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Traffic-Related pollutants and wheezing in children

机译:与交通有关的污染物和儿童喘息

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Background and aims. Traffic related air pollutants from diesel engine exhaust are found in fine and ultrafine particulates. The Cincinnati Childrens Allergy and Air Pollution Birth Cohort Study was initiated to determine if early exposure to these pollutants increased risk for development of early atopic sensitization and allergic respiratory disease phenotypes in children. Materials and methods. Over 700 infants born to at least one atopic parent were recruited to participate in a birth cohort study. Participants received annual medical evaluations and skin testing to two foods and 15 aeroallergens from ages 1-4 and again at age seven. Indoor home assessments were conducted at age one. Outdoor traffic related air pollutant exposure was estimated using proximity and land use regression (LUR) modeling. Clinical outcomes were based upon case definitions for wheezing at ages one and three and allergic rhinitis at age three. Results. At age 1 exposure to stop and go traffic was associated with wheezing during infancy and recurrent wheezing was twice more likely among African-American infants. Exposure to high levels of elemental carbon attributable to traffic (ECAT) estimated with a LUR model predicted recurrent wheezing at age 1 as well as multiple wheezing phenotypes at age 3. Exposure to high levels of endotoxin combined with multiple dogs during the first year reduced risk for recurrent wheezing during the first year of life. Early sensitization to tree pollen aeroallergens in foods (egg white, milk) in infancy increased likelihood of allergic rhinitis during age 3. Conclusion. High exposure to traffic related air pollutants represent independent risk factors for wheezing during infancy and early childhood. Further studies are needed to explore long-term effects of traffic exposure on development of asthma in childhood. Scientific significance. Reduction and mitigation of exposure to traffic related air pollutants could reduce risk of respiratory illnesses during childhood.
机译:背景和目标。柴油机排气中与交通有关的空气污染物存在于细颗粒和超细颗粒中。辛辛那提儿童过敏和空气污染出生队列研究已启动,以确定早期接触这些污染物是否增加儿童早期特应性过敏和过敏性呼吸道疾病表型发展的风险。材料和方法。招募了至少700名婴儿,至少一名异位父母的婴儿参加了一项出生队列研究。参与者接受了从1-4岁到七岁的两种食物和15种空气过敏原的年度医学评估和皮肤测试。室内家居评估是在1岁时进行的。使用接近和土地利用回归(LUR)模型估算与户外交通有关的空气污染物暴露。临床结果基于病例定义,分别为一岁和三岁时的喘息和三岁时的过敏性鼻炎。结果。在1岁时,在婴儿期出现的喘息与停走交通有关,非裔美国人婴儿经常性喘息的可能性是后者的两倍。使用LUR模型估算的高水平可归因于交通的元素碳(ECAT)预测在1岁时会反复发作喘息,并在3岁时出现多种喘息表型。第一年接触高浓度内毒素和多只狗可降低风险在生命的第一年反复发作喘息。婴儿期早期对食物(例如蛋清,牛奶)中的树花粉气敏原致敏,在3岁时增加了过敏性鼻炎的可能性。结论。与交通相关的空气污染物的高度暴露是婴儿期和儿童早期喘息的独立危险因素。需要进行进一步的研究,以探索交通暴露对儿童哮喘发展的长期影响。具有科学意义。减少和减轻与交通相关的空气污染物的接触可以减少儿童时期患呼吸道疾病的风险。

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