Effect of early‐life exposure to PM 2 .5 on childhood asthma/wheezing: a birth cohort study
Effect of early‐life exposure to PM 2 .5 on childhood asthma/wheezing: a birth cohort study
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生命早期接触 PM 2 .5 对儿童哮喘/喘息的影响：出生队列研究
DOI：
10.1111/pai.13822
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Tao Liu
中科院分区：
文献类型：
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作者：
Guimin Chen;He Zhou;Guanhao He;Sui Zhu;Xiaoli Sun;Yufeng Ye;Hanwei Chen;Jianpeng Xiao;Jianxiong Hu;Fangfang Zeng;Pan Yang;Yanhui Gao;Zhongrong He;Jiong Wang;Ganxiang Cao;Yumeng Chen;Hao Feng;Wenjun Ma;Chaoqun Liu;Tao Liu
尽管已有研究调查了早期暴露于细颗粒物（PM2.5）与儿童哮喘/喘鸣之间的关系，但结果不一致，易感暴露窗口仍在很大程度上未知。进行了一项前瞻性出生队列研究，招募妊娠早期的孕妇，并对其及其子女进行随访，直至3-4岁。哮喘/喘息的诊断是从儿童的医疗记录中提取的。时空土地利用回归（ST-LUR）模型被用来评估母亲在怀孕期间暴露于PM2.5和他们的孩子出生后的暴露。采用考克斯比例风险模型和加速失效时间模型（违反比例风险假设），对出生前后PM2.5暴露对儿童哮喘/喘鸣风险的影响进行评估，共纳入3725名儿童，其中392名儿童（10.52%）被诊断为哮喘/喘鸣。出生前和出生后暴露于PM2.5与哮喘/喘息的风险呈正相关。在整个妊娠期间（4.8 μg/m3）和从出生到随访结束期间（1.5 μg/m3）PM2.5暴露的每个四分位距（IQR）增量与校正的风险比（HR）1.44 [95%置信区间（CI）：1.13，1.85和2.74（95% CI：2.59，2.91）]相关。亚组分析显示，在假腺体阶段，PM2.5暴露的HR更高（6-16孕周[GW：IQR = 4.8 μg/m3，HR = 1.10，95% CI：1.02，1.18）和小管期（16-24 GW：IQR = 4.8 μg/m3，HR = 1.13，95% CI：1.03，1.23），且在生后前3年也表现出显著的影响（IQR = 1.5 μg/m3，HR = 2.37，95%CI：=2.24，2.51）。出生前后较高的PM2.5暴露可能增加儿童哮喘/喘息的风险。假腺期、小管期和出生后的前三年可能是暴露窗口的关键易感期。
Although studies have investigated the association between early-life exposure to fine particulate matter (PM2.5 ) and childhood asthma/wheezing, results are inconsistent and the susceptible exposure window remains largely unknown.A prospective birth cohort study was conducted to recruit pregnant women during their early pregnancy, and to follow up them and their children up to 3-4 years old. Diagnosis of asthma/wheezing was extracted from children's medical records. A spatiotemporal land-use regression (ST-LUR) model was used to assess maternal exposure to PM2.5 during pregnancy and their children's exposure after birth. The Cox proportional hazards model and accelerated failure time model (for violation of proportional hazards assumption) were applied to estimate the effects of prenatal and postnatal exposures to PM2.5 on the risk of childhood asthma/wheezing.A total of 3725 children were included, and 392 children (10.52%) were diagnosed with asthma/wheezing. Both prenatal and postnatal exposures to PM2.5 were positively associated with the risk of asthma/wheezing. Each interquartile range (IQR) increment in PM2.5 exposure during the entire pregnancy (4.8 μg/m3 ) and the period from birth to the end of follow-up (1.5 μg/m3 ) was associated with adjusted hazard ratios (HRs) of 1.44 [95% confidence interval (CI): 1.13, 1.85 and 2.74 (95% CI: 2.59, 2.91), respectively. Subgroup analyses showed greater HRs for PM2.5 exposures during the pseudoglandular stage (6-16 gestational weeks [GWs: IQR = 4.8 μg/m3 , HR = 1.10, 95% CI: 1.02, 1.18) and canalicular stage (16-24 GWs: IQR = 4.8 μg/m3 , HR = 1.13, 95% CI:1.03, 1.23) than other stages, and also showed significant effects in the first three-year period after birth (IQR = 1.5 μg/m3 , HR = 2.37, 95% CI: =2.24, 2.51).Higher prenatal and postnatal PM2.5 exposures may increase the risk of childhood asthma/wheezing. The pseudoglandular stage, canalicular stage, and the first three years after birth may be key susceptible to exposure windows.