Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
J Allergy Clin Immunol. 2012 Jan;129(1):240-6. doi: 10.1016/j.jaci.2011.11.001. Epub 2011 Nov 21.
The role of exposure to air pollution in the development of allergic sensitization remains unclear.
We sought to assess the development of sensitization until school age related to longitudinal exposure to air pollution from road traffic.
More than 2500 children in the birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiological Survey) from Stockholm, Sweden, were followed with repeated questionnaires and blood sampling until 8 years of age. Outdoor concentrations of nitrogen oxides, as a marker of exhaust particles, and particles with an aerodynamic diameter of less than 10 μm (PM(10)), mainly representing road dust, were assigned to residential, day care, and school addresses by using dispersion models. Time-weighted average exposures were linked to levels of IgE against common inhalant and food allergens at 4 and 8 years of age.
Air pollution exposure during the first year of life was associated with an increased risk of pollen sensitization at 4 years of age (odds ratio, 1.83; 95% confidence interval, 1.02-3.28) for a 5th to 95th difference in exposure to nitrogen oxides. At 8 years, there was no general increase in the risk of sensitization; however, the risk of food sensitization was increased, particularly among children free of sensitization at 4 years of age (odds ratio, 2.30; 95% confidence interval, 1.10-4.82). Results were similar by using PM(10). No associations between air pollution exposure after the first year of life and sensitization were seen.
Traffic-related air pollution exposure does not seem to increase the overall risk of sensitization to common inhalant and food allergens up to school age, but sensitization to certain allergens might be related to exposure during infancy.
空气污染暴露在过敏性致敏发展中的作用尚不清楚。
我们旨在评估与道路交通相关的空气污染的纵向暴露与儿童至学龄期致敏发展的关系。
在瑞典斯德哥尔摩的 BAMSE(儿童、过敏、环境、斯德哥尔摩、流行病学调查)出生队列中,超过 2500 名儿童接受了多次问卷调查和血液采样,直至 8 岁。使用扩散模型将室外氮氧化物浓度(作为尾气颗粒的标志物)和粒径小于 10μm 的颗粒(PM(10))分配到住宅、日托和学校地址。时间加权平均暴露与 4 岁和 8 岁时对常见吸入性和食物过敏原的 IgE 水平相关联。
生命第一年的空气污染暴露与 4 岁时花粉致敏风险增加相关(比值比,1.83;95%置信区间,1.02-3.28),5 岁至 95 岁的氮氧化物暴露差异为一个等级。8 岁时,致敏风险一般没有增加;然而,食物致敏的风险增加了,特别是在 4 岁时没有致敏的儿童中(比值比,2.30;95%置信区间,1.10-4.82)。使用 PM(10)也得到了类似的结果。在生命的第二年及以后,没有发现空气污染暴露与致敏之间的关联。
交通相关的空气污染暴露似乎不会增加儿童至学龄期对常见吸入性和食物过敏原的整体致敏风险,但某些过敏原的致敏可能与婴儿期的暴露有关。