https://scholars.lib.ntu.edu.tw/handle/123456789/542715
標題: | Fine particulate matter exposure during pregnancy and infancy and incident asthma | 作者: | Jung, C.-R. Chen, W.-T. Tang, Y.-H. Bing-Fang Hwang |
公開日期: | 2019 | 卷: | 143 | 期: | 6 | 起(迄)頁: | 2254-2.26E+08 | 來源出版物: | Journal of Allergy and Clinical Immunology | 摘要: | Background: Lung development is a multistage process from conception to the postnatal period, disruption of which by air pollutants can trigger later respiratory morbidity. Objective: We sought to evaluate the effects of weekly average fine particulate matter (particulate matter with an aerodynamic diameter less than 2.5 μm [PM2.5]) exposure during pregnancy and infancy on asthma and identify vulnerable times to help elucidate possible mechanisms of the effects of PM2.5 on asthma symptoms. Methods: A birth cohort study including 184,604 children born during 2004-2011 in Taichung City was retrieved from the Taiwan Maternal and Child Health Database and followed until 2014. A daily satellite-based hybrid model was applied to estimate PM2.5 exposure for each subject. A Cox proportional hazard model combined with a distributed lag nonlinear model was used to evaluate the associations of asthma with PM2.5 exposure during pregnancy and infancy. Results: The birth cohort contained 34,336 asthmatic patients, and the mean age of children given a diagnosis of asthma was 3.39 ± 1.78 years. Increased exposure to PM2.5 during gestational weeks 6 to 22 and 9 to 46 weeks after birth were significantly associated with an increased incidence of asthma. The exposure-response relationship indicated that the hazard ratio (HR) of asthma increased steeply at PM2.5 exposure of greater than 93 μg/m3 during pregnancy. Additionally, the HRs remained significant with postnatal exposure to PM2.5 between 26 and 72 μg/m3 (range, 1.01-1.07 μg/m3), followed by a sharp increase in HRs at PM2.5 exposure of greater than 73 μg/m3. Conclusion: Both prenatal and postnatal exposures to PM2.5 were associated with later development of asthma. The vulnerable time windows might be within early gestation and midgestation and infancy. © 2019 American Academy of Allergy, Asthma & Immunology |
URI: | https://www.scopus.com/inward/record.url?eid=2-s2.0-85064608060&partnerID=40&md5=b17337b4569165384b5377667fd5dcec https://scholars.lib.ntu.edu.tw/handle/123456789/542715 |
DOI: | 10.1016/j.jaci.2019.03.024 | SDG/關鍵字: | immunoglobulin E; adult; air pollutant; allergic asthma; Article; asthma; child health; cohort analysis; controlled study; disease association; female; gestational age; human; ICD-9; incidence; infant; lung development; major clinical study; male; maternal exposure; maternal smoking; particulate matter; pregnancy; prenatal exposure; prenatal period; priority journal; sex difference; Taiwan; adverse event; asthma; maternal exposure; particulate matter; preschool child; proportional hazards model; Air Pollutants; Asthma; Child, Preschool; Female; Humans; Infant; Male; Maternal Exposure; Particulate Matter; Pregnancy; Prenatal Exposure Delayed Effects; Proportional Hazards Models; Taiwan |
顯示於: | 大氣科學系 |
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