Evidence map›Paper›PMID 18709160›Full record

ArticleEnvironmental health perspectives2008

Interactions between glutathione S-transferase P1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease.

Erik Melén, Fredrik Nyberg, Cecilia M Lindgren, Niklas Berglind, Marco Zucchelli, Emma Nordling, Jenny Hallberg, Magnus Svartengren, Ralf Morgenstern, Juha Kere and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 138 citations in OpenAlex.

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  5. The role of gene-ambient air pollution interactions in paediatric asthma.European respiratory review : an official journal of the European Respiratory Society · 2022
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  12. Dietary total antioxidant capacity in early school age and subsequent allergic disease.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017
    Article
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  19. Epidemiology and natural history of atopic diseases.European clinical respiratory journal · 2015
    Review
  20. 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

13 authors at 4 institutions in 2 countries.

Erik MelénInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. erik.melen@ki.se
Fredrik Nyberg
Cecilia M Lindgren
Niklas Berglind
Marco Zucchelli
Emma Nordling
Jenny Hallberg
Magnus Svartengren
Ralf Morgenstern
Juha Kere
Tom Bellander
Magnus Wickman
Göran Pershagen
Karolinska Institutet · SEStockholm County Council · SECentre for Human Genetics · GBKarolinska University Hospital · SE

Funding

Wellcome Trust 090532
6 · The paper itself

Abstract

backgroundAir pollutants may induce airway inflammation and sensitization due to generation of reactive oxygen species. The genetic background to these mechanisms could be important effect modifiers.

objectiveOur goal was to assess interactions between exposure to air pollution and single nucleotide polymorphisms (SNPs) in the beta2-adrenergic receptor (ADRB2), glutathione S-transferase P1 (GSTP1), and tumor necrosis factor (TNF) genes for development of childhood allergic disease.

methodsIn a birth cohort originally of 4,089 children, we assessed air pollution from local traffic using nitrogen oxides (traffic NO(x)) as an indicator based on emission databases and dispersion modeling and estimated individual exposure through geocoding of home addresses. We measured peak expiratory flow rates and specific IgE for inhalant and food allergens at 4 years of age, and selected children with asthma symptoms up to 4 years of age (n = 542) and controls (n = 542) for genotyping.

resultsInteraction effects on allergic sensitization were indicated between several GSTP1 SNPs and traffic NO(x) exposure during the first year of life (p(nominal) < 0.001-0.06). Children with Ile105Val/Val105Val genotypes were at increased risk of sensitization to any allergen when exposed to elevated levels of traffic NO(x) (for a difference between the 5th and 95th percentile of exposure: odds ratio = 2.4; 95% confidence interval, 1.0-5.3). In children with TNF-308 GA/AA genotypes, the GSTP1-NO(x) interaction effect was even more pronounced. We observed no conclusive interaction effects for ADRB2.

conclusionThe effect of air pollution from traffic on childhood allergy appears to be modified by GSTP1 and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.

Indexed as

Environmental ExposureAir PollutantsChildCohort StudiesFood HypersensitivityGenetic Predisposition to DiseaseGenetic TestingGlutathione S-Transferase piHumansHypersensitivityNitrogen OxidesPeak Expiratory Flow RatePolymorphism, Single NucleotideReceptors, Adrenergic, beta-2SwedenTumor Necrosis FactorsAir PollutantsGlutathione S-Transferase piGSTP1 protein, humanNitrogen OxidesReceptors, Adrenergic, beta-2Tumor Necrosis FactorsVehicle EmissionsADRB2air pollutionallergyasthmageneticsGSTP1interactionnitrogen oxidespolymorphismTNF

Identifiers

PMID18709160
PMCPMC2516580
OpenAlexW1987396961

What OpenQuestion holds

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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.