraph

Article in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

George AdamsLydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, U.K.
Oliver WagstaffLydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, U.K.ORCID https://orcid.org/0000-0003-0769-639X
Dave ToppingManchester Environmental Research Institute, Faculty of Science and Engineering, University of Manchester, Manchester M13 9PT, U.K.ORCID https://orcid.org/0000-0001-8247-9649
David BroughLydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, U.K.ORCID https://orcid.org/0000-0002-2250-2381
Gloria Lopez-CastejonLydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, U.K.
Riccardo D'EliaChemical Biological and Radiological Division, Dstl Porton Down, Salisbury SP4 0JQ, U.K.
Sheena M CruickshankLydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, U.K.ORCID https://orcid.org/0000-0002-3047-5475

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poor air quality, and particularly particulate matter (PM), is detrimental to health, contributing to chronic inflammatory conditions and worsening the outcomes to infections. PM has major impacts on barrier tissues including the lungs, gut, and skin. These tissues are lined by epithelial cells that can initiate and contribute to immune responses, but we still do not fully understand how they respond to PM. Furthermore, PM is multifactorial, and which components may be the most triggering for immune responses are not known. We evaluated the impact of a range of PM components including transition metals and components of diesel exhaust particulates (DEP) on lung-, gut-, and skin-derived epithelial cells. Differences in toxicity were observed between components, with the polyaromatic hydrocarbon 1, 2-naphthoquinone extremely toxic at concentrations of 100 μg/mL, contrasting with 2-nitrofluorenone and 2-methyl-4-nitrophenol. At lower nonlethal concentrations, 1, 2-naphthoquinone promoted epithelial cell production of the chemokines CXCL1 and CXCL2 that are associated with neutrophil recruitment, contrasting with other pollutants evaluated. Furthermore, 1, 2-naphthoquinone caused broad transcriptional changes in the lung epithelial cells. These results highlight the potential dangers of discrete components of PM such as 1, 2-naphthoquinone on epithelial function, indicating the potential to alter the immune landscape in the lung.

Identifiers

PMID42395944
PMCPMC13325352

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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.