Talk:Abnormal Development - Air Pollution
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Cite this page: Hill, M.A. (2021, August 3) Embryology Abnormal Development - Air Pollution. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Air_Pollution
Ha S, Yeung E, Bell E, Insaf T, Ghassabian A, Bell G, Muscatiello N & Mendola P. (2019). Prenatal and early life exposures to ambient air pollution and development. Environ. Res. , 174, 170-175. PMID: 30979514 DOI.
Prenatal and early life exposures to ambient air pollution and development.
Abstract BACKGROUND: Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5 μm (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES: We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN: Prospective cohort. SETTINGS: New York State excluding New York City. PARTICIPANTS: 4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES: Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES: Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000 m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS: Compared to those >1000 m away from a major roadway, those resided 50-100 m [RR: 2.12 (1.00-4.52)] and 100-500 m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10 μg/m3 increase in PM2.5 and 0.7%-1.7% for a 10 ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS: In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted. Copyright © 2019 Elsevier Inc. All rights reserved.
KEYWORDS: Air pollution; Child development; Major roadway; Neurodevelopment; Traffic PMID: 30979514 PMCID: PMC6541527 [Available on 2020-07-01] DOI: 10.1016/j.envres.2019.03.064
Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health
Environ Int. 2019 Feb 28;126:363-376. doi: 10.1016/j.envint.2019.02.028. [Epub ahead of print]
Ladd-Acosta C1, Feinberg JI2, Brown SC3, Lurmann FW4, Croen LA5, Hertz-Picciotto I6, Newschaffer CJ7, Feinberg AP8, Fallin MD2, Volk HE9.
Abstract BACKGROUND: Prenatal air pollution exposure has been linked to many adverse health conditions in the offspring. However, little is known about the mechanisms underlying these associations. Epigenetics may be one plausible biologic link. Here, we sought to identify site-specific and global DNA methylation (DNAm) changes, in developmentally relevant tissues, associated with prenatal exposure to nitrogen dioxide (NO2) and ozone (O3). Additionally, we assessed whether sex-specific changes in methylation exist and whether DNAm changes are consistently observed across tissues. METHODS: Genome-scale DNAm measurements were obtained using the Infinium HumanMethylation450k platform for 133 placenta and 175 cord blood specimens from Early Autism Risk Longitudinal Investigation (EARLI) neonates. Ambient NO2 and O3 exposure levels were based on prenatal address locations of EARLI mothers and the Environmental Protection Agency's AirNOW monitoring network using inverse distance weighting. We computed sample-level aggregate methylation measures for each of 5 types of genomic regions including genome-wide, open sea, shelf, shore, and island regions. Linear regression was performed for each genomic region; per-sample aggregate methylation measures were modeled as a function of quantitative exposure level with covariate adjustment. In addition, bumphunting was performed to identify differentially methylated regions (DMRs) associated with prenatal O3 and NO2 exposures in each tissue and by sex, with adjustment for technical and biological sources of variation. RESULTS: We identified global and locus-specific changes in DNA methylation related to prenatal exposure to NO2 and O3 in 2 developmentally relevant tissues. Neonates with increased prenatal O3 exposure had lower aggregate levels of DNAm at CpGs located in open sea and shelf regions of the genome. We identified 6 DMRs associated with prenatal NO2 exposure, including 3 sex-specific. An additional 3 sex-specific DMRs were associated with prenatal O3 exposure levels. DMRs initially detected in cord blood samples (n = 4) showed consistent exposure-related changes in DNAm in placenta. However, the DMRs initially detected in placenta (n = 5) did not show DNAm differences in cord blood and, thus, they appear to be tissue-specific. CONCLUSIONS: We observed global, locus, and sex-specific methylation changes associated with prenatal NO2 and O3 exposures. Our findings support DNAm is a biologic target of prenatal air pollutant exposures and highlight epigenetic involvement in sex-specific differential susceptibility to environmental exposure effects in 2 developmentally relevant tissues. Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved. KEYWORDS: DNA methylation; Epigenetic; Genome-scale; Placenta; Prenatal air pollution exposure; Sex differences PMID: 30826615 DOI: 10.1016/j.envint.2019.02.028
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
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
PLoS Med. 2015 Mar 3;12(3):e1001792. doi: 10.1371/journal.pmed.1001792. eCollection 2015 Mar.
Sunyer J1, Esnaola M2, Alvarez-Pedrerol M2, Forns J2, Rivas I3, López-Vicente M2, Suades-González E4, Foraster M2, Garcia-Esteban R2, Basagaña X2, Viana M5, Cirach M2, Moreno T5, Alastuey A5, Sebastian-Galles N6, Nieuwenhuijsen M2, Querol X5. Author information Abstract BACKGROUND: Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development. METHODS AND FINDINGS: We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). Chronic traffic air pollution (elemental carbon [EC], nitrogen dioxide [NO2], and ultrafine particle number [UFP; 10-700 nm]) was measured twice during 1-wk campaigns both in the courtyard (outdoor) and inside the classroom (indoor) simultaneously in each school pair. Cognitive development was assessed with the n-back and the attentional network tests, in particular, working memory (two-back detectability), superior working memory (three-back detectability), and inattentiveness (hit reaction time standard error). Linear mixed effects models were adjusted for age, sex, maternal education, socioeconomic status, and air pollution exposure at home. Children from highly polluted schools had a smaller growth in cognitive development than children from the paired lowly polluted schools, both in crude and adjusted models (e.g., 7.4% [95% CI 5.6%-8.8%] versus 11.5% [95% CI 8.9%-12.5%] improvement in working memory, p = 0.0024). Cogently, children attending schools with higher levels of EC, NO2, and UFP both indoors and outdoors experienced substantially smaller growth in all the cognitive measurements; for example, a change from the first to the fourth quartile in indoor EC reduced the gain in working memory by 13.0% (95% CI 4.2%-23.1%). Residual confounding for social class could not be discarded completely; however, the associations remained in stratified analyses (e.g., for type of school or high-/low-polluted area) and after additional adjustments (e.g., for commuting, educational quality, or smoking at home), contradicting a potential residual confounding explanation. CONCLUSIONS: Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development. PMID: 25734425 PMCID: PMC4348510 DOI: 10.1371/journal.pmed.1001792