您的位置：山东大学 -> 科技期刊社 -> 《山东大学学报（医学版）》

山东大学学报 (医学版) ›› 2018, Vol. 56 ›› Issue (11): 111-115.doi: 10.6040/j.issn.1671-7554.0.2018.780

• • 上一篇    

青岛人群孕期多环芳烃暴露对婴幼儿发育的影响

崔静1,孙治涛1,谢萌2,张倩3,王炳玲1,高汝钦1   

  1. 1.青岛市疾病预防控制中心, 青岛市预防医学研究院, 山东 青岛 266033;2.山东省疾病预防控制中心计划免疫所, 山东 济南 250014;3.青岛市黄岛区妇幼保健计划生育服务一中心, 山东 青岛 266000
  • 发布日期:2022-09-27
  • 通讯作者: 王炳玲. E-mail:binglingw@yeah.com
  • 基金资助:
    国家自然科学基金面上项目(81372955);中国疾控妇幼保健中心合生元母婴营养与健康研究基金(2017FYH008);山东省医药卫生科技发展计划(2016WS0309);青岛市医疗卫生优秀人才培养项目(2017-2019)

Effects of polycyclic aromatic hydrocarbons exposure during pregnancy on the development of infant in Qingdao City, China

CUI Jing1, SUN Zhitao1, XIE Meng2, ZHANG Qian3, WANG Bingling1, GAO Ruqin1   

  1. 1. Qingdao Municipal Center for Disease Control and Prevention, Qingdao Institute of Preventive Medicine, Qingdao 266033, Shandong, China;
    2. Division of Expanded Immunization Program, Shandong Center for Disease Control and Prevention, Jinan 250014, Shandong, China;
    3. Maternal and Child Health Care of Family Planning Service Center of Huangdao District, Qingdao 266000, Shandong, China
  • Published:2022-09-27

PDF (PC)

8

摘要： 目的 采用出生队列研究设计,探讨青岛人群孕期多环芳烃(PAHs)暴露水平对6月、12月龄婴幼儿发育的影响。 方法 选择2014年1~12月间出生的348例婴幼儿作为研究对象进行脐带血PAH-DNA加合物测定,使用盖泽尔发育诊断量表测定婴幼儿6月、12月龄的发育商(DQ),Spearman相关检验分析PAH-DNA加合物与6月、12月龄DQs的相关性,线性回归模型分析PAH-DNA加合物对12月龄DQs的影响。 结果 研究对象的PAH-DNA加合物的检出率为52.4%,6月龄五个功能区的DQs得分在66~118间,12月龄的在72~156间。Spearman相关性分析结果显示,检出的PAH-DNA加合物水平与12月龄的大动作行为(r=-0.188)、精细动作行为(r=-0.196)、个人社交行为(r=-0.180)均呈负相关关系,且差异有统计学意义(P<0.05)。在调整了幼儿性别、孕妇年龄、出生体质量、母亲文化水平后,检出的PAH-DNA加合物与12月龄幼儿的适应性行为、大动作行为、精细动作行为、语言行为、个人社交行为呈负相关(P<0.05)。 结论 孕期PAHs暴露可能对12月龄儿童发育产生不利影响,故降低孕期PAHs暴露水平对婴幼儿早期发育损伤具有一定的预防作用。

关键词: 多环芳烃, 神经发育, 婴幼儿, 多环芳烃-DNA加合物

Abstract: Objective To explore the effects of polycyclic aromatic hydrocarbons(PAHs)exposure during pregnancy on the development of infants aged 6 and 12 months in a birth cohort in Qingdao City. Methods A total of 348 infants born during Jan. and Dec. 2014 were enrolled in this analysis. PAH-DNA adduct of umbilical cord blood was determined, and development quotients(DQs)were measured at the ages of 6 and 12 months with Gesell Development Inventory. The correlation between PAH-DNA adduct and DQs at the ages of 6 and 12 months was assessed with Spearman correlation analysis. The effects of PAH-DNA adduct on the DQs at the age of 12 months was evaluated with linear regression models. Results The detection rate of PAH-DAN adduct was 52.4%. The DQs of 5 functional areas ranged from 66 to 118 at the age of 6 months, and ranged from 72 to 156 at the age of 12 months. Spearman correlation 山 东 大 学 学 报 (医 学 版)56卷11期 -崔静,等.青岛人群孕期多环芳烃暴露对婴幼儿发育的影响 \=-analysis showed that the PAH-DNA adduct levels were negatively correlated with the DQs of gross motor(r=0.188), fine motor(r=0.196), and personal social behavior(r=0.180)at the age of 12 months, and the differences were statistically significant(P<0.05). After the gender of infants, age of pregnant woman, birth weight, and educational levels of pregnant woman were adjusted, the PAH-DNA adduct levels were negatively correlated with the DQs of adaptive, gross motor, fine motor, language, and personal social behavior at the age of 12 months(P<0.05). Conclusion PAHs exposure during pregnancy may have adverse effects on the development of 12-month-old infants. Reducing PAHs exposure has certain preventive effects on the early developmental damage in infants.

