scholarly journals Prenatal and postnatal traffic pollution exposure, DNA methylation in Shank3 and MeCP2 promoter regions, H3K4me3 and H3K27me3 and sociability in rats’ offspring

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Qinfeng Zhou ◽  
Yu Tian ◽  
Chenlu Xu ◽  
Juling Wang ◽  
Yongtang Jin
Keyword(s):  
Dna Methylation ◽  
Air Pollution ◽  
Early Life ◽  
Noise Pollution ◽  
Traffic Pollution ◽  
Male Rats ◽  
Promoter Regions ◽  
Increased Risk ◽  
Analysis Experiment ◽  
Pollution Exposure

Abstract Background Road traffic air pollution is linked with an increased risk of autistic spectrum disorder (ASD). The aim of this study is to assess the effect of exposure to prenatal or postnatal traffic-related air pollution combining concomitant noise pollution on ASD-related epigenetic and behavioral alternations on offspring. Methods A 2 × 2 factorial analysis experiment was designed. Wistar rats were exposed at different sites (L group: green space; H group: crossroads) and timings (E group: full gestation; P group: 21 days after birth) at the same time, and air pollutants of nitrogen dioxide (NO2) and fine particles (PM2.5) were meanwhile sampled. On postnatal day 25, brains from offspring of each group were extracted to determine the levels of DNA methylation in Shank3 (three parts: Shank3_01, Shank3_02, Shank3_03) and MeCP2 (two parts: MeCP2_01, MeCP2_02) promoter regions, H3K4me3 and H3K27me3 after three-chamber social test. Meanwhile, the Shank3 and MeCP2 levels were quantified. Results The concentrations of PM2.5 (L: 58.33 µg/m3; H: 88.33 µg/m3, P < 0.05) and NO2 (L: 52.76 µg/m3; H: 146.03 µg/m3, P < 0.01) as well as the intensity of noise pollution (L: 44.4 dB (A); H: 70.1 dB (A), P < 0.001) differed significantly from 18:00 to 19:00 between experimental sites. Traffic pollution exposure (P = 0.006) and neonatal exposure (P = 0.001) led to lower weight of male pups on PND25. Male rats under early-life exposure had increased levels of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.001, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.94 µg/mg; EH: 11.98; PL: 17.14; PH: 14.78, timing P < 0.05), and reduced levels of H3K27me3 (EL: 71.07 µg/mg; EH: 44.76; PL: 29.15; PH: 28.67, timing P < 0.001; site P < 0.05) in brain compared to those under prenatal exposure. There was, for female pups, a same pattern of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.05, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.27 µg/mg; EH: 11.55; PL: 16.11; PH: 15.44, timing P < 0.001), but the levels of H3K27me3 exhibited an inverse trend concerning exposure timing. Hypermethylation at the MeCP2 and Shank3 promoter was correlated with the less content of MeCP2 (female: EL: 32.23 ng/mg; EH: 29.58; PL: 25.01; PH: 23.03, timing P < 0.001; site P < 0.05; male: EL: 31.05 ng/mg; EH: 32.75; PL: 23.40; PH: 25.91, timing P < 0.001) and Shank3 (female: EL: 5.10 ng/mg; EH: 5.31; PL: 4.63; PH: 4.82, timing P < 0.001; male: EL: 5.40 ng/mg; EH: 5.48; PL: 4.82; PH: 4.87, timing P < 0.001). Rats with traffic pollution exposure showed aberrant sociability preference and social novelty, while those without it behaved normally. Conclusions Our findings suggest early life under environmental risks is a crucial window for epigenetic perturbations and then abnormalities in protein expression, and traffic pollution impairs behaviors either during pregnancy or after birth.

