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Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: results from the TAG Study.

Abstract

BACKGROUND

Associations between traffic-related air pollution (TRAP) and allergic rhinitis remain inconsistent, possibly because of unexplored gene-environment interactions.

OBJECTIVE

In a pooled analysis of 6 birth cohorts (Ntotal = 15,299), we examined whether TRAP and genetic polymorphisms related to inflammation and oxidative stress predict allergic rhinitis and sensitization.

METHODS

Allergic rhinitis was defined with a doctor diagnosis or reported symptoms at age 7 or 8 years. Associations between nitrogen dioxide, particulate matter 2.5 (PM2.5) mass, PM2.5 absorbance, and ozone, estimated for each child at the year of birth, and single nucleotide polymorphisms within the GSTP1, TNF, TLR2, or TLR4 genes with allergic rhinitis and aeroallergen sensitization were examined with logistic regression. Models were stratified by genotype and interaction terms tested for gene-environment associations.

RESULTS

Point estimates for associations between nitrogen dioxide, PM2.5 mass, and PM2.5 absorbance with allergic rhinitis were elevated, but only that for PM2.5 mass was statistically significant (1.37 [1.01, 1.86] per 5 μg/m(3)). This result was not robust to single-cohort exclusions. Carriers of at least 1 minor rs1800629 (TNF) or rs1927911 (TLR4) allele were consistently at an increased risk of developing allergic rhinitis (1.19 [1.00, 1.41] and 1.24 [1.01, 1.53], respectively), regardless of TRAP exposure. No evidence of gene-environment interactions was observed.

CONCLUSION

The generally null effect of TRAP on allergic rhinitis and aeroallergen sensitization was not modified by the studied variants in the GSTP1, TNF, TLR2, or TLR4 genes. Children carrying a minor rs1800629 (TNF) or rs1927911 (TLR4) allele may be at a higher risk of allergic rhinitis.

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  • Publisher Full Text

    • Grapherence [↓14]

    Authors+Show Affiliations

    Fuertes E
    ,

    School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada.

    Brauer M
    ,
    MacIntyre E
    ,
    Bauer M
    ,
    Bellander T
    ,
    von Berg A
    ,
    Berdel D
    ,
    Brunekreef B
    ,
    Chan-Yeung M
    ,
    Gehring U
    ,
    Herbarth O
    ,
    Hoffmann B
    ,
    Kerkhof M
    ,
    Klümper C
    ,
    Koletzko S
    ,
    Kozyrskyj A
    ,
    Kull I
    ,
    Heinrich J
    ,
    Melén E
    ,
    Pershagen G
    ,
    Postma D
    ,
    Tiesler CM
    ,
    Carlsten C
    ,
    TAG Study Group

    Source

    MeSH

    Air Pollutants
    Air Pollution
    Child
    Cohort Studies
    Female
    Gene-Environment Interaction
    Glutathione S-Transferase pi
    Humans
    Male
    Polymorphism, Single Nucleotide
    Rhinitis, Allergic
    Rhinitis, Allergic, Perennial
    Toll-Like Receptor 2
    Toll-Like Receptor 4
    Tumor Necrosis Factor-alpha
    Vehicle Emissions

