Talk:Abnormal Development - Air Pollution
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Cite this page: Hill, M.A. (2026, April 18) Embryology Abnormal Development - Air Pollution. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Air_Pollution |
2019
The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study
Environ Int. 2019 Jan;122:316-321. doi: 10.1016/j.envint.2018.11.030. Epub 2018 Nov 16.
Liu C1, Li Q2, Yan L3, Wang H4, Yu J4, Tang J4, Yao H4, Li S5, Zhang Y6, Guo Y7. Author information Abstract BACKGROUND: Few studies from western countries have linked prenatal exposure to ambient particulate matter <2.5 μm (PM2.5) with increased risk of congenital anomalies. However, the results are mixed. Particularly, evidence is limited for Chinese pregnant women. METHODS: In this retrospective cohort study, we matched the data of all pregnant women laboured in public hospitals during 2015-2016 in Yinchuan, a capital city of northwest China and the data of daily average PM2.5, nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone (O3) concentrations of the nearest monitor station. We calculated a time-dependent exposure over the entire pregnancy for each woman. We used a time varying Cox proportional hazards model to explore the association between PM2.5 exposure and the risk of congenital anomalies, after adjusting for individual confounders and other pollutants. RESULTS: A total of 39,386 singleton live births were included in the study, and 530 (1.35%) were with congenital anomalies. An increase of 10 μg/m3 in PM2.5 exposure over the entire pregnancy was significantly associated with increased risk of congenital anomalies, with hazard ratio (HR) of 1.35 [95% confidence interval (95%CI): 1.16, 1.58]. For subtype analyses, PM2.5 exposure exhibited a significant association with cardiac anomalies and other unclassifiable anomalies, with HRs of 1.60 (95%CI: 1.24, 2.08) and 1.42 (95%CI: 1.07, 1.89), respectively. The impacts of PM2.5 exposure on orofacial anomalies and musculoskeletal anomalies were not significant. CONCLUSION: Our results indicate high concentration of PM2.5 could increase the risk of congenital anomalies among Chinese, especially for cardiac anomalies. Self-protective measures involving reducing PM2.5 pollution exposure during pregnancy as well as environmental policies aiming to restrict PM2.5 emission could be helpful to reduce the burden of cognitional anomalies. Copyright © 2018 Elsevier Ltd. All rights reserved. KEYWORDS: Cardiac anomalies; Congenital anomalies; PM(2.5) exposure PMID: 30455103 DOI: 10.1016/j.envint.2018.11.030
2018
Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children
Biol Psychiatry. 2018 Aug 15;84(4):295-303. doi: 10.1016/j.biopsych.2018.01.016. Epub 2018 Jan 31.
Guxens M1, Lubczyńska MJ2, Muetzel RL3, Dalmau-Bueno A2, Jaddoe VWV4, Hoek G5, van der Lugt A6, Verhulst FC7, White T8, Brunekreef B9, Tiemeier H10, El Marroun H3.
Abstract BACKGROUND: Air pollution exposure during fetal life has been related to impaired child neurodevelopment, but it is unclear if brain structural alterations underlie this association. The authors assessed whether air pollution exposure during fetal life alters brain morphology and whether these alterations mediate the association between air pollution exposure during fetal life and cognitive function in school-age children. METHODS: We used data from a population-based birth cohort set up in Rotterdam, The Netherlands (2002-2006). Residential levels of air pollution during the entire fetal period were calculated using land-use regression models. Structural neuroimaging and cognitive function were performed at 6 to 10 years of age (n = 783). Models were adjusted for several socioeconomic and lifestyle characteristics. RESULTS: Mean fine particle levels were 20.2 μg/m3 (range, 16.8-28.1 μg/m3). Children exposed to higher particulate matter levels during fetal life had thinner cortex in several brain regions of both hemispheres (e.g., cerebral cortex of the precuneus region in the right hemisphere was 0.045 mm thinner (95% confidence interval, 0.028-0.062) for each 5-μg/m3 increase in fine particles). The reduced cerebral cortex in precuneus and rostral middle frontal regions partially mediated the association between exposure to fine particles and impaired inhibitory control. Air pollution exposure was not associated with global brain volumes. CONCLUSIONS: Exposure to fine particles during fetal life was related to child brain structural alterations of the cerebral cortex, and these alterations partially mediated the association between exposure to fine particles during fetal life and impaired child inhibitory control. Such cognitive impairment at early ages could have significant long-term consequences. Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved. KEYWORDS: Child development; Cognition; Cohort studies; Environmental pollution; Neuroimaging; Particulate matter PMID: 29530279 DOI: 10.1016/j.biopsych.2018.01.016