Epigenome-wide analysis of long-term air pollution exposure and DNA methylation in monocytes: results from the Multi-Ethnic Study of Atherosclerosis

Epigenetics ◽  
2021 ◽  
pp. 1-17
Author(s):  
Gloria C. Chi ◽  
Yongmei Liu ◽  
James W. MacDonald ◽  
Lindsay M. Reynolds ◽  
Daniel A. Enquobahrie ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Air Pollution ◽  
Ethnic Study ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

scholarly journals Childhood cancer and traffic-related air pollution exposure in pregnancy and early life

2013 ◽  
Vol 2013 (1) ◽  
pp. 3811
Author(s):  
Julia Heck ◽  
Jun Wu ◽  
Christina Lombardi ◽  
Travis Meyers ◽  
Michelle Wilhelm ◽  
...  
Keyword(s):  
Air Pollution ◽  
Childhood Cancer ◽  
Early Life ◽  
Air Pollution Exposure ◽  
Pollution Exposure ◽  
In Pregnancy

scholarly journals Early Pregnancy Exposure to Ambient Air Pollution among Late-Onset Preeclamptic Cases Is Associated with Placental DNA Hypomethylation of Specific Genes and Slower Placental Maturation

Toxics ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 338
Author(s):  
Karin Engström ◽  
Yumjirmaa Mandakh ◽  
Lana Garmire ◽  
Zahra Masoumi ◽  
Christina Isaxon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Air Pollution ◽  
Early Pregnancy ◽  
Late Onset ◽  
Dispersion Model ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Dna Hypomethylation ◽  
Increased Risk

Exposure to ambient air pollution during pregnancy has been associated with an increased risk of preeclampsia (PE). Some suggested mechanisms behind this association are changes in placental DNA methylation and gene expression. The objective of this study was to identify how early pregnancy exposure to ambient nitrogen oxides (NOx) among PE cases and normotensive controls influence DNA methylation (EPIC array) and gene expression (RNA-seq). The study included placentas from 111 women (29 PE cases/82 controls) in Scania, Sweden. First-trimester NOx exposure was assessed at the participants’ residence using a dispersion model and categorized via median split into high or low NOx. Placental gestational epigenetic age was derived from the DNA methylation data. We identified six differentially methylated positions (DMPs, q < 0.05) comparing controls with low NOx vs. cases with high NOx and 14 DMPs comparing cases and controls with high NOx. Placentas with female fetuses showed more DMPs (N = 309) than male-derived placentas (N = 1). Placentas from PE cases with high NOx demonstrated gestational age deceleration compared to controls with low NOx (p = 0.034). No differentially expressed genes (DEGs, q < 0.05) were found. In conclusion, early pregnancy exposure to NOx affected placental DNA methylation in PE, resulting in placental immaturity and showing sexual dimorphism.

scholarly journals Early life air pollution exposure elevates general psychopathology risk at the transition to adulthood

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Aaron Reuben ◽  
Louise Arseneault ◽  
Andrew Beddows ◽  
Sean D. Beevers ◽  
Terrie E. Moffitt ◽  
...  
Keyword(s):  
Air Pollution ◽  
Transition To Adulthood ◽  
Early Life ◽  
General Psychopathology ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Air pollution exposure associates with increased risk of neonatal jaundice

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Liqiang Zhang ◽  
Weiwei Liu ◽  
Kun Hou ◽  
Jintai Lin ◽  
Changqing Song ◽  
...  
Keyword(s):  
Air Pollution ◽  
Neonatal Jaundice ◽  
Increased Risk ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Air pollution and the development of asthma from birth until young adulthood

2020 ◽  
Vol 56 (1) ◽  
pp. 2000147 ◽  
Author(s):  
Ulrike Gehring ◽  
Alet H. Wijga ◽  
Gerard H. Koppelman ◽  
Judith M. Vonk ◽  
Henriette A. Smit ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Early Adulthood ◽  
Childhood And Adolescence ◽  
Asthma Incidence ◽  
Mite Allergy ◽  
Increased Risk ◽  
Air Pollution Exposure ◽  
Pollution Exposure ◽  
The Impact

