Association of Prenatal Ambient Air Pollution Exposure With Placental Mitochondrial DNA Copy Number, Telomere Length and Preeclampsia

Background: Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage.Objective: To study the association between prenatal exposure to ambient nitrogen oxides (NOx, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn.Methods: This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NOx exposure assessment in southern Scania, Sweden. Hourly concentrations of NOx were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics.Results: Exposure was categorized into low and high exposures by median cut-offs during first [11.9 μg/m3; interquartile range (IQR) 7.9, 17.9], second (11.6 μg/m3; IQR: 7.1, 21.1), third trimesters (11.9 μg/m3; IQR: 7.7, 19.5) and entire pregnancy (12.0 μg/m3; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NOx exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; p = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; p = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (−0.20; 95% CI: −0.36, −0.04; p = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NOx exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NOx exposure and PE.Conclusion: In this region with relatively low levels of air pollution, ambient NOx exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.

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Ambient air pollution, blood mitochondrial DNA copy number and telomere length in a panel of diabetes patients

Inhalation Toxicology ◽

10.3109/08958378.2015.1075090 ◽

2015 ◽

Vol 27 (10) ◽

pp. 481-487 ◽

Cited By ~ 10

Author(s):

Yongjie Xia ◽

Renjie Chen ◽

Cuicui Wang ◽

Jing Cai ◽

Lianghui Wang ◽

...

Keyword(s):

Air Pollution ◽

Mitochondrial Dna ◽

Telomere Length ◽

Copy Number ◽

Ambient Air ◽

Ambient Air Pollution ◽

Dna Copy Number ◽

Mitochondrial Dna Copy Number ◽

Diabetes Patients

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Associations Between Ambient Air Pollution And Mitochondrial Dna Copy Number And Telomere Length In A Panel Of Elderly Residents Of Shanghai, China

ISEE Conference Abstracts ◽

10.1289/isee.2015.2015-2665 ◽

2015 ◽

Vol 2015 (1) ◽

pp. 2665

Author(s):

Yongjie Xia ◽

Renjie, Chen ◽

Jing Cai ◽

Haidong Kan

Keyword(s):

Air Pollution ◽

Mitochondrial Dna ◽

Telomere Length ◽

Copy Number ◽

Ambient Air ◽

Ambient Air Pollution ◽

Dna Copy Number ◽

Mitochondrial Dna Copy Number

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Sperm mtDNA copy number, telomere length, and seminal spermatogenic cells in relation to ambient air pollution: Results of a cross-sectional study in Jing-Jin-Ji region of China

Journal of Hazardous Materials ◽

10.1016/j.jhazmat.2020.124308 ◽

2020 ◽

pp. 124308

Author(s):

Lixiao Zhou ◽

Lipeng Li ◽

Guimin Hao ◽

Binghua Li ◽

Sujuan Yang ◽

...

Keyword(s):

Air Pollution ◽

Telomere Length ◽

Copy Number ◽

Ambient Air ◽

Cross Sectional Study ◽

Ambient Air Pollution ◽

Spermatogenic Cells ◽

Sectional Study ◽

Mtdna Copy Number ◽

Cross Sectional

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Relationship between Air Pollutant Exposure and Gynecologic Cancer Risk

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph18105353 ◽

2021 ◽

Vol 18 (10) ◽

pp. 5353

Author(s):

Qiwei Yu ◽

Liqiang Zhang ◽

Kun Hou ◽

Jingwen Li ◽

Suhong Liu ◽

...

Keyword(s):

Air Pollution ◽

Cancer Risk ◽

Air Pollutants ◽

Gynecological Cancer ◽

Gynecologic Cancer ◽

Ambient Air ◽

Air Pollutant ◽

Ambient Air Pollution ◽

Short Term Exposure ◽

Increased Risk

Exposure to air pollution has been suggested to be associated with an increased risk of women’s health disorders. However, it remains unknown to what extent changes in ambient air pollution affect gynecological cancer. In our case–control study, the logistic regression model was combined with the restricted cubic spline to examine the association of short-term exposure to air pollution with gynecological cancer events using the clinical data of 35,989 women in Beijing from December 2008 to December 2017. We assessed the women’s exposure to air pollutants using the monitor located nearest to each woman’s residence and working places, adjusting for age, occupation, ambient temperature, and ambient humidity. The adjusted odds ratios (ORs) were examined to evaluate gynecologic cancer risk in six time windows (Phase 1–Phase 6) of women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the highest ORs were found in Phase 4 (240 days). Then, the higher adjusted ORs were found associated with the increased concentrations of each pollutant (PM2.5, CO, O3, and SO2) in Phase 4. For instance, the adjusted OR of gynecological cancer risk for a 1.0-mg m−3 increase in CO exposures was 1.010 (95% CI: 0.881–1.139) below 0.8 mg m−3, 1.032 (95% CI: 0.871–1.194) at 0.8–1.0 mg m−3, 1.059 (95% CI: 0.973–1.145) at 1.0–1.4 mg m−3, and 1.120 (95% CI: 0.993–1.246) above 1.4 mg m−3. The ORs calculated in different air pollution levels accessed us to identify the nonlinear association between women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the gynecological cancer risk. This study supports that the gynecologic risks associated with air pollution should be considered in improved public health preventive measures and policymaking to minimize the dangerous effects of air pollution.

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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 ◽

10.3390/toxics9120338 ◽

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.

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Abstract P043: Does The Severity of Coronary Artery Disease Explain The Increased Risk of Death and Myocardial Infarction From Ambient Air Pollution Exposure?

