Evidence map›Paper›PMID 27836898›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells.

Claire E McCarthy, Parker F Duffney, Robert Gelein, Thomas H Thatcher, Alison Elder, Richard P Phipps, Patricia J Sime

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Protocol for differentiating primary human small airway epithelial cells at the air-liquid interface.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Proinflammatory Effects inAnnals of the American Thoracic Society · 2020
    Article
  7. Review
  8. Review
  9. Cigarette smoke dampens antiviral signaling in small airway epithelial cells by disrupting TLR3 cleavage.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  10. Article
  11. Comparison of in vitro toxicological effects of biomass smoke from different sources of animal dung.Toxicology in vitro : an international journal published in association with BIBRA · 2017
    Article
  12. Low-level arsenic causes chronic inflammation and suppresses expression of phagocytic receptors.Environmental science and pollution research international · 2017
    Article
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 at 1 institution in 1 country.

Claire E McCarthyDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Parker F DuffneyDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Robert GeleinDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Thomas H ThatcherDivision of Pulmonary and Critical Care Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.ORCID http://orcid.org/0000-0001-7177-3041
Alison ElderDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Richard P PhippsDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Patricia J SimeDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; Patricia_Sime@urmc.rochester.edu.
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
Novel therapies for cigarette smoke induced lung injuryR01HL120908 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2014 to 2017
$1.6M
NHLBI NIH HHS R01 HL120908NIEHS NIH HHS P30 ES001247NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

Animal dung is a biomass fuel burned by vulnerable populations who cannot afford cleaner sources of energy, such as wood and gas, for cooking and heating their homes. Exposure to biomass smoke is the leading environmental risk for mortality, with over 4,000,000 deaths each year worldwide attributed to indoor air pollution from biomass smoke. Biomass smoke inhalation is epidemiologically associated with pulmonary diseases, including chronic obstructive pulmonary disease (COPD), lung cancer, and respiratory infections, especially in low and middle-income countries. Yet, few studies have examined the mechanisms of dung biomass smoke-induced inflammatory responses in human lung cells. Here, we tested the hypothesis that dung biomass smoke causes inflammatory responses in human lung cells through signaling pathways involved in acute and chronic lung inflammation. Primary human small airway epithelial cells (SAECs) were exposed to dung smoke at the air-liquid interface using a newly developed, automated, and reproducible dung biomass smoke generation system. The examination of inflammatory signaling showed that dung biomass smoke increased the production of several proinflammatory cytokines and enzymes in SAECs through activation of the activator protein (AP)-1 and arylhydrocarbon receptor (AhR) but not nuclear factor-κB (NF-κB) pathways. We propose that the inflammatory responses of lung cells exposed to dung biomass smoke contribute to the development of respiratory diseases.

Indexed as

BiomassSignal TransductionAnimalsAzo CompoundsCyclooxygenase 2CytokinesEpithelial CellsHorsesHumansInflammationJNK Mitogen-Activated Protein KinasesLungNF-kappa BParticulate MatterPyrazolesReceptors, Aryl Hydrocarbon2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazophenyl)amideAzo CompoundsCyclooxygenase 2CytokinesJNK Mitogen-Activated Protein KinasesNF-kappa BParticulate MatterPyrazolesReceptors, Aryl HydrocarbonSmokeTranscription Factor AP-1biomass smokeinflammatory responsesparticulatesrespiratory toxicologysmall airway epithelial cells

Identifiers

PMID27836898
PMCPMC5206396
OpenAlexW2553053875

What OpenQuestion holds

Textmetadata
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.