Interactions between Glutathione S-Transferase P1, Tumor Necrosis Factor, and Traffic-Related Air Pollution for Development of Childhood Allergic Disease
2008

Air Pollution and Childhood Allergic Disease: The Role of Genetics

Sample size: 982 publication 10 minutes Evidence: moderate

Author Information

Author(s): Melén Erik, Nyberg Fredrik, Lindgren Cecilia M., Berglind Niklas, Zucchelli Marco, Nordling Emma, Hallberg Jenny, Svartengren Magnus, Morgenstern Ralf, Kere Juha, Bellander Tom, Wickman Magnus, Pershagen Göran

Primary Institution: Karolinska Institutet, Stockholm, Sweden

Hypothesis

The study aims to assess interactions between exposure to air pollution and genetic variants in the GSTP1 and TNF genes for the development of childhood allergic disease.

Conclusion

The effect of air pollution from traffic on childhood allergy is modified by GSTP1 and TNF gene variants.

Supporting Evidence

  • Children with certain GSTP1 genotypes had a 2.4 times increased risk of sensitization to allergens when exposed to high levels of traffic NOx.
  • Interaction effects were significant for GSTP1 SNPs and traffic NOx exposure during the first year of life.
  • TNF-308 GA/AA genotypes showed a pronounced interaction effect with GSTP1 on allergic sensitization.

Takeaway

Kids who are exposed to more traffic pollution and have certain genes are more likely to develop allergies.

Methodology

The study used a birth cohort of 4,089 children, assessing air pollution exposure and genotyping children with asthma symptoms and controls.

Potential Biases

Potential bias due to reliance on parental reporting and the possibility of false-positive findings.

Limitations

The study relied on parental reports for asthma diagnosis, which may not be confirmed by objective measurements.

Participant Demographics

Children from the BAMSE study, primarily from urban and suburban areas of Stockholm.

Statistical Information

P-Value

p<0.001

Confidence Interval

95% CI, 1.0–5.3

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1289/ehp.11117

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