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      Maternal exposure to ambient fine particulate matter and fetal growth in Shanghai, China

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          Abstract

          Background

          Fetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM 2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.

          Methods

          A total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM 2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM 2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO 2, NO 2, PM 10 and O 3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).

          Results

          The full model showed that with each 10 μg/m 3 increase in PM 2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (− 9.06, − 1.91), 5.57 (− 6.66, − 4.47), and 5.47 (− 6.39, − 4.55), respectively; the mean EFW decreased by 14.49 (− 16.05, − 13.49) grams by Hadlock’s third formula and 13.56 (− 14.71, − 12.50) grams by Shepard’s formula with each 10 μg/m 3 increase in PM 2.5 exposure.

          Conclusions

          A negative correlation existed between maternal PM 2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

          Electronic supplementary material

          The online version of this article (10.1186/s12940-019-0485-3) contains supplementary material, which is available to authorized users.

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          Most cited references29

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          Air Pollution and Noncommunicable Diseases

          Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (particulate matter with an aerodynamic diameter  103 million disability-adjusted life years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe.
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            Ambient particulate air pollution induces oxidative stress and alterations of mitochondria and gene expression in brown and white adipose tissues

            Background Prior studies have demonstrated a link between air pollution and metabolic diseases such as type II diabetes. Changes in adipose tissue and its mitochondrial content/function are closely associated with the development of insulin resistance and attendant metabolic complications. We investigated changes in adipose tissue structure and function in brown and white adipose depots in response to chronic ambient air pollutant exposure in a rodent model. Methods Male ApoE knockout (ApoE-/-) mice inhaled concentrated fine ambient PM (PM < 2.5 μm in aerodynamic diameter; PM2.5) or filtered air (FA) for 6 hours/day, 5 days/week, for 2 months. We examined superoxide production by dihydroethidium staining; inflammatory responses by immunohistochemistry; and changes in white and brown adipocyte-specific gene profiles by real-time PCR and mitochondria by transmission electron microscopy in response to PM2.5 exposure in different adipose depots of ApoE-/- mice to understand responses to chronic inhalational stimuli. Results Exposure to PM2.5 induced an increase in the production of reactive oxygen species (ROS) in brown adipose depots. Additionally, exposure to PM2.5 decreased expression of uncoupling protein 1 in brown adipose tissue as measured by immunohistochemistry and Western blot. Mitochondrial number was significantly reduced in white (WAT) and brown adipose tissues (BAT), while mitochondrial size was also reduced in BAT. In BAT, PM2.5 exposure down-regulated brown adipocyte-specific genes, while white adipocyte-specific genes were differentially up-regulated. Conclusions PM2.5 exposure triggers oxidative stress in BAT, and results in key alterations in mitochondrial gene expression and mitochondrial alterations that are pronounced in BAT. We postulate that exposure to PM2.5 may induce imbalance between white and brown adipose tissue functionality and thereby predispose to metabolic dysfunction.
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              Air Pollution Exposure During Pregnancy, Ultrasound Measures of Fetal Growth, and Adverse Birth Outcomes: A Prospective Cohort Study

              Background: Air pollution exposure during pregnancy might have trimester-specific effects on fetal growth. Objective: We prospectively evaluated the associations of maternal air pollution exposure with fetal growth characteristics and adverse birth outcomes in 7,772 subjects in the Netherlands. Methods: Particulate matter with an aerodynamic diameter < 10 μm (PM10) and nitrogen dioxide (NO2) levels were estimated using dispersion modeling at the home address. Fetal head circumference, length, and weight were estimated in each trimester by ultrasound. Information on birth outcomes was obtained from medical records. Results: In cross-sectional analyses, NO2 levels were inversely associated with fetal femur length in the second and third trimester, and PM10 and NO2 levels both were associated with smaller fetal head circumference in the third trimester [–0.18 mm, 95% confidence interval (CI): –0.24, –0.12 mm; and –0.12 mm, 95% CI: –0.17, –0.06 mm per 1-μg/m3 increase in PM10 and NO2, respectively]. Average PM10 and NO2 levels during pregnancy were not associated with head circumference and length at birth or neonatally, but were inversely associated with birth weight (–3.6 g, 95% CI: –6.7, –0.4 g; and –3.4 g, 95% CI: –6.2, –0.6 g, respectively). Longitudinal analyses showed similar patterns for head circumference and weight, but no associations with length. The third and fourth quartiles of PM10 exposure were associated with preterm birth [odds ratio (OR) = 1.40, 95% CI: 1.03, 1.89; and OR = 1.32; 95% CI: 0.96, 1.79, relative to the first quartile]. The third quartile of PM10 exposure, but not the fourth, was associated with small size for gestational age at birth (SGA) (OR = 1.38; 95% CI: 1.00, 1.90). No consistent associations were observed for NO2 levels and adverse birth outcomes. Conclusions: Results suggest that maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth. PM10 exposure was positively associated with preterm birth and SGA.
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                Author and article information

                Contributors
                zhijuancao@tongji.edu.cn
                menglulu586@163.com
                zy861201@163.com
                liuchao1020@gmail.com
                yyjenny1214@163.com
                xiujuan_su@tongji.edu.cn
                qingyanf@semc.gov.cn
                wangdf@semc.gov.cn
                86 21 20261428 , huajing_mih@163.com
                Journal
                Environ Health
                Environ Health
                Environmental Health
                BioMed Central (London )
                1476-069X
                16 May 2019
                16 May 2019
                2019
                : 18
                : 49
                Affiliations
                [1 ]ISNI 0000000123704535, GRID grid.24516.34, Department of Women and Children’s Health Care, Shanghai First Maternity and Infant Hospital, , Tongji University School of Medicine, ; Shanghai, China
                [2 ]ISNI 0000000123704535, GRID grid.24516.34, College of Architecture and Urban Planning, , Tongji University, ; Siping Rd. 1239, Shanghai, 200082 China
                [3 ]Shanghai Environmental Monitoring Centre, Shanghai, China
                Author information
                http://orcid.org/0000-0002-7037-3748
                Article
                485
                10.1186/s12940-019-0485-3
                6524254
                31096994
                5863d599-c7fa-427a-bbb0-4633e8493f7f
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 20 December 2018
                : 23 April 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81703233
                Award ID: 81673179
                Award ID: 81602860
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100008410, Shanghai Municipal Population and Family Planning Commission;
                Award ID: 20184Y0078
                Award ID: 20174Y0100
                Award Recipient :
                Funded by: Shanghai Sailing Program
                Award ID: 18YF1419600
                Award Recipient :
                Funded by: Fundamental Research Funds for Central Universities
                Award ID: 22120180038
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                Public health
                pm2.5,ultrasound measures,maternal exposure,fetal growth restriction,china
                Public health
                pm2.5, ultrasound measures, maternal exposure, fetal growth restriction, china

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