Tags

Type your tag names separated by a space and hit enter

Effects of prenatal exposure to air particulate matter on the risk of preterm birth and roles of maternal and cord blood LINE-1 methylation: A birth cohort study in Guangzhou, China.
Environ Int. 2019 12; 133(Pt A):105177.EI

Abstract

BACKGROUND

Epidemiological studies have found that increased risk of preterm birth (PTB) is associated with higher prenatal exposure to PM10 and PM2.5, but few studies have been conducted to assess the impacts of extremely fine particulate matter (PM1) which may have more toxic effects than other types of ambient particulate air pollution (PM). Several studies have separately investigated the associations between DNA methylation and PTB risk and PM. Maternal LINE-1 methylation level negatively correlated with prenatal exposure to PM and risk of PTB. A comprehensive picture is lacking regarding the associations between prenatal exposure to PM, LINE-1 methylation, and risk of PTB.

OBJECTIVES

This study aimed to estimate the effects of exposure to ambient PM (PM10, PM2.5, and PM1) of different sizes during pregnancy on risk of PTB, identify susceptible exposure windows, and illustrate the roles of LINE-1 methylation in the associations between PM and PTB risk.

METHODS

The Birth Cohort Study on Prenatal Environments and Offspring Health (PEOH) has been ongoing since 2016 in Guangzhou, China. A total of 4928 pregnant women were recruited during early pregnancy, and 4278 (86.8%) were successfully followed-up. Each individual weekly exposure to PM10 and PM2.5 from 3 months before pregnancy to childbirth was assessed using a spatiotemporal land use regression model, and the weekly PM1 exposure was estimated by employing a generalized additive model. Maternal and cord blood LINE-1 methylation levels (%5mC) were tested using bisulfite-PCR pyrosequencing. A distributed lag nonlinear model incorporated with a Cox proportional hazard model was applied to assess the effect of weekly-specific maternal PM exposure on PTB risk, and a multiple-linear regression model was employed to investigate the associations between PM exposure and LINE-1 methylation levels of maternal and cord bloods. We also assessed the associations between LINE-1 methylation levels and PTB risk by using a logistic regression model.

RESULTS

The risk of PTB was positively associated with PM2.5 and PM1 concentrations during the 12th to 20th gestational weeks, and the strongest association was in the fourth quartile (Q4) versus the first quartile (Q1) and observed during the 16th gestational week (PM2.5: harzard ratio [HR] = 1.18, 95%CI: 1.04-1.35, IQR = 11.94 μg/m3. PM1: HR = 1.20, 95%CI: 1.03-1.39, IQR = 11.36 μg/m3). We observed significantly negative associations of PM10(β = -0.51%5mC per 10 μg/m3, P = 0.014), PM2.5 (β = -0.66%5mC per 10 μg/m3, P = 0.032) and PM1 (β = -0.67%5mC per 10 μg/m3, P = 0.032) concentrations with cord blood LINE-1 methylation levels, and a negative association between PM1 concentration and maternal LINE-1 methylation level (β = -0.86%5mC per 10 μg/m3, P = 0.034).

CONCLUSION

Higher prenatal exposure to PM1 and PM2.5 during the 12th to 20th gestational weeks was associated with increased risk of PTB. Maternal and fetal LINE-1 methylation alternation might be an underlying mechanism of PM that increasing the risk of PTB.

Authors+Show Affiliations

Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangzhou Panyu Central Hospital, Guangzhou 511400, China.Guangzhou Panyu Central Hospital, Guangzhou 511400, China.Department of Environmental and Occupational Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510080, China.School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510080, China.Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia.School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China; General Practice Center, Nanhai Hospital, Southern Medical University, Foshan 528200, China.General Practice Center, Nanhai Hospital, Southern Medical University, Foshan 528200, China.Food Safety and Health Research Center, School of Public Health, Southern Medical University, Guangzhou 510515, China; Department of Environmental and Occupational Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China. Electronic address: cnzhangbo@126.com.Guangdong Provincial Institute of Public Health, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou 511430, China; General Practice Center, Nanhai Hospital, Southern Medical University, Foshan 528200, China. Electronic address: gztt_2002@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

