摘要
背景：考虑到儿童早期生命脆弱性的差异，臭氧(O3)引起的幼儿哮喘和喘息(AW)的生命过程尚不完全清楚。
方法：我们于2018年至2021年在中国济南进行了出生队列研究，以阐明O3暴露导致儿童AW的发病模式。采用反距离加权模型进行个体暴露评估。采用时间依赖的Cox比例风险模型和logistic模型研究了O3暴露对AW的影响。采用主成分分析、相互作用分析和分布滞后模型对生命周期法进行分析。
结果：6501名2岁儿童的AW累积发病率为1.4%。O3水平高与AW相关(HR: 2.10, 95% CI: 1.31, 3.37)。在调整出生前的影响后，只有出生后暴露于O3与AW相关，OR为1.82(1.08,3.12)。此外，调整其他空气污染物后，高O3暴露对AW个体效应的HR为2.44(1.53,3.89)。有趣的是，O3与其他污染物主成分相互作用的P值以及开窗特征变量均小于0.1。此外，出生前31～37周和出生后1～105周O3暴露IQR的增加与AW的HRs的增加有关。
结论：出生后高水平的O3暴露可导致幼儿AW。重要的是，AW发病模型可能包括危险因素累积和敏感期模型。具体来说，生命早期存在两个敏感窗口，高水平O3和其他污染物以及打开窗口对哮喘诱发作用的相关损害。
A life course approach to asthma and wheezing among young children caused by ozone: A prospective birth cohort in northern China.
Bai S, Cui L, Du S, Zhao X,
Abstrast
Background: Given differences in vulnerability of children in early life, a life course approach to asthma and wheezing (AW) in young children caused by ozone (O3) is not fully understood..
Methods: We conducted a birth cohort in Jinan, China from 2018 to 2021 to elucidate the onset model of childhood AW due to O3 exposure. An inverse distance weighted model was used for individual exposure assessment. The time-dependent Cox proportional-hazard model and logistic model were used to investigate the effects of O3 exposure on AW. Principal component analysis, interaction analysis, and distributed lag model were used to analyze the life course approach.
Results: The cumulative incidence rate for AW among 6501 children aged 2 was 1.4%. A high level of O3 was related to AW (HR: 2.10, 95% CI: 1.31, 3.37). Only O3 exposure after birth was associated with AW, with an OR of 1.82 (1.08, 3.12), after adjusting for the effect before birth. Furthermore, adjusting for other air pollutants, the HR for the individual effect of high O3 exposure on AW was 2.44 (1.53, 3.89). Interestingly, P values for interactions for O3 and the principal components of other pollutants, as well as the characteristic variable of open windows were less than 0.1. Moreover, an increase in the IQR of O3 exposure at the 31st to 37th weeks before birth and the 1st to 105th weeks after birth was associated with an increase in the HRs for AW.
Conclusions: High-level of O3 exposure after birth could lead to AW among young children. Importantly, the AW onset model may include the risk factors accumulation and the sensitive period model. Specifically, there are two sensitive windows in early life, and the correlated insults between the high level of O3 and other pollutants as well as open windows in the asthma-inducing effect.
背景：考虑到儿童早期生命脆弱性的差异，臭氧(O3)引起的幼儿哮喘和喘息(AW)的生命过程尚不完全清楚。
方法：我们于2018年至2021年在中国济南进行了出生队列研究，以阐明O3暴露导致儿童AW的发病模式。采用反距离加权模型进行个体暴露评估。采用时间依赖的Cox比例风险模型和logistic模型研究了O3暴露对AW的影响。采用主成分分析、相互作用分析和分布滞后模型对生命周期法进行分析。
结果：6501名2岁儿童的AW累积发病率为1.4%。O3水平高与AW相关(HR: 2.10, 95% CI: 1.31, 3.37)。在调整出生前的影响后，只有出生后暴露于O3与AW相关，OR为1.82(1.08,3.12)。此外，调整其他空气污染物后，高O3暴露对AW个体效应的HR为2.44(1.53,3.89)。有趣的是，O3与其他污染物主成分相互作用的P值以及开窗特征变量均小于0.1。此外，出生前31～37周和出生后1～105周O3暴露IQR的增加与AW的HRs的增加有关。
结论：出生后高水平的O3暴露可导致幼儿AW。重要的是，AW发病模型可能包括危险因素累积和敏感期模型。具体来说，生命早期存在两个敏感窗口，高水平O3和其他污染物以及打开窗口对哮喘诱发作用的相关损害。
(中日友好医院呼吸与危重症医学科 万静萱 摘译 林江涛 审校)
(Environ Res 2023 Jun 01;226; doi: 10.1016/j.envres.2023.115687.IF: 5.715)
(Environ Res 2023 Jun 01;226; doi: 10.1016/j.envres.2023.115687.IF: 5.715)
A life course approach to asthma and wheezing among young children caused by ozone: A prospective birth cohort in northern China.
Bai S, Cui L, Du S, Zhao X,
Abstrast
Background: Given differences in vulnerability of children in early life, a life course approach to asthma and wheezing (AW) in young children caused by ozone (O3) is not fully understood..
Methods: We conducted a birth cohort in Jinan, China from 2018 to 2021 to elucidate the onset model of childhood AW due to O3 exposure. An inverse distance weighted model was used for individual exposure assessment. The time-dependent Cox proportional-hazard model and logistic model were used to investigate the effects of O3 exposure on AW. Principal component analysis, interaction analysis, and distributed lag model were used to analyze the life course approach.
Results: The cumulative incidence rate for AW among 6501 children aged 2 was 1.4%. A high level of O3 was related to AW (HR: 2.10, 95% CI: 1.31, 3.37). Only O3 exposure after birth was associated with AW, with an OR of 1.82 (1.08, 3.12), after adjusting for the effect before birth. Furthermore, adjusting for other air pollutants, the HR for the individual effect of high O3 exposure on AW was 2.44 (1.53, 3.89). Interestingly, P values for interactions for O3 and the principal components of other pollutants, as well as the characteristic variable of open windows were less than 0.1. Moreover, an increase in the IQR of O3 exposure at the 31st to 37th weeks before birth and the 1st to 105th weeks after birth was associated with an increase in the HRs for AW.
Conclusions: High-level of O3 exposure after birth could lead to AW among young children. Importantly, the AW onset model may include the risk factors accumulation and the sensitive period model. Specifically, there are two sensitive windows in early life, and the correlated insults between the high level of O3 and other pollutants as well as open windows in the asthma-inducing effect.
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