Interactions between Glutathione S- Transferase P1, Tumor Necrosis Factor, and Traffic-Related Air Pollution for Development of Childhood Allergic Disease

Autor: Fredrik Nyberg, Niklas Berglind, Emma Nordling, Erik Melén, Magnus Wickman, Cecilia M. Lindgren, Tom Bellander, Marco Zucchelli, Jenny Hallberg, G Pershagen, Ralf Morgenstern, Magnus Svartengren, Juha Kere
Rok vydání: 2008
Předmět:
Health
Toxicology and Mutagenesis
air pollution
TNF
Peak Expiratory Flow Rate
medicine.disease_cause
polymorphism
Cohort Studies
GSTP1
0302 clinical medicine
genetics
Child
Sensitization
Vehicle Emissions
chemistry.chemical_classification
Air Pollutants
0303 health sciences
biology
Chemistry
Environmental exposure
3. Good health
nitrogen oxides
medicine.anatomical_structure
Glutathione S-transferase
ADRB2
Children's Health
Tumor Necrosis Factors
Tumor necrosis factor alpha
Glutathione S-Transferase pi
Food Hypersensitivity
interaction
Polymorphism
Single Nucleotide
03 medical and health sciences
Hypersensitivity
medicine
Humans
Genetic Predisposition to Disease
Genetic Testing
030304 developmental biology
Sweden
Reactive oxygen species
Research
Public Health
Environmental and Occupational Health
Environmental Exposure
asthma
allergy
030228 respiratory system
13. Climate action
Immunology
biology.protein
Receptors
Adrenergic
beta-2
Oxidative stress
Zdroj: Environmental Health Perspectives
ISSN: 1552-9924
0091-6765
DOI: 10.1289/ehp.11117
Popis: BACKGROUND: Air 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. OBJECTIVE: Our 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. METHODS: In 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. RESULTS: Interaction 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. CONCLUSION: The 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.
Databáze: OpenAIRE
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