{"title":"空气污染与突发性感音神经性听力损失风险的相关性:一项孟德尔随机研究。","authors":"Xiaoli Luo, Wenqi Zuo, Quanwei Ren, Linlin Wang, Di Wu, Yilin Xiang, Shixun Zhong","doi":"10.1038/s41598-025-92952-3","DOIUrl":null,"url":null,"abstract":"<p><p>Numerous compelling epidemiological studies have linked air pollution to Sudden Sensorineural Hearing Loss (SSNHL). However, the causal relationship behind this association has not yet been established. We employed a Two-Sample Mendelian Randomization (MR) approach to investigate the causal relationship between air pollution (nitrogen dioxide, nitrogen oxides, PM<sub>2.5</sub>, PM<sub>10</sub>, and PM<sub>2.5-10</sub>) and SSNHL.Independent genetic variants associated with air pollution and SSNHL were selected as instrumental variables (IVs) at a genome-wide significance level. All summary data were obtained from GWAS databases. The primary method used for MR analysis was the Inverse Variance Weighted (IVW) method, supplemented by various MR analyses method, including weighted median, simple mode, weighted mode, and MR-Egger, to ensure robustness. Cochran's Q test was employed for heterogeneity assessment. To identify potential pleiotropy, we utilized MR-Egger regression and the MR-PRESSO global test. Additionally, sensitivity analyses were performed using the leave-one-out approach. The MR analysis using the IVW method showed no substantial evidence supporting a direct causal relationship between air pollution and the risk of SSNHL (Nitrogen dioxide: P = 0.488, Nitrogen oxides: P = 0.572, PM<sub>2.5</sub>: P = 0.480, PM<sub>10</sub>: P = 0.225, and PM<sub>2.5-10</sub>: P = 0.608). There was no evidence of heterogeneity or pleiotropy, and sensitivity analyses based on the leave-one-out approach indicated that individual single nucleotide polymorphisms (SNPs) did not affect the robustness of the results.This study found no substantial evidence to support a causal relationship between air pollution and the risk of SSNHL in the European population.</p>","PeriodicalId":21811,"journal":{"name":"Scientific Reports","volume":"15 1","pages":"28921"},"PeriodicalIF":3.9000,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12331894/pdf/","citationCount":"0","resultStr":"{\"title\":\"Correlation of air pollution and risk of sudden sensorineural hearing loss: a Mendelian randomization study.\",\"authors\":\"Xiaoli Luo, Wenqi Zuo, Quanwei Ren, Linlin Wang, Di Wu, Yilin Xiang, Shixun Zhong\",\"doi\":\"10.1038/s41598-025-92952-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Numerous compelling epidemiological studies have linked air pollution to Sudden Sensorineural Hearing Loss (SSNHL). However, the causal relationship behind this association has not yet been established. We employed a Two-Sample Mendelian Randomization (MR) approach to investigate the causal relationship between air pollution (nitrogen dioxide, nitrogen oxides, PM<sub>2.5</sub>, PM<sub>10</sub>, and PM<sub>2.5-10</sub>) and SSNHL.Independent genetic variants associated with air pollution and SSNHL were selected as instrumental variables (IVs) at a genome-wide significance level. All summary data were obtained from GWAS databases. The primary method used for MR analysis was the Inverse Variance Weighted (IVW) method, supplemented by various MR analyses method, including weighted median, simple mode, weighted mode, and MR-Egger, to ensure robustness. Cochran's Q test was employed for heterogeneity assessment. To identify potential pleiotropy, we utilized MR-Egger regression and the MR-PRESSO global test. Additionally, sensitivity analyses were performed using the leave-one-out approach. The MR analysis using the IVW method showed no substantial evidence supporting a direct causal relationship between air pollution and the risk of SSNHL (Nitrogen dioxide: P = 0.488, Nitrogen oxides: P = 0.572, PM<sub>2.5</sub>: P = 0.480, PM<sub>10</sub>: P = 0.225, and PM<sub>2.5-10</sub>: P = 0.608). 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引用次数: 0
摘要
许多令人信服的流行病学研究将空气污染与突发性感音神经性听力损失(SSNHL)联系起来。然而,这种关联背后的因果关系尚未确定。我们采用双样本孟德尔随机化(MR)方法来研究空气污染(二氧化氮、氮氧化物、PM2.5、PM10和PM2.5-10)与SSNHL之间的因果关系。在全基因组显著水平上选择与空气污染和SSNHL相关的独立遗传变异作为工具变量(IVs)。所有汇总数据均来自GWAS数据库。MR分析采用的主要方法是方差反加权(IVW)法,辅以加权中位数、简单模式、加权模式、MR- egger等多种MR分析方法,以保证鲁棒性。异质性评价采用Cochran’s Q检验。为了确定潜在的多效性,我们使用了MR-Egger回归和MR-PRESSO全局检验。此外,使用留一方法进行敏感性分析。使用IVW方法的MR分析显示,空气污染与SSNHL风险之间没有直接因果关系(二氧化氮:P = 0.488,氮氧化物:P = 0.572, PM2.5: P = 0.480, PM10: P = 0.225, PM2.5: P = 0.608)。没有证据表明存在异质性或多效性,基于留一方法的敏感性分析表明,个体单核苷酸多态性(snp)不会影响结果的稳健性。这项研究没有发现实质性的证据来支持欧洲人群中空气污染与SSNHL风险之间的因果关系。
Correlation of air pollution and risk of sudden sensorineural hearing loss: a Mendelian randomization study.
Numerous compelling epidemiological studies have linked air pollution to Sudden Sensorineural Hearing Loss (SSNHL). However, the causal relationship behind this association has not yet been established. We employed a Two-Sample Mendelian Randomization (MR) approach to investigate the causal relationship between air pollution (nitrogen dioxide, nitrogen oxides, PM2.5, PM10, and PM2.5-10) and SSNHL.Independent genetic variants associated with air pollution and SSNHL were selected as instrumental variables (IVs) at a genome-wide significance level. All summary data were obtained from GWAS databases. The primary method used for MR analysis was the Inverse Variance Weighted (IVW) method, supplemented by various MR analyses method, including weighted median, simple mode, weighted mode, and MR-Egger, to ensure robustness. Cochran's Q test was employed for heterogeneity assessment. To identify potential pleiotropy, we utilized MR-Egger regression and the MR-PRESSO global test. Additionally, sensitivity analyses were performed using the leave-one-out approach. The MR analysis using the IVW method showed no substantial evidence supporting a direct causal relationship between air pollution and the risk of SSNHL (Nitrogen dioxide: P = 0.488, Nitrogen oxides: P = 0.572, PM2.5: P = 0.480, PM10: P = 0.225, and PM2.5-10: P = 0.608). There was no evidence of heterogeneity or pleiotropy, and sensitivity analyses based on the leave-one-out approach indicated that individual single nucleotide polymorphisms (SNPs) did not affect the robustness of the results.This study found no substantial evidence to support a causal relationship between air pollution and the risk of SSNHL in the European population.
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