Evidence map›Paper›PMID 26335830›Full record

ReviewInternational forum of allergy & rhinology2015

Asthma risk factors.

Elina Toskala, David W Kennedy

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International forum of allergy & rhinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05915845 (Effects of Laura Mitchell's Relaxation Versus Papworth Exercise on Dyspnea, Fatigue, and Sleep Quality in Ashmatic Patient), which is not on this map. Cited by 127 papers, 14 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 14 pooled it
3.0field-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.

NCT05915845 naunknown statusnot on this mapstarted 2023, after this paper: background citation

Effects of Laura Mitchell's Relaxation Versus Papworth Exercise on Dyspnea, Fatigue, and Sleep Quality in Ashmatic Patient

TypeinterventionalSponsorRiphah International UniversityRan2023 to 2023Enrolled46ConditionsAsthmaticArmsLaura Mitchell's Relaxation technique, Papworth exercise
3 · Its place in the literature

Who cites it

127 citing papers in PubMed, 14 syntheses or guidelines pooled it, 206 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
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  11. Sex Differences in Exercise-Induced Bronchoconstriction in Athletes: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2020
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  12. The C79G Polymorphism of the β2-Adrenergic Receptor Gene, ADRB2, and Susceptibility to Pediatric Asthma: Meta-Analysis from Review of the Literature.Medical science monitor : international medical journal of experimental and clinical research · 2019
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  18. Association of genetic variants in the autophagy gene ATG4B with asthma.medRxiv : the preprint server for health sciences · 2026
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67 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Elina ToskalaDepartment of Otorhinolaryngology-Head and Neck Surgery, Temple University, Philadelphia, PA.
David W KennedyDepartment of Otorhinolaryngology-Head and Neck Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Temple University · USUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBronchial asthma is one of the most common chronic diseases in childhood, with a current prevalence of 6% to 9%, but a prevalence that is increasing at an alarming rate. Asthma is a complex genetic disorder with strong environmental influence. It imposes a growing burden on our society in terms of morbidity, quality of life, and healthcare costs. Despite large-scale efforts, only a few asthma genes have been confirmed, suggesting that the genetic underpinning of asthma is highly complex.

methodsA review of the literature was performed regarding atopic and nonatopic asthma risk factors, including environmental risk factors and genetic studies in adults and children.

resultsSeveral environmental risk factors have been identified to increase the risk of developing asthma such as exposure to air pollution and tobaccos smoke as well as occupational risk factors. In addition atopy, stress, and obesity all can increases the risk for asthma in genetically susceptible persons.

conclusionAsthma represents a dysfunctional interaction with our genes and the environment to which they are exposed, especially in fetal and early infant life. The increasing prevalence of asthma in all age groups indicate that our living environment and immunity are in imbalance with each other reacting with airway inflammation to the environmental exposures and often non-harmful proteins, such as allergens causing the current "asthma and allergy epidemic." Because of the close relationship between asthma and chronic rhinosinusitis, it is important that otolaryngologists have a good understanding of asthma, the etiologic factors associated with disease, and its evaluation and management.

Indexed as

AsthmaEnvironmentGenetic Predisposition to DiseaseHumansRisk Factorsair pollutionallergensasthmaatopyenvironmental risk factorsepigeneticsgenetic risk factorshygiene hypothesismicrobesrisk factors

Identifiers

PMID26335830
PMCPMC7159773
OpenAlexW2156555691

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.