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    23639307

    Citation

    Fuertes, Elaine, et al. "Childhood Allergic Rhinitis, Traffic-related Air Pollution, and Variability in the GSTP1, TNF, TLR2, and TLR4 Genes: Results From the TAG Study." The Journal of Allergy and Clinical Immunology, vol. 132, no. 2, 2013, pp. 342-52.e2.
    Fuertes E, Brauer M, MacIntyre E, et al. Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: results from the TAG Study. J Allergy Clin Immunol. 2013;132(2):342-52.e2.
    Fuertes, E., Brauer, M., MacIntyre, E., Bauer, M., Bellander, T., von Berg, A., ... Carlsten, C. (2013). Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: results from the TAG Study. The Journal of Allergy and Clinical Immunology, 132(2), pp. 342-52.e2. doi:10.1016/j.jaci.2013.03.007.
    Fuertes E, et al. Childhood Allergic Rhinitis, Traffic-related Air Pollution, and Variability in the GSTP1, TNF, TLR2, and TLR4 Genes: Results From the TAG Study. J Allergy Clin Immunol. 2013;132(2):342-52.e2. PubMed PMID: 23639307.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: results from the TAG Study. AU - Fuertes,Elaine, AU - Brauer,Michael, AU - MacIntyre,Elaina, AU - Bauer,Mario, AU - Bellander,Tom, AU - von Berg,Andrea, AU - Berdel,Dietrich, AU - Brunekreef,Bert, AU - Chan-Yeung,Moira, AU - Gehring,Ulrike, AU - Herbarth,Olf, AU - Hoffmann,Barbara, AU - Kerkhof,Marjan, AU - Klümper,Claudia, AU - Koletzko,Sibylle, AU - Kozyrskyj,Anita, AU - Kull,Inger, AU - Heinrich,Joachim, AU - Melén,Erik, AU - Pershagen,Göran, AU - Postma,Dirkje, AU - Tiesler,Carla M T, AU - Carlsten,Chris, AU - ,, Y1 - 2013/04/30/ PY - 2012/08/30/received PY - 2013/02/05/revised PY - 2013/03/06/accepted PY - 2013/5/4/entrez PY - 2013/5/4/pubmed PY - 2013/10/19/medline KW - APMoSPHERE KW - Air Pollution Modelling for Support to Policy on Health and Environmental Risk in Europe KW - BAMSE KW - CAPPS KW - Canadian Asthma Primary Prevention Study KW - Childhood allergic rhinitis KW - Children, Allergy, Milieu, Stockholm, Epidemiological Survey KW - GINIplus KW - GSTP1 KW - German Infant study on the influence of Nutritional Intervention plus environmental and genetic influences on allergy development KW - Glutathione-S-transferase pi 1 KW - LISAplus KW - LUR KW - Land-use regression KW - Lifestyle related factors, Immune System and the development of Allergies in Childhood plus the influence of traffic emissions and genetics study KW - NO(2) KW - Nitrogen dioxide KW - OR KW - Odds ratio KW - PIAMA KW - PM KW - Particulate matter KW - Prevention and Incidence of Asthma and Mite Allergy KW - SAGE KW - SNP KW - Single nucleotide polymorphism KW - Study of Asthma, Genes, and Environment KW - TAG KW - TLR KW - TLR4 KW - TNF KW - TRAP KW - Toll-like receptor KW - Traffic, Asthma, and Genetics KW - Traffic-related air pollution KW - air pollution KW - genetics KW - interaction SP - 342 EP - 52.e2 JF - The Journal of allergy and clinical immunology JO - J. Allergy Clin. Immunol. VL - 132 IS - 2 N2 - BACKGROUND: Associations between traffic-related air pollution (TRAP) and allergic rhinitis remain inconsistent, possibly because of unexplored gene-environment interactions. OBJECTIVE: In a pooled analysis of 6 birth cohorts (Ntotal = 15,299), we examined whether TRAP and genetic polymorphisms related to inflammation and oxidative stress predict allergic rhinitis and sensitization. METHODS: Allergic rhinitis was defined with a doctor diagnosis or reported symptoms at age 7 or 8 years. Associations between nitrogen dioxide, particulate matter 2.5 (PM2.5) mass, PM2.5 absorbance, and ozone, estimated for each child at the year of birth, and single nucleotide polymorphisms within the GSTP1, TNF, TLR2, or TLR4 genes with allergic rhinitis and aeroallergen sensitization were examined with logistic regression. Models were stratified by genotype and interaction terms tested for gene-environment associations. RESULTS: Point estimates for associations between nitrogen dioxide, PM2.5 mass, and PM2.5 absorbance with allergic rhinitis were elevated, but only that for PM2.5 mass was statistically significant (1.37 [1.01, 1.86] per 5 μg/m(3)). This result was not robust to single-cohort exclusions. Carriers of at least 1 minor rs1800629 (TNF) or rs1927911 (TLR4) allele were consistently at an increased risk of developing allergic rhinitis (1.19 [1.00, 1.41] and 1.24 [1.01, 1.53], respectively), regardless of TRAP exposure. No evidence of gene-environment interactions was observed. CONCLUSION: The generally null effect of TRAP on allergic rhinitis and aeroallergen sensitization was not modified by the studied variants in the GSTP1, TNF, TLR2, or TLR4 genes. Children carrying a minor rs1800629 (TNF) or rs1927911 (TLR4) allele may be at a higher risk of allergic rhinitis. SN - 1097-6825 UR - https://www.unboundmedicine.com/medline/citation/23639307/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(13)00427-2 DB - PRIME DP - Unbound Medicine ER -