Liu Qingyang
College of Ecology and Environment, Nanjing Forestry University, Nanjing 210037, China.
Toxics. 2025 Sep 4;13(9):753. doi: 10.3390/toxics13090753.
Arsenic, a naturally occurring metalloid, poses a significant global public health threat due to widespread environmental contamination. Despite its well-documented carcinogenicity, critical gaps remain in understanding the health impacts of chronic low-level airborne exposure and the multi-modal mechanisms driving inorganic arsenic toxicity. This narrative review synthesizes recent molecular research and population health data to explain how airborne inorganic arsenic causes harm through multiple biological pathways. Key novel insights include (1) a comprehensive analysis of inorganic arsenic-induced oxidative stress and epigenetic dysregulation, revealing transgenerational effects via germline epigenetic markers; (2) a critical evaluation of the linear no-threshold (LNT) model, demonstrating its overestimation of low-dose risks by 2-3× compared to threshold-based evidence; and (3) descriptions of mechanistic links between inorganic arsenic speciation, organ-specific pathologies (e.g., neurodevelopmental impairments, cardiovascular diseases), and pollution mitigation strategies. This study connects molecular mechanisms with public health strategies to improve arsenic risk assessment. It focuses on how inorganic arsenic alters gene regulation (epigenetics) and combines exposure from multiple sources, while also clarifying uncertainties about low-dose effects and refining safety standards.
砷是一种天然存在的类金属，由于广泛的环境污染，对全球公众健康构成重大威胁。尽管其致癌性已有充分记录，但在了解慢性低水平空气暴露的健康影响以及驱动无机砷毒性的多模式机制方面仍存在关键差距。这篇叙述性综述综合了近期的分子研究和人群健康数据，以解释空气中的无机砷如何通过多种生物学途径造成危害。关键的新见解包括：（1）对无机砷诱导的氧化应激和表观遗传失调进行全面分析，揭示通过种系表观遗传标记产生的跨代效应；（2）对线性无阈值（LNT）模型进行批判性评估，表明与基于阈值的证据相比，其对低剂量风险的高估达2至3倍；（3）描述无机砷形态、器官特异性病理（如神经发育障碍、心血管疾病）和污染缓解策略之间的机制联系。本研究将分子机制与公共卫生策略联系起来，以改进砷风险评估。它关注无机砷如何改变基因调控（表观遗传学）并整合多种来源的暴露，同时也阐明了低剂量效应的不确定性并完善安全标准。
