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This is associated with increases in levels of inflammatory mediators, including tumor necrosis factor (TNF)\u03b1 in the lung and upregulation of its receptor TNFR1. Dysregulated production of TNF\u03b1 and TNF\u03b1 signaling has been implicated in lung injury, oxidative and nitrosative stress, apoptosis, and necrosis, which contribute to tissue damage, chronic inflammation, airway hyperresponsiveness, and tissue remodeling. These findings suggest that targeting production of TNF\u03b1 or TNF\u03b1 activity may represent an efficacious approach to mitigating lung toxicity induced by both mustards and radiation. 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