31622906

Citation

Liu, Xin, et al. "Effects of Prenatal Exposure to Air Particulate Matter On the Risk of Preterm Birth and Roles of Maternal and Cord Blood LINE-1 Methylation: a Birth Cohort Study in Guangzhou, China." Environment International, vol. 133, no. Pt A, 2019, p. 105177.
Liu X, Ye Y, Chen Y, et al. Effects of prenatal exposure to air particulate matter on the risk of preterm birth and roles of maternal and cord blood LINE-1 methylation: A birth cohort study in Guangzhou, China. Environ Int. 2019;133(Pt A):105177.
Liu, X., Ye, Y., Chen, Y., Li, X., Feng, B., Cao, G., Xiao, J., Zeng, W., Li, X., Sun, J., Ning, D., Yang, Y., Yao, Z., Guo, Y., Wang, Q., Zhang, Y., Ma, W., Du, Q., Zhang, B., & Liu, T. (2019). Effects of prenatal exposure to air particulate matter on the risk of preterm birth and roles of maternal and cord blood LINE-1 methylation: A birth cohort study in Guangzhou, China. Environment International, 133(Pt A), 105177. https://doi.org/10.1016/j.envint.2019.105177
Liu X, et al. Effects of Prenatal Exposure to Air Particulate Matter On the Risk of Preterm Birth and Roles of Maternal and Cord Blood LINE-1 Methylation: a Birth Cohort Study in Guangzhou, China. Environ Int. 2019;133(Pt A):105177. PubMed PMID: 31622906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of prenatal exposure to air particulate matter on the risk of preterm birth and roles of maternal and cord blood LINE-1 methylation: A birth cohort study in Guangzhou, China. AU - Liu,Xin, AU - Ye,Yufeng, AU - Chen,Yi, AU - Li,Xiaona, AU - Feng,Baixiang, AU - Cao,Ganxiang, AU - Xiao,Jianpeng, AU - Zeng,Weilin, AU - Li,Xing, AU - Sun,Jiufeng, AU - Ning,Dan, AU - Yang,Yi, AU - Yao,Zhenjiang, AU - Guo,Yuming, AU - Wang,Qiong, AU - Zhang,Yonghui, AU - Ma,Wenjun, AU - Du,Qingfeng, AU - Zhang,Bo, AU - Liu,Tao, Y1 - 2019/10/14/ PY - 2019/05/16/received PY - 2019/08/10/revised PY - 2019/09/09/accepted PY - 2019/10/18/pubmed PY - 2019/10/18/medline PY - 2019/10/18/entrez KW - Birth cohort study KW - LINE-1 methylation KW - Particulate matter KW - Preterm birth KW - Susceptible exposure window SP - 105177 EP - 105177 JF - Environment international JO - Environ Int VL - 133 IS - Pt A N2 - BACKGROUND: Epidemiological studies have found that increased risk of preterm birth (PTB) is associated with higher prenatal exposure to PM10 and PM2.5, but few studies have been conducted to assess the impacts of extremely fine particulate matter (PM1) which may have more toxic effects than other types of ambient particulate air pollution (PM). Several studies have separately investigated the associations between DNA methylation and PTB risk and PM. Maternal LINE-1 methylation level negatively correlated with prenatal exposure to PM and risk of PTB. A comprehensive picture is lacking regarding the associations between prenatal exposure to PM, LINE-1 methylation, and risk of PTB. OBJECTIVES: This study aimed to estimate the effects of exposure to ambient PM (PM10, PM2.5, and PM1) of different sizes during pregnancy on risk of PTB, identify susceptible exposure windows, and illustrate the roles of LINE-1 methylation in the associations between PM and PTB risk. METHODS: The Birth Cohort Study on Prenatal Environments and Offspring Health (PEOH) has been ongoing since 2016 in Guangzhou, China. A total of 4928 pregnant women were recruited during early pregnancy, and 4278 (86.8%) were successfully followed-up. Each individual weekly exposure to PM10 and PM2.5 from 3 months before pregnancy to childbirth was assessed using a spatiotemporal land use regression model, and the weekly PM1 exposure was estimated by employing a generalized additive model. Maternal and cord blood LINE-1 methylation levels (%5mC) were tested using bisulfite-PCR pyrosequencing. A distributed lag nonlinear model incorporated with a Cox proportional hazard model was applied to assess the effect of weekly-specific maternal PM exposure on PTB risk, and a multiple-linear regression model was employed to investigate the associations between PM exposure and LINE-1 methylation levels of maternal and cord bloods. We also assessed the associations between LINE-1 methylation levels and PTB risk by using a logistic regression model. RESULTS: The risk of PTB was positively associated with PM2.5 and PM1 concentrations during the 12th to 20th gestational weeks, and the strongest association was in the fourth quartile (Q4) versus the first quartile (Q1) and observed during the 16th gestational week (PM2.5: harzard ratio [HR] = 1.18, 95%CI: 1.04-1.35, IQR = 11.94 μg/m3. PM1: HR = 1.20, 95%CI: 1.03-1.39, IQR = 11.36 μg/m3). We observed significantly negative associations of PM10(β = -0.51%5mC per 10 μg/m3, P = 0.014), PM2.5 (β = -0.66%5mC per 10 μg/m3, P = 0.032) and PM1 (β = -0.67%5mC per 10 μg/m3, P = 0.032) concentrations with cord blood LINE-1 methylation levels, and a negative association between PM1 concentration and maternal LINE-1 methylation level (β = -0.86%5mC per 10 μg/m3, P = 0.034). CONCLUSION: Higher prenatal exposure to PM1 and PM2.5 during the 12th to 20th gestational weeks was associated with increased risk of PTB. Maternal and fetal LINE-1 methylation alternation might be an underlying mechanism of PM that increasing the risk of PTB. SN - 1873-6750 UR - https://www.unboundmedicine.com/medline/citation/31622906/Effects_of_prenatal_exposure_to_air_particulate_matter_on_the_risk_of_preterm_birth_and_roles_of_maternal_and_cord_blood_LINE_1_methylation:_A_birth_cohort_study_in_Guangzhou_China_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0160-4120(19)31649-6 DB - PRIME DP - Unbound Medicine ER -