Evidence map›Paper›PMID 26837756›Full record

ReviewSeminars in immunopathology2016

TRP channels and traffic-related environmental pollution-induced pulmonary disease.

Armen N Akopian, E Robert Fanick, Edward G Brooks

Abstract readReview
In one paragraph

Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. TRP channels in airway sensory nerves.Neuroscience letters · 2021
    Review
  10. TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. The influence of PMExperimental and therapeutic medicine · 2019
    Article
  14. Article
  15. Observational
  16. Article
  17. 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 at 3 institutions in 1 country.

Armen N AkopianDepartment of Endodontics, School of Dentistry, UT Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
E Robert FanickOffice of Automotive Engineering, Southwest Research Institute, San Antonio, TX, 78228, USA.
Edward G BrooksDepartment of Pediatrics, Division of Immunology and Infectious Disease, School of Medicine, UT Health Science Center at San Antonio, San Antonio, TX, 78229, USA. brookse@uthscsa.edu.
Southwest Research Institute · USThe University of Texas Health Science Center at Houston · USThe University of Texas Health Science Center at San Antonio · US

Funding

Southwest Center for Occupational and Environmental HealthT42OH008421 · OH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FELKNOR, SARAH A. · 2005 to 2024
$24.1M
Prolactin regulation of postoperative pain in males and femalesR01GM112747 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AKOPIAN, ARMEN N · 2015 to 2018
$1.2M
Mechanisms of airway neurogenic inflammation by asthma-inducing allergensR21AI101325 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AKOPIAN, ARMEN N · 2012 to 2013
$362k
ACL HHS T42OH008421NIAID NIH HHS R21 AI101325NIGMS NIH HHS R01 GM112747
6 · The paper itself

Abstract

Environmental pollutant exposures are major risk factors for adverse health outcomes, with increased morbidity and mortality in humans. Diesel exhaust (DE) is one of the major harmful components of traffic-related air pollution. Exposure to DE affects several physiological systems, including the airways, and pulmonary diseases are increased in highly populated urban areas. Hence, there are urgent needs to (1) create newer and lesser polluting fuels, (2) improve exhaust aftertreatments and reduce emissions, and (3) understand mechanisms of actions for toxic effects of both conventional and cleaner diesel fuels on the lungs. These steps could aid the development of diagnostics and interventions to prevent the negative impact of traffic-related air pollution on the pulmonary system. Exhaust from conventional, and to a lesser extent, clean fuels, contains particulate matter (PM) and more than 400 additional chemical constituents. The major toxic constituents are nitrogen oxides (NOx) and polycyclic aromatic hydrocarbons (PAHs). PM and PAHs could potentially act via transient receptor potential (TRP) channels. In this review, we will first discuss the associations between DE from conventional as well as clean fuel technologies and acute and chronic airway inflammation. We will then review possible activation and/or potentiation of TRP vanilloid type 1 (TRPV1) and ankyrin 1 (TRPA1) channels by PM and PAHs. Finally, we will discuss and summarize recent findings on the mechanisms whereby TRPs could control the link between DE and airway inflammation, which is a primary determinant leading to pulmonary disease.

Indexed as

Air PollutionAnimalsCalciumEnvironmental ExposureEnvironmental PollutionGene ExpressionHumansLung DiseasesParticulate MatterReactive Oxygen SpeciesTransient Receptor Potential ChannelsVehicle EmissionsCalciumParticulate MatterReactive Oxygen SpeciesTransient Receptor Potential ChannelsVehicle EmissionsAcute lung injuryAsthmaClean dieselDiesel exhaust particles (DEP)Polycyclic aromatic hydrocarbons (PAHs)TRPA1TRPV1

Identifiers

PMID26837756
PMCPMC4896490
OpenAlexW2292265050

What OpenQuestion holds

Textmetadata
LicenceTDM
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.