School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada.
J Allergy Clin Immunol. 2013 Aug;132(2):342-52.e2. doi: 10.1016/j.jaci.2013.03.007. Epub 2013 Apr 30.
Associations between traffic-related air pollution (TRAP) and allergic rhinitis remain inconsistent, possibly because of unexplored gene-environment interactions.
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.
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.
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.
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.
交通相关空气污染（TRAP）与过敏性鼻炎之间的关联仍不一致，这可能是由于尚未探索到的基因-环境相互作用所致。
在对 6 个出生队列（Ntotal=15299）的汇总分析中，我们研究了 TRAP 和与炎症和氧化应激相关的遗传多态性是否可预测过敏性鼻炎和致敏。
在 7 或 8 岁时通过医生诊断或报告的症状来定义过敏性鼻炎。使用逻辑回归检查每个孩子出生当年的二氧化氮、细颗粒物 2.5（PM2.5）质量、PM2.5 吸收率和臭氧的估计值与 GSTP1、TNF、TLR2 或 TLR4 基因中的单核苷酸多态性与过敏性鼻炎和变应原致敏之间的关联。对基因-环境关联进行分层，并测试基因型和交互项。
与过敏性鼻炎相关的二氧化氮、PM2.5 质量和 PM2.5 吸收率的点估计值升高，但仅 PM2.5 质量具有统计学意义（每增加 5μg/m3，增加 1.37[1.01，1.86]）。此结果在排除单个队列后并不稳健。至少携带 1 个 minor rs1800629（TNF）或 rs1927911（TLR4）等位基因的个体患过敏性鼻炎的风险持续增加（分别为 1.19[1.00，1.41]和 1.24[1.01，1.53]），而与 TRAP 暴露无关。未观察到基因-环境相互作用的证据。
所研究的 GSTP1、TNF、TLR2 或 TLR4 基因中的变体并未改变 TRAP 对过敏性鼻炎和变应原致敏的普遍无效作用。携带 minor rs1800629（TNF）或 rs1927911（TLR4）等位基因的儿童患过敏性鼻炎的风险可能更高。
