交通相关的污染物和儿童喘息
2012/02/29
背景和目的：交通相关的空气污染物（车辆排出的废气）包括细颗粒和超细颗粒。辛辛那提儿童过敏与空气污染出生队列研究旨在评价这些污染物的早期暴露是否能增加儿童早期过敏性致敏和过敏性呼吸道疾病表现型的风险。
材料与方法：超过700名新出生婴儿入选此项队列研究，其父母至少有一人存在特应性。1～4岁和7岁时，每年对婴儿进行医学评价，对2种食物和15种空气过敏原进行皮肤针刺试验。1岁时进行室内评价。采用接近度和土地使用回归（LUR）模型，评价室外交通相关空气污染物。基于1岁和3岁时喘息和3岁是的过敏性鼻炎，评价临床转归。
结果：1岁时，交通暴露与幼年喘息相关，非洲裔美国婴儿反复发作性喘息是其他儿童的2倍以上。基于LUR模型估计的交通相关高水平碳元素暴露（ECAT）能预测1岁时反复发作性喘息和3岁时多种喘息表现型。1岁以内内毒素和狗过敏原高水平暴露，能降低1岁内反复喘息的风险。幼年对食物（蛋清和牛奶）中树花粉早期致敏能增加3岁时过敏性鼻炎的风险。
结论：高水平交通相关空气污染物暴露是幼年和儿童早期反复喘息的一个独立危险因素。有必要进行更多的试验，研究交通废气暴露对儿童期哮喘的长期影响。
科学重要性：减少交通相关空气污染物暴露能降低儿童期呼吸系统疾病风险。
材料与方法：超过700名新出生婴儿入选此项队列研究，其父母至少有一人存在特应性。1～4岁和7岁时，每年对婴儿进行医学评价，对2种食物和15种空气过敏原进行皮肤针刺试验。1岁时进行室内评价。采用接近度和土地使用回归（LUR）模型，评价室外交通相关空气污染物。基于1岁和3岁时喘息和3岁是的过敏性鼻炎，评价临床转归。
结果：1岁时，交通暴露与幼年喘息相关，非洲裔美国婴儿反复发作性喘息是其他儿童的2倍以上。基于LUR模型估计的交通相关高水平碳元素暴露（ECAT）能预测1岁时反复发作性喘息和3岁时多种喘息表现型。1岁以内内毒素和狗过敏原高水平暴露，能降低1岁内反复喘息的风险。幼年对食物（蛋清和牛奶）中树花粉早期致敏能增加3岁时过敏性鼻炎的风险。
结论：高水平交通相关空气污染物暴露是幼年和儿童早期反复喘息的一个独立危险因素。有必要进行更多的试验，研究交通废气暴露对儿童期哮喘的长期影响。
科学重要性：减少交通相关空气污染物暴露能降低儿童期呼吸系统疾病风险。
（林江涛 审校）
J Asthma. 2012 Feb;49(1):5-7. Epub 2012 Jan 3.
J Asthma. 2012 Feb;49(1):5-7. Epub 2012 Jan 3.
Source
Department of Internal Medicine, University of Cincinnati College of Medicine , Cincinnati, OH , USA .
Department of Internal Medicine, University of Cincinnati College of Medicine , Cincinnati, OH , USA .
Abstract
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 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.
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 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.
J Asthma. 2012 Feb;49(1):5-7. Epub 2012 Jan 3.
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母乳喂养预防6岁内儿童现患哮喘
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