Traffic-related Air Pollution, Lung Function, and Host Vulnerability New Insights from the PARIS Birth Cohort
Traffic-related Air Pollution, Lung Function, and Host Vulnerability New Insights from the PARIS Birth Cohort
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DOI：
10.1513/annalsats.201711-900oc
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发表时间：
2018-05-01
影响因子：
8.3
通讯作者：
Momas, Isabelle
中科院分区：
文献类型：
--
作者：
Bougas, Nicolas;Ranciere, Fanny;Momas, Isabelle
理论基础：虽然交通相关的空气污染对呼吸恶化的影响已经有了很好的记录，但它对儿童肺功能的影响仍然不清楚。目的：我们的目的是调查出生前、早期和终生交通相关的空气污染暴露与8-9岁的肺功能的关系，研究性别、8-9岁的致敏和早期下呼吸道感染的可能影响。方法：我们对来自巴黎(污染和哮喘风险婴儿研究)出生队列的788名儿童进行了这项研究。8~9岁时在体检时进行肺功能检查。使用氮氧化物背景测量来估计怀孕每三个月期间与交通相关的空气污染暴露。出生后与交通相关的空气污染暴露通过居住和托儿所/学校地址的氮氧化物空气扩散模型进行评估。结果：胎儿期氮氧化物水平较高，特别是孕中期，与用力肺活量的25%~75%的用力呼气流量较低有关，但产前氮氧化物水平与用力肺活量、1秒用力呼气量或1秒用力呼气量/用力肺活量比值之间无显著相关性。在8-9岁早期下呼吸道感染或致敏的儿童中，出生后与交通相关的空气污染暴露与肺功能低下有关，但在整个队列中不相关。在早期反复下呼吸道感染的儿童中，终生氮氧化物暴露的四分位数增加与1秒内较低的用力呼气量(-62.6ml；95%可信区间=-107.0~-18.1)和用力肺活量(-55.7ml；95%可信区间=-109.5~-1.8%)有关，但与1秒内用力呼气量/用力肺活量比率无关。在致敏儿童中，出生后早期较多的氮氧化物暴露与较低的1秒用力呼气量/用力肺活量比率(-0.65%；95%可信区间=-1.25~-0.05)有关。结论：本研究提供了新的线索，提示早期反复下呼吸道感染或变态反应可增强出生后交通相关空气污染暴露与肺功能降低的相关性。
Rationale: Although the effects of traffic-related air pollution on respiratory exacerbations have been well documented, its impact on lung function in childhood remains unclear.Objectives: Our aim was to investigate the associations of prenatal, early, and lifetime traffic-related air pollution exposure with lung function at 8-9 years studying possible effect modification by sex, sensitization at 8-9 years, and early lower respiratory tract infections.Methods: We conducted this study among 788 children from the PARIS (Pollution and Asthma Risk an Infant Study) birth cohort. Lung function tests were performed during the medical examination at 8-9 years. Traffic-related air pollution exposure during each trimester of pregnancy was estimated using nitrogen oxides background measurements. Postnatal traffic-related air pollution exposure was assessed by a nitrogen oxides air dispersion model at both residential and daycare/school addresses. Associations between lung function and traffic-related air pollution exposure were analyzed by multiple linear regression models.Results: Higher prenatal nitrogen oxides levels, especially during the second trimester of pregnancy, were associated with a lower forced expiratory flow at 25-75% of the forced vital capacity, but there were no significant associations between prenatal nitrogen oxide levels and forced vital capacity, forced expiratory volume during 1 second, or the forced expiratory volume during 1 second/forced vital capacity ratio overall. Postnatal traffic-related air pollution exposure was associated with lower lung function among children with early lower respiratory tract infections or sensitization at 8-9 years, but not in the full cohort. In children with early repeated lower respiratory tract infections, an interquartile increase in lifetime nitrogen oxides exposure was associated with both a lower forced expiratory volume during 1 second (-62.6 ml; 95% confidence interval = - 107.0 to -18.1) and forced vital capacity (- 55.7 ml; 95% confidence interval = -109.5 to -1.8), but was not associated with the forced expiratory volume during 1 second/forced vital capacity ratio. There was an association between greater early postnatal nitrogen oxide exposure and a lower forced expiratory volume during 1 second/forced vital capacity ratio among sensitized children (-0.65%; 95% confidence interval = -1.25 to -0.05).Conclusions: This study sheds new light, suggesting associations between postnatal traffic-related air pollution exposure and reduced lung function may be enhanced by early, repeated lower respiratory tract infections or allergic sensitization.