The Affiliated Guangzhou Twelfth People's Hospital, Guangzhou Medical University, Guangzhou 510620, China; Key Laboratory of Occupational Environment and Health, Guangzhou Twelfth People's Hospital, Guangzhou 510620, China.
Key Laboratory of Occupational Environment and Health, Guangzhou Twelfth People's Hospital, Guangzhou 510620, China.
Sci Total Environ. 2024 Nov 15;951:175743. doi: 10.1016/j.scitotenv.2024.175743. Epub 2024 Aug 23.
Noise and air pollution are significant environmental threats with proven adverse health effects. However, the causality between these ambient exposures and disease is still largely unknown. This study aims to provide genetic evidence for this gap and investigates the dual role of inflammatory factors, emphasizing the need for integrated public health strategies.
We included noise and air pollution as exposures, 91 inflammatory factors as mediators, and 26 diseases as outcomes. We explored causal relationships using Mendelian randomization. To ensure the reliability, we screened single nucleotide polymorphisms (SNPs) closely associated with exposure as instrumental variables (IVs), and assessed the pleiotropy and heterogeneity of these IVs.
Our results suggest that "Hearing difficulty/problems with background noise" increases the risk of hypertension, bronchitis, and menopause; loud music exposure frequency increases the risk of bronchitis; noisy workplace raises the risk of hypertension, coronary heart disease, narcolepsy, and irritable bowel syndrome; NO increases the risk of myocardial infarction and chronic heart failure; NO increases the risk of pneumonia and inflammatory diseases of female pelvic organs; and PM increases the risk of myocardial infarction, narcolepsy, and type 2 diabetes; PM increases the risk of developing pneumonia and type 2 diabetes. Furthermore, we found that nine inflammatory factors play a mediating role, of which four play a mediating role in increasing the risk of morbidity and eight play a mediating role in protection against ambient exposures. Finally, we selected SNPs significantly associated with exposure and outcome for enrichment analysis.
This study provides the first genetic evidence linking noise and air pollution to various diseases, highlighting the dual mediating role of inflammatory factors. Our findings align with the "One Health" framework, emphasizing the interconnectedness of environmental and human health. Integrated public health strategies considering these complex biological responses are essential for promoting overall well-being.
噪声和空气污染是具有显著健康危害的重要环境威胁。然而，这些环境暴露与疾病之间的因果关系在很大程度上仍不清楚。本研究旨在为这一空白提供遗传证据，并研究炎症因子的双重作用，强调需要采取综合公共卫生策略。
我们将噪声和空气污染作为暴露因素，91 种炎症因子作为中介因素，26 种疾病作为结果因素。我们使用孟德尔随机化方法探索因果关系。为了确保可靠性，我们筛选了与暴露密切相关的单核苷酸多态性（SNP）作为工具变量（IVs），并评估了这些 IVs 的多效性和异质性。
我们的研究结果表明，“听力困难/背景噪声问题”会增加患高血压、支气管炎和更年期的风险；频繁接触吵闹音乐会增加患支气管炎的风险；嘈杂的工作场所会增加患高血压、冠心病、发作性睡病和肠易激综合征的风险；NO 会增加患心肌梗死和慢性心力衰竭的风险；NO 会增加患肺炎和女性盆腔器官炎症性疾病的风险；PM 会增加患心肌梗死、发作性睡病和 2 型糖尿病的风险；PM 会增加患肺炎和 2 型糖尿病的风险。此外，我们发现九个炎症因子在其中发挥了中介作用，其中四个炎症因子在增加发病风险方面发挥了中介作用，八个炎症因子在保护免受环境暴露方面发挥了中介作用。最后，我们选择了与暴露和结果显著相关的 SNP 进行富集分析。
本研究首次提供了遗传证据，将噪声和空气污染与各种疾病联系起来，强调了炎症因子的双重中介作用。我们的研究结果与“One Health”框架一致，强调了环境和人类健康的相互联系。考虑到这些复杂的生物学反应，综合公共卫生策略对于促进整体健康至关重要。