Key words: Polycyclic aromatic hydrocarbons, Neurodevelopment, Infant, PAH-DNA adduct

中图分类号: 

  • R114
[1] Perera F, Tang D, Whyatt R, et al. DNA damage from polycyclic aromatic hydrocarbons measured by benzo[a] pyrene-DNA adducts in mothers and newborns from Northern Manhattan, the World Trade Center Area, Poland, and China[J]. Cancer Epidemiol Biomark Prev, 2005, 14(3): 709-714.
[2] Kim JJ. Ambient air pollution: health hazards to children[J]. Pediatrics, 2004, 114(6): 1699-1707.
[3] Sanyal MK, Li YL. Deleterious effects of polynuclear aromatic hydrocarbon on blood vascular system of the rat fetus[J]. Birth Defects Res B Dev Reprod Toxicol, 2007, 80(5): 367-373.
[4] Dong W, Wang L, Thornton C, et al. Benzo(a)pyrene decreases brain and ovarian aromatase mRNA expression in Fundulus heteroclitus[J]. Aquat Toxicol, 2008, 88(4): 289-300.
[5] Takeda K, Tsukue N, Yoshida S. Endocrine-disrupting activity of chemicals in diesel exhaust and diesel exhaust particles[J]. Environ Sci, 2004, 11(1): 33-45.
[6] Wormley DD, Chirwa S, Nayyar T, et al. Inhaled benzo(a)pyrene impairs long-term potentiation in the F1 generation rat dentate gyrus[J]. Cell Mol Biol(Noisy-le-grand), 2004, 50(6): 715-721.
[7] Archibong AE, Inyang F, Ramesh A, et al. Alteration of pregnancy-related hormones and fetal survival in F-344 rats exposed by inhalation to benzo(a)pyrene[J]. Reprod Toxicol, 2002, 16(6): 801-808.
[8] 谢萌. 出生队列儿童1岁龄多环芳烃暴露对其神经发育的影响[D]. 青岛:青岛大学, 2017.
[9] Perera FP, Li Z, Whyatt R, et al. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5 years[J]. Pediatrics, 2009, 124(2): 195-202.
[10] Perera FP, Rauh V, Whyatt RM, et al. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among Inner-City children[J]. Environ Health Perspect, 2006, 114(8): 1287-1292.
[11] Perera F, Li TY, Zhou ZJ, et al. Benefits of reducing prenatal exposure to coal-burning pollutants to childrens neurodevelopment in China[J]. Environ Health Perspect, 2008, 116(10): 1396-400.
[12] Kalia V, Perera F, Tang D. Environmental Pollutants and Neurodevelopment: Review of Benefits From Closure of a Coal-Burning Power Plant in Tongliang, China[J]. Glob Pediatr Health, 2017, 31, 4: 2333794X17721609. doi: 10.1177/2333794X17721609. eCollection 2017.
[13] Perera F, Li TY, Zhou ZJ, et al. Benefits of reducing prenatal exposure to coal-burning pollutants to childrens neurodevelopment in China[J]. Environ Health Perspect, 2008, 116(10): 1396-400.
[14] Perera FP, Rauh V, Tsai WY, et al. Effects of transplacental exposure to environmental pollutants on birth outcomes in a multiethnic population[J]. Environ Health Perspect, 2003, 111(2): 201-205.
[15] Perera FP, Rauh V, Whyatt RM, et al. A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures[J]. Neurotoxicology, 2005, 26(4): 573-587.