BackgroundAir pollution is associated with asthma development in children and adults, but the impact on asthma development during the transition from adolescence to adulthood is unclear. Adult studies lack historical exposures and consequently cannot assess the relevance of exposure during different periods of life. We assessed the relevance of early-life and more recent air pollution exposure for asthma development from birth until early adulthood.MethodsWe used data of 3687 participants of the prospective Dutch PIAMA (Prevention and Incidence of Asthma and Mite Allergy) birth cohort and linked asthma incidence until age 20 years to estimated concentrations of nitrogen dioxide (NO2), particulate matter with a diameter <2.5 μm (PM2.5), <10 μm (PM10), and 2.5–10 μm, and PM2.5 absorbance (“soot”) at the residential address. We assessed overall and age-specific associations with air pollution exposure with discrete time-hazard models, adjusting for potential confounders.ResultsOverall, we found higher incidence of asthma until the age of 20 years with higher exposure to all pollutants at the birth address (adjusted odds ratio (95% CI) ranging from 1.09 (1.01–1.18) for PM10 to 1.20 (1.10–1.32) for NO2) per interquartile range increase) that were rather persistent with age. Similar associations were observed with more recent exposure defined as exposure at the current home address. In two-pollutant models with particulate matter, associations with NO2 persisted.ConclusionsExposure to air pollution, especially from motorised traffic, early in life may have long-term consequences for asthma development, as it is associated with an increased risk of developing asthma through childhood and adolescence into early adulthood.

Epigenome-Wide Meta-Analysis of DNA Methylation in Children related to Prenatal Particulate Air Pollution Exposure

2018 ◽  
Vol 2017 (1) ◽  
pp. 172
Author(s):  
Olena Gruzieva ◽  
Carrie V. Breton ◽  
Herman T. den Dekker ◽  
Akram Ghantous ◽  
Allan C. Just ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Air Pollution ◽  
Meta Analysis ◽  
Particulate Air Pollution ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Association between Exposure to Noise and Air Pollution and Metabolic Syndrome

2021 ◽  
Author(s):  
Mina Arabian ◽  
Masoud Mirzaei ◽  
Mohammad Javad Zare Sakhvidi ◽  
Sara Jambarsang ◽  
Mohsen Mirzaei
Keyword(s):  
Metabolic Syndrome ◽  
Air Pollution ◽  
Traffic Noise ◽  
Noise Pollution ◽  
Kriging Model ◽  
Wide Range ◽  
Air Pollution Exposure ◽  
Pollution Modeling ◽  
Adjusted Model ◽  
Pollution Exposure

Abstract Background: In addition to the classical risk factors environmental pollution such as traffic noise and air pollution are suggested to be a risk factor for Metabolic Syndrome (MetS). In this study, we examined the between exposure to noise and air pollution (PM2.5) and MetS.Methods: This study was performed on 3513 participants in a prospective study on the health of the people of Yazd (YaHS). A wide range of demographic, anthropometric and blood biochemistry data were gathered during 2014-2015. Data on personal level noise and air pollution (PM2.5) at residential address were collected through air pollution maps. Air and noise pollution modeling was performed using Kriging model. Using weighted logistic regressiARAon, we reported the odds ratio (95% confidence interval) of MetS for a unit increase in exposure to the pollutants. Results: The prevalence of MetS in the total population was 43.7%. No association was found with MetS between noise exposures in the range (54.1-62.3) dB (A). There was a positive relationship between air pollution exposure in the range (32.82 - 16.38) micrograms per cubic meter and MetS in the raw model and after adjusting for the effect of age and sex, increased air pollution exposure, chance The incidence of MetS increases by 8% (95% CI = 1.06 - 1.10), while the fully adjusted model did not find a positive and significant relationship. Conclusion: We did not find any association between noise and air pollution with MetS in the fully adjusted model.

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