Toxicology of Airborne Inorganic Arsenic: Oxidative Stress, Molecular Mechanisms, and Organ-Specific Pathologies

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.