[16] Herbstman JB, Tang D, Zhu D, et al. Prenatal exposure to polycyclic aromatic hydrocarbons, benzo[a] pyrene-DNA adducts, and genomic DNA methylation in cord blood[J]. Environ Health Perspect, 2012, 120(5): 733-738.
[17] Pereira RD, De Long NE, Wang RC, et al. Angiogenesis in the placenta: the role of reactive oxygen species signaling[J]. Biomed Res Int, 2015, 2015(8): 814543. doi: 10.1155/2015/814543. Epub 2015 Jan 29. Review.
[18] Lee J, Kalia V, Perera F, et al. Prenatal airborne polycyclic aromatic hydrocarbon exposure, LINE1 methylation and child development in a Chinese cohort[J]. Environ Int, 2017, 99: 315-320.
[19] Saunders CR, Das SK, Ramesh A, et al. Benzo(a)pyrene-induced acute neurotoxicity in the F-344 rat: role of oxidative stress[J]. J Appl Toxicol, 2006, 26(5): 427-438.
[20] Block ML, Calderón-Garcidueñas L. Air pollution: mechanisms of neuroinflammation and CNS disease[J]. Trends Neurosci, 2009, 32(9): 506-516.
[21] Perera F, Phillips DH, Wang Y, et al. Prenatal exposure to polycyclic aromatic hydrocarbons/aromatics, BDNF and child development[J]. Environ Res, 2015, 142(3): 602-608.
[22] Brown LA, Khousbouei H, Goodwin JS, et al. Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo(a)pyrene[J]. Neurotoxicology, 2007, 28(5): 965-978.
[23] Dutta K, Ghosh D, Nazmi A, et al. A common carcinogen benzo[a] pyrene causes neuronal death in mouse via microglial activation[J]. PLoS One, 2010, 5(4): e9984. doi: 10.1371/journal.pone.0009984.
[24] Dejmek J, Solanský I, Benes I, et al. The impact of polycyclic aromatic hydrocarbons and fine particles on pregnancy outcome[J]. Environ Health Perspect, 2000, 108(12): 1159-1164.
[1] 王增敏,韩金燕,李桂梅. GnRHa联合rhGH治疗婴幼儿灰结节错构瘤1例并文献复习[J]. 山东大学学报 (医学版), 2022, 60(2): 48-53.
[2] 马燕燕,龚瑶琴. 人脑类器官在神经发育疾病研究中的应用[J]. 山东大学学报 (医学版), 2021, 59(9): 22-29.
[3] 曹萌,王丽珩,彭秀苗,崔亮亮. 2016~2020年济南市两城区大气PM2.5中多环芳烃浓度特征及慢性健康风险评估[J]. 山东大学学报 (医学版), 2021, 59(12): 87-95.
[4] 吴义良,张林峰,李圆,刘筱雯,徐广琪,高峰,吕仁荣,霍然. 超高频超声与高频超声在浅表性婴幼儿血管瘤中的应用[J]. 山东大学学报（医学版）, 2016, 54(12): 72-76.
[5] 徐荣建，王法刚，党伟,曹永倩，林莉,韦浩，赵君，国丽. 激光治疗对婴幼儿皮肤血管瘤患者血浆VEGF及bFGF表达的影响[J]. 山东大学学报(医学版), 2013, 51(4): 96-99.
[6] . 大前庭水管综合征婴幼儿患者ASSR和ABR听力学特点[J]. 山东大学学报(医学版), 2009, 47(8): 89-92.
[7] 张爱华 杨达宽. 持续超滤在婴幼儿体外循环手术中的临床应用[J]. 山东大学学报(医学版), 2009, 47(5): 99-101.
[8] 石广永,张供,李跃华. 改良超滤在婴幼儿心内直视手术中的临床应用[J]. 山东大学学报(医学版), 2008, 46(6): 628-630.
[9] 边致强,刘亚群,李笃民,崔凤玉. 多层螺旋CT对婴幼儿先天性感音性耳聋的诊断价值[J]. 山东大学学报(医学版), 2007, 45(12): 1257-1260.
[10] 孙文秀,王学禹,温兆春,高玉兴,王如明. 婴幼儿毒鼠强中毒特点及血液灌流疗效观察[J]. 山东大学学报(医学版), 2006, 44(5): 524-527.
[11] 孙文秀,王学禹,温兆春,高玉兴,王如明. 婴幼儿毒鼠强中毒特点及血液灌流疗效观察[J]. 山东大学学报(医学版), 2006, 44(5): 524-527.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
版权所有 © 2018 《山东大学学报(医学版)》编辑部　
地址:山东大学科技期刊社（济南市历城区山大南路27号山东大学中心校区明德楼B座721室） 电话: 0531-88366918 E-mail: xbyxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发