Air Pollution and the Risk of Birth Defects in Anqing City, China

Yao, Cijiang; Chen, Yanyan; Zhu, Xiaoxia; Liu, Ying; Zhang, Jian; Hou, Lijuan; Xu, Yachun; Zhang, Chao; Cao, Jiyu

doi:10.1097/jom.0000000000000676

Cited by 16 publications

(5 citation statements)

References 26 publications

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“…Conversely, they differed from those obtained by Dadvand et al [ 32 ], which showed an inverse relationship between maternal exposure to SO 2 and risk of ventricular septal defect similarly to Strickland et al [ 23 ] and Hansen et al [ 24 ]. More recently, the association between the exposure to ambient SO 2 during pregnancy and an increase in birth risk defects has been confirmed in a retrospective study conducted in Anqing city of Eastern China [ 39 ].…”

Section: Air Pollutant Exposure and Chd Risk: Epidemiological Evidmentioning

confidence: 93%

Genetic and Epigenetic Mechanisms Linking Air Pollution and Congenital Heart Disease

Vecoli

Pulignani

Andreassi

2016

JCDD

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Epidemiological studies strongly suggest that parental air pollutants exposure during the periconceptional period may play a major role in causing fetal/newborn malformations, including a frequent heterogeneity in the methods applied and a difficulty in estimating the clear effect of environmental toxicants. Moreover, only some couples exposed to toxicants during the pre-conception period give birth to a child with congenital anomalies. The reasons for such phenomena remain elusive but they can be explained by the individual, innate ability to metabolize these contaminants that eventually defines the ultimate dose of a biological active toxicant. In this paper, we reviewed the major evidence regarding the role of parental air pollutant exposure on congenital heart disease (CHD) risk as well as the modulating effect on detoxification systems. Finally, major epigenetic alterations induced by adverse environment contaminants have been revised as possible mechanisms altering a correct heart morphogenesis.

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Section: Air Pollutant Exposure and Chd Risk: Epidemiological Evidmentioning

confidence: 93%

Genetic and Epigenetic Mechanisms Linking Air Pollution and Congenital Heart Disease

Vecoli

Pulignani

Andreassi

2016

JCDD

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“…[13] The retrospective cohort study in Anqing city, Eastern China, suggested that exposure to ambient sulfur dioxide (SO 2 ) during pregnancy may increase the risk of birth defects. [12] The study in Lanzhou, China, investigated a cohort of 8969 singleton live births by using inverse distance weighting way for exposure assessment found positive associations for congenital malformations of cardiac septa with PM 10 exposures in the second trimester and the entire pregnancy, and SO 2 exposures in the entire pregnancy. [11] In a word, there were differences in the studies in the selection of subgroups of birth defects, exposure window, exposure assessment method and adjustments for confounding factors, and the representativeness problem that each study conducted in different areas.…”

Section: Introductionmentioning

confidence: 99%

The association between ambient air pollution and birth defects in four cities in Hunan province, China, from 2014 to 2016

Xiong¹,

Zenghui

Wang³

et al. 2019

Medicine

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This study was performed to assess whether air pollution was positively associated with birth defects and if a specific pregnancy stage played a role. This was a population-based case-control study comprising 153,822 perinatal births in four cities located in Hunan province, China, during the period 2014 to 2016. Exposure to SO2, NO2, and PM10 in each pregnant woman in the first 3 months before pregnancy, and in the first and third trimester was assessed. The risk of birth defects related to SO2 in the first 3 months before pregnancy was between 1.191 and 1.566. In the first trimester stage the risk was between 1.104 and 1.348. The risk of birth defects related to NO2 before pregnancy was 1.285 (95%CI: 1.180–1.399), in the first trimester stage the risk was between 1.280 (95%CI: 1.197–1.368) and 1.380 (95%CI: 1.293–1.473). In the third month before delivery the risk was 1.484 (95%CI: 1.366–1.613). The risk of birth defects related to PM10 in the first month of pregnancy was 1.098 (95%CI: 1.057–1.140), and in the third month before delivery the risk was 1.296 (95%CI: 1.222–1.375). SO2 had a greater effect on the prophase of pregnancy, while NO2 and PM10 had an effect in the late third trimester.

