Air pollution during pregnancy and placental adaptation in the levels of global DNA methylation

Maghbooli, Zhila; Hossein–Nezhad, Arash; Adabi, Elham; Asadollahpour, Effat; Sadeghi, Mahsa; Mohammadnabi, Sara; Rad, Leila Zakeri; Hosseini, Ali-asghar Malek; Radmehr, Mehrnaz; Faghihi, Fatemeh; Aghaei, Atoosa; Omidifar, Abolfazl; Aghababei, Yasaman; Behzadi, Hadis

doi:10.1371/journal.pone.0199772

Cited by 90 publications

(65 citation statements)

References 25 publications

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“…The result indicates that the exposure to PM2.5 in the first trimester might have the biggest effect on birth weight. It might be because that the exposure to air pollution in the first trimester could lead to placental adaptation through epigenetic modification …”

Section: Discussionmentioning

confidence: 99%

Effect of PM2.5 on macrosomia in China: A nationwide prospective cohort study

Chen

Wang

Li³

et al. 2019

Pediatric Obesity

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Background: Macrosomia is associated with both neonatal complications and adult diseases (obesity, diabetes mellitus, etc.). Previous studies have reported maternal exposure to PM2.5 might influence metabolism and fetal development and cause adverse pregnancy outcomes. Studies conducted in areas with low PM2.5 concentration have found relationship between gestational PM2.5 exposure and birth weight. However, the impact of air pollution on macrosomia has not been studied, especially in highly polluted areas.Objective: To evaluate the association between fine particulate matter (PM2.5) exposure during pregnancy and the risk of macrosomia.Methods: Data from preconception health examination and prenatal and postnatal records were collected from 1 January 2010 to 31 December 2012 in the National Free Preconception Health Examination Project. Monthly mean of PM2.5 concentration during pregnancy was estimated from satellite data using an ensemble machine learning model. A newborn with birth weight above 4000 g was defined as macrosomia. Logistic regression models were used to examine the association between maternal exposure to PM2.5 and the risk of macrosomia, after adjusting for maternal age, pre-pregnancy body mass index, parity, neonatal sex, duration of gestation, seasonality, educational level, smoking and drinking habits, past history of diabetes mellitus and hypertension, and family history of diabetes mellitus. Restricted cubic spline models were used to evaluate the dose-response relationship between the risk of macrosomia and PM2.5 concentration. Results:Of 177 841 singleton nonlow birth weight newborns included, 14 598 (8.2%) had macrosomia. The mean PM2.5 concentrations were 70.7, 71.5, and 80.9 μg/m 3 in the first, second, and third trimesters. In full-adjusted logistic regression models, significant associations were found between increased risk of macrosomia and every 10 μg/m 3 increase of PM2.5 concentration over the first (odds ratio [OR]: 1.045; 95% CI, 1.037-1.052), second (OR: 1.035; 95% CI, 1.028-1.043), and third (OR: 1.033; 95% CI, 1.026-1.039) trimesters. There was a /journal/ijpo 1 of 7 nonlinear does-response association between PM2.5 concentration and the risk of macrosomia.Conclusions: Maternal exposure to PM2.5 during pregnancy was associated with an increased risk of macrosomia in China.

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Section: Discussionmentioning

confidence: 99%

Effect of PM2.5 on macrosomia in China: A nationwide prospective cohort study

Chen

Wang

Li³

et al. 2019

Pediatric Obesity

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“…Various types of cellular stress seem to affect epigenetic alterations that may lead to deleterious consequences. Exposure to fine particle air pollution affects DNA methylation status in blood cells [ 178 , 179 , 180 , 181 , 182 , 183 ] and placenta [ 184 ]. Cigarette smoking has adverse effects on health and is associated with changes in epigenetic marks.…”

Section: Epigenetics and Agingmentioning

confidence: 99%

Polyamine Metabolism and Gene Methylation in Conjunction with One-Carbon Metabolism

Soda

2018

IJMS

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Recent investigations have revealed that changes in DNA methylation status play an important role in aging-associated pathologies and lifespan. The methylation of DNA is regulated by DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) in the presence of S-adenosylmethionine (SAM), which serves as a methyl group donor. Increased availability of SAM enhances DNMT activity, while its metabolites, S-adenosyl-l-homocysteine (SAH) and decarboxylated S-adenosylmethionine (dcSAM), act to inhibit DNMT activity. SAH, which is converted from SAM by adding a methyl group to cytosine residues in DNA, is an intermediate precursor of homocysteine. dcSAM, converted from SAM by the enzymatic activity of adenosylmethionine decarboxylase, provides an aminopropyl group to synthesize the polyamines spermine and spermidine. Increased homocysteine levels are a significant risk factor for the development of a wide range of conditions, including cardiovascular diseases. However, successful homocysteine-lowering treatment by vitamins (B6, B12, and folate) failed to improve these conditions. Long-term increased polyamine intake elevated blood spermine levels and inhibited aging-associated pathologies in mice and humans. Spermine reversed changes (increased dcSAM, decreased DNMT activity, aberrant DNA methylation, and proinflammatory status) induced by the inhibition of ornithine decarboxylase. The relation between polyamine metabolism, one-carbon metabolism, DNA methylation, and the biological mechanism of spermine-induced lifespan extension is discussed.

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“…Furthermore, it is well known that in Italy urban pollutants decrease from inlands to offshore and near the coastal environment and are associated with interstitial pneumonia. 7 On the basis of several publicly available data from government's environmental, health, and statistical institutions for the latest 3 years, we calculated that the Northern regions have an OR of 11.44 (95% CI, 10.707-12.238) for COVID-19 incidence risk in subjects living in inland areas with PM 10 levels of greater than or equal to 40 mg/m 3 and NO 2 levels of greater than or equal to 40 mg/m 3 for at least 3 months/y, whereas the Central-Southern regions, including major islands, have an OR of 0.97 (95% CI, 0.898-1.068) with same values in the same time course; that is, there is no relevant risk association between the onset of COVID-19 following SARS-CoV-2 infections and major urban pollutants. Furthermore, we calculated from data of the Italian Government ''Institute of STATistics'' (ISTAT) and the National Institute of Health that the OR of COVID-19 risk incidence in subjects with asthma living permanently in Northern inland macro area was 1.44 (95% CI, 1.395-1.488), whereas in the Central-Southern macro area (including Sardinia and Sicily), the OR was 0.76 (95% CI, 0.721-0.807).…”

mentioning

confidence: 99%

“…2 According to our opinion, one possible leading factor in the paradoxical bimodal distribution of COVID-19 cases in Italy, very high in the Northern part and slightly modest in the Central-Southern part, is not only the favorable genetic endowment of ACE I/D polymorphism but also the presence of environmental O 3 , because ozone, besides being a nontoxic asthma trigger, is able to modulate the pulmonary microbiome, thus assessing the correct cross-talk between airway bacteria and the immune surveillance of lung physiology, whereas PM 10 alters this interelationship. [5][6][7] It is possible therefore to suggest that the increasing asthma prevalence from North to South is a sign of the different impact of the troposphere ozone in Italy.…”

mentioning

confidence: 99%