<?xml version="1.0" encoding="UTF-8" standalone="no" ?><xml><records><record><database name="vuoto - Copia" path="F:\vuoto - Copia">vuoto - Copia</database><source-app name="Reference Manager 11.0" version="11.0.0.359">Reference Manager 11.0</source-app><rec-number>5</rec-number><ref-type name="Journal">1</ref-type><contributors><authors><author><style face="normal" font="default">Chen,G</style></author><author><style face="normal" font="default"> Zhou,H</style></author><author><style face="normal" font="default"> He,G</style></author><author><style face="normal" font="default"> Zhu,S</style></author><author><style face="normal" font="default"> Sun,X</style></author><author><style face="normal" font="default"> Ye,Y</style></author><author><style face="normal" font="default"> Chen,H</style></author><author><style face="normal" font="default"> Xiao,J</style></author><author><style face="normal" font="default"> Hu,J</style></author><author><style face="normal" font="default"> Zeng,F</style></author><author><style face="normal" font="default"> Yang,P</style></author><author><style face="normal" font="default"> Gao,Y</style></author><author><style face="normal" font="default"> He,Z</style></author><author><style face="normal" font="default"> Wang,J</style></author><author><style face="normal" font="default"> Cao,G</style></author><author><style face="normal" font="default"> Chen,Y</style></author><author><style face="normal" font="default"> Feng,H</style></author><author><style face="normal" font="default"> Ma,W</style></author><author><style face="normal" font="default"> Liu,C</style></author><author><style face="normal" font="default"> Liu,T</style></author></authors></contributors><titles><title><style face="normal" font="default">Effect of early-life exposure to PM2.5 on childhood asthma/wheezing: a birth cohort study</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><volume><style face="normal" font="default">33</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">air pollution</style></keyword><keyword><style face="normal" font="default"> asthma</style></keyword><keyword><style face="normal" font="default"> birth cohort</style></keyword><keyword><style face="normal" font="default"> children</style></keyword><keyword><style face="normal" font="default"> PMID</style></keyword><keyword><style face="normal" font="default"> pregnancy</style></keyword><keyword><style face="normal" font="default"> wheezing</style></keyword></keywords><dates><year Day="1" Month="6" Year="2022">2022/6/1</year><pub-dates><date Day="27" Month="6" Year="2022">2022/6/27</date></pub-dates></dates><publisher><style face="normal" font="default">John Wiley &amp; Sons, Ltd</style></publisher><isbn><style face="normal" font="default">0905-6157</style></isbn><abstract><style face="normal" font="default">BackgroundAlthough 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.MethodsA 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.ResultsA 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).ConclusionHigher 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.</style></abstract><work-type><style face="normal" font="default">10.1111/pai.13822</style></work-type><urls><web-urls><url ppv-ref="no">https://onlinelibrary.wiley.com/doi/10.1111/pai.13822</url></web-urls></urls><misc3><style face="normal" font="default">10.1111/pai.13822</style></misc3></record></records></xml>