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“…Twenty of the 70 studies included in the review (29%) investigated the role of urban air pollution and CHD in urban areas from sources such as traffic amd coal-fired power stations [83][84][85][86][87][88][89][90][91][92][93][94][95][96][97][98][99][100][101][102]. These studies examined criteria pollutants such as NO 2 , SO 2 , CO, O 3 , PM2.5 and PM10 measured from fixed monitoring stations.…”

Section: Urban Air Pollutionmentioning

confidence: 99%

“…All the studies represented case control studies and assigned exposure to the vulnerable window of cardiogenesis between the 3rd and 5th week post conception [103]. Generally, CO was associated with septal defects, pulmonary valve stenosis or pulmonary artery stenosis [83,88] but other studies reported inverse associations between CO and ventricular septal and conotruncal defects [84]; NO 2 was associated with coarctation of aorta, pulmonary valve stenosis and patent ductus arteriosus [92,93,99,102] but others found no associations with CHD [96]; SO 2 was associated with aortic valve stenosis, septal defects, CHD [91,96,99] and others found no associations with CHD and its subtypes [85,88]; O 3 was associated with pulmonary valve stenosis, pulmonary artery stenosis, patent ductus arteriosus and septal defects [84,94] and no associations were found with CHD in other studies [86,87,100]; PM10 was associated with patent ductus arteriosus, pulmonary valve stenosis, ventricular septal defects, transposition of the great arteries, multiple CHD, tetralogy of Fallot [84,89,90,94,98,99] whilst other studies found no associations with CHD [83,[95][96][97]; PM2.5 was associated with transposition of the great arteries, hypoplastic left heart syndrome and ventricular septal defects [90,93,97] and others found no associations [89,100]. One study by Stingone et al examined multipollutant exposures from urban air pollutants and found associations with left ventricular outflow tract obstruction…”

Section: Urban Air Pollutionmentioning

confidence: 99%

Environmental pollution and the development of congenital heart disease: A scoping review

Ngwezi¹,

Hornberger²,

Osornio-Vargas³

2018

apr

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Introduction: Congenital heart disease (CHD) is the most common congenital anomaly in infancy affecting 1% of all live births worldwide of which the etiology in most affected children is unknown. The role of environmental pollutants from various sources is increasingly gaining attention. To explore the existing breadth of knowledge on this topic, we undertook a scoping review of studies examining the role of environmental pollution in relation to the development of CHD.Methods: We searched various databases for studies reporting CHD and exposures to chemicals using Medical Subject Headings (MeSH) and non-MeSH including criteria pollutants (e.g. CO, SO 2, NO 2 ), occupational, non-occupational, industrial chemicals and emissions reported in pollutant release and transfer registers (PRTR) from 1980 to 2018. Results:We identified 70 studies that were grouped into the categories of outdoor industrial chemical pollution; urban air pollution; occupational; and non-occupational exposures. There were no marked differences in proportions of studies in the first three categories, which ranged between 29-33%. Nonoccupational exposures accounted for 7% of the studies. Proximity to industrial facilities and hazardous waste sites was associated with CHD in a modest number of studies that used PRTR. Urban criteria pollutants were consistently associated with CHD. Maternal occupational exposures were more commonly studied compared to paternal exposures and organic solvents were associated with CHD in these studies. There were limited studies that examined non-occupational and multipollutant exposures. Conclusion:We identified associations between various chemicals and CHD, employing diverse methods of exposure assessment. Most studies examined single pollutant exposures and have demonstrated inconclusive findings. Future studies should examine multiple pollutant exposures and CHD. In addition to monitored data, exploratory studies could exploit PRTR in countries where such registers exist. Furthermore, multicenter studies that examine larger populations of affected patients could facilitate the discovery of the relationship between specific chemicals and CHD subtypes.

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Air Pollution and the Risk of Birth Defects in Anqing City, China

Abstract: The results suggested that exposure to ambient SO2 during pregnancy may increase the risk of birth defects.

Cited by 16 publications

References 26 publications

Genetic and Epigenetic Mechanisms Linking Air Pollution and Congenital Heart Disease

Genetic and Epigenetic Mechanisms Linking Air Pollution and Congenital Heart Disease

The association between ambient air pollution and birth defects in four cities in Hunan province, China, from 2014 to 2016

Environmental pollution and the development of congenital heart disease: A scoping review

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