Bernstein David I
Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0563, USA.
J Asthma. 2012 Feb;49(1):5-7. doi: 10.3109/02770903.2011.641049. Epub 2012 Jan 3.
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.
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.
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.
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.
柴油发动机尾气排放的交通相关空气污染物存在于细颗粒物和超细颗粒物中。辛辛那提儿童过敏与空气污染出生队列研究旨在确定早期接触这些污染物是否会增加儿童早期特应性致敏和过敏性呼吸道疾病表型的发生风险。
招募了700多名至少有一位特应性父母的婴儿参与一项出生队列研究。参与者在1至4岁以及7岁时接受年度医学评估和针对两种食物及15种气传变应原的皮肤测试。在1岁时进行家庭室内评估。使用距离和土地利用回归（LUR）模型估算室外交通相关空气污染物暴露情况。临床结局基于1岁和3岁时喘息以及3岁时过敏性鼻炎的病例定义。
1岁时接触走走停停的交通状况与婴儿期喘息相关，非裔美国婴儿反复喘息的可能性是其他婴儿的两倍。用LUR模型估算的交通相关元素碳（ECAT）高暴露水平可预测1岁时反复喘息以及3岁时多种喘息表型。出生后第一年接触高浓度内毒素并饲养多只宠物狗可降低1岁内反复喘息的风险。婴儿期对食物（蛋清、牛奶）中的树木花粉气传变应原早期致敏会增加3岁时患过敏性鼻炎的可能性。
高暴露于交通相关空气污染物是婴儿期和幼儿期喘息的独立危险因素。需要进一步研究来探讨交通暴露对儿童哮喘发展的长期影响。科学意义：减少和减轻交通相关空气污染物暴露可降低儿童期呼吸道疾病风险。
