Delayed complications of sulfur mustard poisoning: a focus on inflammation and telomere footprint.

Abstract

Sulfur mustard (SM), a potent alkylating agent, has been widely used in chemical warfare, causing severe acute and long-term health complications. While its immediate toxic effects are well documented, the late-onset complications remain poorly understood. Chronic exposure to SM has been linked to persistent oxidative stress, inflammation, and genomic instability, contributing to the progression of various diseases, including pulmonary fibrosis, chronic obstructive pulmonary disease (COPD), and cancer. This review explores the emerging role of telomere biology in the delayed pathophysiology of SM exposure. Evidence suggests that telomere shortening and dysregulation of telomeric repeat-containing RNA (TERRA) may serve as key molecular indicators of SM-induced aging and cellular dysfunction. Furthermore, inflammatory pathways, particularly NF-κB and TGF-β signaling, appear to be closely associated with telomere attrition, perpetuating chronic inflammation and fibrosis. By integrating oxidative stress, inflammation, and telomere dynamics, we propose a novel model linking telomere biology to SM-induced late complications. Understanding these mechanisms could pave the way for targeted therapeutic strategies, including antioxidant and epigenetic interventions, to mitigate long-term effects. Future research should focus on validating telomere-based biomarkers for early detection and exploring novel interventions to alleviate SM-induced chronic health conditions.