电子垃圾拆解区化学污染物复合暴露对儿童听觉系统发育的影响

Exposure to environmental pollutants can cause adverse effects on the development of auditory system in children. Our previous studies indicated that higher concentration of heavy metals and organic pollutants, such as lead, mercury, cadmium, polychlorinated biphenyls, polybrominated diphenyl ethers, and polycyclic aromatic hydrocarbons, may correlate with hearing loss in children from Guiyu, an electronic waste recycling area. Epidemiological investigation also showed an increased morbidity of child hearing loss in this region. Therefore, we hypothesize that co-exposure to multiple heavy metals and organic pollutants may cause ototoxicity in children and consequently results in hearing loss. To demonstrate the relationship between the sources, levels and distribution of these pollutants and their contribution to ototoxicity and hearing loss, we designed the project to find out ototoxicity-related exposure biomarkers and endpoint effects by measuring pollutant concentrations in blood, urine and cerumen samples from preschool children and examining the hearing threshold and cochlea function through pure tone audiometry (PTA) and distortion product otoacoustic emissions (DPOAE). Besides, a cohort study is conducted to determine the crucial age during which the cochlea development mostly susceptible to chemical pollutants. Furthermore, to elucidate the genetic mechanisms of hearing loss induced by chemical pollutants, epigenetic studies are intended to identify the relevant susceptible genes and gene-environment interactions by detecting the methylation status of genes associated with ototoxicity and verifying the related miRNA expression. We hope this work will provide evidences for the prevention and control of hearing loss in children, especially those living in contaminated areas.

环境污染物暴露会影响儿童听觉系统的正常发育。我们前期研究显示：贵屿电子垃圾拆解区儿童体内铅、汞、镉、多氯联苯、多溴联苯醚、多环芳烃等多种重金属和有机污染物水平均高于对照组，且听力损失与上述污染物暴露水平有关，流行病学调查也表明该地区耳聋患儿发病率较高。我们认为多种重金属和有机污染物暴露可联合作用引起耳毒性，造成儿童听力损失。为此，本项目将通过纯音听阈和畸变产物耳声发射检测听力阈值和耳蜗功能；采集儿童血液、尿液、耵聍等样本，检测多种污染物的暴露水平，揭示污染物暴露种类、浓度、分布与耳蜗功能状态和听力损失之间的关系，找出耳毒性依次重要的污染物，分析污染物之间的联合毒性作用。通过队列研究，阐明耳蜗功能在发育过程中最容易受到污染物影响的关键期；通过检测与听力损失相关基因的甲基化状态、听觉功能相关miRNA的表达状态，探讨污染物暴露对儿童听觉系统影响的表观遗传学机制，为防控儿童听力损失提供科学依据。

环境污染物暴露会影响儿童听觉系统的正常发育。我们前期研究显示：贵屿电子垃圾拆解区儿童体内铅、汞、镉、多氯联苯、多溴联苯醚、多环芳烃等多种重金属和有机污染物水平均高于参照组，且听力损失与上述污染物暴露水平有关，流行病学调查也表明该地区耳聋患儿发病率较高。重金属和有机污染物暴露可联合作用引起耳毒性，造成儿童听力损失。本项目通过纯音听阈和畸变产物耳声发射检测听力阈值和耳蜗功能；采集儿童血液、尿液、耵聍等样本，检测多种污染物的暴露水平，揭示了污染物暴露种类、浓度、分布与耳蜗功能状态和听力损失之间的关系。研究结果发现：电子垃圾拆解区贵屿学龄前儿童体内重金属（Mg、Ca、Mn、Fe、Co、Cu、Zn、As、Mo、Cd、Sb、Hg、Ti、Pb）及有机污染物（PCBs、PBDEs及ΣOHPAH)水平均高于参照组；铅、镉等重金属暴露会增加儿童听力损失的风险，有机污染物PCBs和PBDEs对儿童听力影响存在交互效应；通过队列研究，检测与听力损失相关基因的甲基化状态、听觉功能相关miRNA的表达状态，发现cg02978827、position+14、position+4、cg23882545和下游启动子平均甲基化水平与血铅水平呈负相关，cg unknown和position+10甲基化水平与血铅水平呈负相关。这些结果从表观遗传学上证明了污染物暴露与儿童听力损失相关，为防控儿童听力损失提供科学依据。