Inflammatory mechanisms in brain edema from 1,2-dichloroethane poisoning: a review

1,2-Dichloroethane (1,2-DCE) is a synthetic halogenated hydrocarbon widely used in polyvinyl chloride (PVC) production and as an industrial solvent. Prolonged or high-level exposure to 1,2-DCE can cause severe central nervous system injury, with brain edema being one of its major pathological manifestations. Recent studies have revealed that inflammation plays a pivotal role in the onset and progression of 1,2-DCE-induced brain edema. Activation of microglia and astrocytes triggers the release of proinflammatory cytokines such as TNF-<i>α</i>, IL-1β, and IL-6, which in turn disrupt the integrity of the Blood-Brain Barrier (BBB) and increase vascular permeability. Moreover, oxidative stress and mitochondrial dysfunction amplify inflammatory signaling through the Mitogen-Activated Protein Kinase (MAPK)-Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, promoting endothelial injury and cytotoxic edema. This review summarizes current understanding of the inflammatory mechanisms underlying brain edema following 1,2-DCE intoxication, emphasizing the interplay among oxidative stress, cytokine signaling, and BBB disruption. These findings not only elucidate the molecular basis of 1,2-DCE-induced neurotoxicity but also highlight the clinical relevance of targeting inflammation and oxidative stress for therapeutic intervention. In addition, potential therapeutic strategies targeting inflammatory signaling cascades and oxidative damage are discussed, providing insights into future directions for prevention and treatment research.