Evidence map›Paper›PMID 41802872›Full record

ArticleEnvironmental toxicology2026

Variation on Toxic and Inflammatory Potential of Coal Smoke of Different Sources From a Region With High Lung Cancer Risk.

Yongliang Zhang, Wei Hu, Nathanial Rothman, Dingyu Liu, Jihua Li, Jun Xu, Bofu Ning, Roel Vermeulen, Qing Lan, Flemming R Cassee and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Environmental toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

11 authors.

Yongliang ZhangInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.ORCID https://orcid.org/0000-0002-9479-9911
Wei HuOccupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
Nathanial RothmanOccupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
Dingyu LiuNational Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands.
Jihua LiQujing Center of Disease Control and Prevention, Qujing, China.
Jun XuDepartment of Community Medicine, School of Public Health, The University of Hongkong, Pokfulam, Hongkong.
Bofu NingXuanwei Center of Disease Control and Prevention, Xuanwei, China.
Roel VermeulenInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
Qing LanOccupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, USA.
Flemming R CasseeInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
George S DownwardInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.

Funding

NIH HHS HHSN261201400122P
6 · The paper itself

Abstract

Excess lung cancer risk in Xuanwei and Fuyuan, China, has been attributed to household air pollution from use of a locally sourced smoky (bituminous) coal. However, the carcinogenic mechanisms remain unclear. Given the important role of inflammation in lung cancer development, this study compared the proinflammatory potentials of the particulate phase of smoky coal emissions with those of a locally sourced smokeless (anthracite) coal, which poses a lower lung cancer risk. A co-culture model of lung epithelial (Calu-3) and macrophage (differentiated THP-1) cells was exposed to aerosolized particulates, followed by analysis at 24 h exposure (R0) and after 24 h of recovery (R24). Cytotoxicity was minimal, with lactate dehydrogenase (LDH) release consistently under 15% of the total LDH content. Particulate exposure reduced transepithelial electric resistance (TEER) at R0, with partial recovery by R24, indicating sustained epithelial barrier damage. IL-6 release occurred at R0 in a dose-dependent manner but normalized by R24 for most samples. No significant IL-8 release was observed. The inflammatory and toxic potential (TEER reduction and IL-6/IL-8 changes) were similar across coal types and ventilation conditions. The observed potencies showed no correlation with polycyclic aromatic hydrocarbons (PAHs) content and the observed lung cancer risks of the coal samples. In summary, transient inflammation and lasting barrier damage were observed with little contrast between different coal samples. As these results do not explain the variation of lung cancer risks, further studies examining alternative cellular pathways and biological effects are needed to elucidate the mechanisms driving lung cancer in this population.

Indexed as

Air PollutantsCoalLung NeoplasmsSmokeCell LineChinaCoculture TechniquesHumansInflammationInterleukin-6Interleukin-8Particulate MatterAir PollutantsCoalInterleukin-6Interleukin-8Particulate MatterSmokeair‐liquid interfacecoal smokeinflammationin vitro experimentlung cancer

Identifiers

PMID41802872
PMCPMC13656885

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Registered trials

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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.