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      Ambient air pollution and adverse birth outcomes: A review of underlying mechanisms

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          Abstract

          Epidemiological data provide varying degrees of evidence for associations between prenatal exposure to ambient air pollutants and adverse birth outcomes (suboptimal measures of fetal growth, preterm birth and stillbirth). To further assess certainty of effects, this review examines the experimental literature base to identify mechanisms by which air pollution (particulate matter, nitrogen dioxide and ozone) could cause adverse effects on the developing fetus. It likely that this environmental insult impacts multiple biological pathways important for sustaining a healthy pregnancy, depending upon the composition of the pollutant mixture and the exposure window owing to changes in physiologic maturity of the placenta, its circulations and the fetus as pregnancy ensues. The current body of evidence indicates that the placenta is a target tissue, impacted by a variety of critical processes including nitrosative/oxidative stress, inflammation, endocrine disruption, epigenetic changes, as well as vascular dysregulation of the maternal-fetal unit. All of the above can disturb placental function and, as a consequence, could contribute to compromised fetal growth as well increasing the risk of stillbirth. Furthermore, given that there is often an increased inflammatory response associated with preterm labour, inflammation is a plausible mechanism mediating the effects of air pollution on premature delivery. In the light of increased urbanisation and an ever-changing climate, both of which increase ambient air pollution and negatively affect vulnerable populations such as pregnant individuals, it is hoped that the collective evidence may contribute to decisions taken to strengthen air quality policies, reductions in exposure to air pollution and subsequent improvements in the health of those not yet born.

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          Most cited references140

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          Epidemiology and causes of preterm birth

          Summary This paper is the first in a three-part series on preterm birth, which is the leading cause of perinatal morbidity and mortality in developed countries. Infants are born preterm at less than 37 weeks' gestational age after: (1) spontaneous labour with intact membranes, (2) preterm premature rupture of the membranes (PPROM), and (3) labour induction or caesarean delivery for maternal or fetal indications. The frequency of preterm births is about 12–13% in the USA and 5–9% in many other developed countries; however, the rate of preterm birth has increased in many locations, predominantly because of increasing indicated preterm births and preterm delivery of artificially conceived multiple pregnancies. Common reasons for indicated preterm births include pre-eclampsia or eclampsia, and intrauterine growth restriction. Births that follow spontaneous preterm labour and PPROM—together called spontaneous preterm births—are regarded as a syndrome resulting from multiple causes, including infection or inflammation, vascular disease, and uterine overdistension. Risk factors for spontaneous preterm births include a previous preterm birth, black race, periodontal disease, and low maternal body-mass index. A short cervical length and a raised cervical-vaginal fetal fibronectin concentration are the strongest predictors of spontaneous preterm birth.
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            The unique immunological and microbial aspects of pregnancy

            Although healthy pregnancies were traditionally considered to require an anti-inflammatory state, emerging evidence suggests that inflammation is important for a healthy pregnancy. Here, the authors discuss how the immune response varies throughout the main stages of pregnancy, and they consider how bacterial and viral infections can affect immune responses at the maternal–fetal interface.
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              The "Great Obstetrical Syndromes" are associated with disorders of deep placentation.

              Defective deep placentation has been associated with a spectrum of complications of pregnancy including preeclampsia, intrauterine growth restriction, preterm labor, preterm premature rupture of membranes, late spontaneous abortion, and abruptio placentae. The disease of the placental vascular bed that underpins these complications is commonly investigated with targeted biopsies. In this review, we critically evaluate the biopsy technique to summarize the salient types of defective deep placentation, and propose criteria for the classification of defective deep placentation into 3 types based on the degree of restriction of remodeling and the presence of obstructive lesions in the myometrial segment of the spiral arteries. Copyright © 2011 Mosby, Inc. All rights reserved.
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                Author and article information

                Journal
                100935741
                BJOG
                BJOG
                BJOG : an international journal of obstetrics and gynaecology
                1470-0328
                1471-0528
                30 November 2023
                April 2024
                30 November 2023
                01 April 2024
                : 131
                : 5
                : 538-550
                Affiliations
                [1 ]MRC Centre for Environment and Health, School of Public Health, Imperial College London, London, United Kingdom
                [2 ]National Institute for Health and Care Research Health Protection Research Unit in Environmental Exposures and Health, Imperial College London, London, United Kingdom
                [3 ]EGA Institute for Women's Health, Faculty of Population Health Sciences, University College London, London, UK
                [4 ]Mohn Centre for Children’s Health and Wellbeing, School of Public Health, Imperial College London, London, UK
                [5 ]Department of Physiology, Development and Neuroscience, University of Cambridge
                Author notes
                [* ] Correspondence: Julia C. Fussell. National Institute for Health Research Health Protection Research Unit in Environmental Exposures and Health, School of Public Health, Imperial College London, London W12 0BZ, U.K. julia.fussell@ 123456imperial.ac.uk
                Author information
                https://orcid.org/0000-0002-0057-6654
                https://orcid.org/0000-0003-0925-7737
                https://orcid.org/0000-0003-4000-2919
                https://orcid.org/0000-0001-8677-4143
                Article
                EMS191868
                10.1111/1471-0528.17727
                7615717
                38037459
                16d34f0a-b54f-48fe-83ec-13d6b4cbb61f

                This work is licensed under a BY 4.0 International license.

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                Categories
                Article

                Obstetrics & Gynecology
                adverse birth outcomes,ambient air pollution,endocrine disruption,epigenetic changes,inflammation,mechanisms,oxidative stress,placenta

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