Sulfur mustard-induced pulmonary injury: current mechanisms and intervention strategies

Sulfur mustard (SM) is a lipophilic vesicant alkylating agent. It can be absorbed into the body via multiple routes, including the respiratory tract, cornea, and skin, leading to systemic organ damage. The alkylation of DNA, proteins, and nucleic acids by SM produces unique cytotoxicity, and SM is also a potent mutagen and carcinogen. Regardless of the exposure route, the lung is the most vulnerable target organ. Acute respiratory distress syndrome and pulmonary infections are the primary causes of early mortality in SM poisoning. To date, no specific antidote is available for SM. This review aims to discuss the cellular and molecular mechanisms of acute and delayed SM-induced pulmonary injury, with emphasis on DNA damage, oxidative stress, inflammatory response, and apoptosis mechanisms. These mechanisms indicate the potential application of anti-DNA damage, antioxidant, anti-inflammatory, and anti-apoptotic therapies to help mitigate SM-induced pulmonary injuries.