Circulation ◽

10.1161/circ.125.suppl_10.ap043 ◽

2012 ◽

Vol 125 (suppl_10) ◽

Author(s):

Somjot S Brar ◽

Denise Le ◽

Sumit Khandhar ◽

Dong Chang ◽

Lindsay Short ◽

...

Keyword(s):

Air Pollution ◽

Coronary Artery ◽

Ambient Air ◽

Ambient Air Pollution ◽

Left Main ◽

Left Main Disease ◽

Increased Risk ◽

Artery Disease ◽

The Relationship ◽

Road Distance

BACKGROUND: Ambient air pollution from traffic increases cardiovascular morbidity and mortality and is associated with coronary artery calcification. Whether this increased risk is mediated by severity of coronary artery disease (CAD) remains unknown. METHODS: In this pilot study, the relationship between living near a major roadway and multivessel CAD confirmed by invasive coronary angiographic was explored. Subjects undergoing coronary angiography in the Los Angeles metropolitan area in 2009-10 were randomly selected. Investigators blinded to the exposure status reviewed coronary angiograms. Subjects were categorized as having: absence of or non-obstructive CAD, 1-vessel, 2-vessel, or 3-vessel CAD based upon the number of major epicardial vessels with > 70% stenoses. The distance from each subject's residence to the nearest major road was calculated in meters. Multivariate logistic regression was used to explore the relationship between severity of CAD and distance to major roadway. RESULTS: There were 642 subjects undergoing coronary angiography. The mean age (SD) was 64 years (12) and 36% were female. In multivariate analysis log-road distance was a predictor of multivessel CAD, odds ratio (OR) = 0.85 (95%CI, 0.75-0.98; p=0. 02) after adjusting for age, gender, hypertension, and diabetes, and smoking status. Other predictors of multivessel CAD included from the multivariate logist model were: male gender (OR, 3.00, 95% CI, 2.06-4.39; p<0.001), diabetes (OR, 2.49; 95% CI, 1.75-3.54; p<0.001), and hypertension 2.58; 95%CI, 1.28-5.21; p=0.008). The most severe form of CAD, >50% stenosis of the left main artery, was observed in 6.6% of the cohort. In a multivariate model, age (P = 0.002) and diabetes (P = 0.002) were significant predictors of severe left main disease; there was a trend for log-road distance (OR, 0.83; 95% CI, 0.67-1.02; P = 0.079) with left main disease. CONCLUSIONS: Multivessel CAD was strongly associated with traditional risk factors. After adjusting for these factors, living near a major roadway was also a predictor. This study demonstrates the feasibility of exploring the association between angiographic CAD and traffic pollution. Additional studies are needed to better understand the mechanisms underlying the increase in adverse cardiovascular events from air pollution.

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The Relationship Between Air Pollution and All-Cause Mortality in Singapore

Atmosphere ◽

10.3390/atmos11010009 ◽

2019 ◽

Vol 11 (1) ◽

pp. 9 ◽

Cited By ~ 6

Author(s):

Ho ◽

Zheng ◽

Cheong ◽

En ◽

Pek ◽

...

Keyword(s):

Air Pollution ◽

Health Hazard ◽

Ambient Air ◽

Ambient Air Pollution ◽

World Population ◽

Distributed Lag ◽

Increased Risk ◽

All Cause Mortality ◽

Unit Increase ◽

The Relationship

Ambient air pollution is a risk factor for both acute and chronic diseases and poses serious health threats to the world population. We aim to study the relationship between air pollution and all-cause mortality in the context of a city-state exposed to the Southeast Asian haze problem. The primary exposure was ambient air pollution, as measured by the Pollutants Standards Index (PSI). The outcome of interest was all-cause mortality from 2010–2015. A time-stratified case-crossover design was performed. A conditional Poisson regression model, including environmental variables such as PSI, temperature, wind speed, and rainfall, was fitted to the daily count of deaths to estimate the incidence rate ratio (IRR) of mortality per unit increase in PSI, accounting for overdispersion and autocorrelation. To account for intermediate exposure effects (maximum lag of 10 days), a distributed lag non-linear model was used. There were 105,504 deaths during the study period. Increment in PSI was significantly associated with an increased risk of mortality. The adjusted IRR of mortality per the 10-unit increase in PSI was 1.01 (95%CI = 1.00–1.01). The lag effect was stronger when PSI was in the unhealthy range compared to the good and moderate ranges. At lag = 7 days, PSI appeared to have an adverse effect on mortality, although the effect was not significant. These findings provide evidence on the general health hazard of exposure to air pollution and can potentially guide public health policies in the region.

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Short-term effects of air pollution on blood pressure

Scientific Reports ◽

10.1038/s41598-019-56413-y ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 1

Author(s):

You-Jung Choi ◽

Sun-Hwa Kim ◽

Si-Hyuck Kang ◽

Sun-Young Kim ◽

Ok-Jin Kim ◽

...

Keyword(s):

Blood Pressure ◽

Air Pollution ◽

Air Pollutants ◽

Ambient Air ◽

Ambient Air Pollution ◽

Pathophysiological Mechanism ◽

Short Term ◽

Mortality And Morbidity ◽

Short Term Exposure ◽

Increased Risk

AbstractElevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0–8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2–4 hours and 3–5 hours after increased levels of SO2 and CO, respectively (0.24 mmHg and 0.26 mmHg for an interquartile range, respectively). In contrast, O3 and NO2 were associated with significantly increased systolic BP at 3–5 lag hours and at 0–2 lag hours, respectively. BP elevation in association with O3 and NO2 was shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.

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