Purpose: To report the clinical features of 93 eyes of 48 pa-tients with chro nic and delayed-onset mustard gas keratitis. Clinicopathologic correlation in 5 eyes and a review of related literature are presented. Design: Retrospective, n oncomparative case series. Participants: Forty-eight Iranian survivors of Iraqi chemical warfare with chronic or delayed-onset mustard gas keratitis. Methods: We reviewed the symptoms, clinical findings, course, and treatment of our patie nts and reviewed the literature. In 5 patients, histopathologic features of corn eal and conjunctival specimens were evaluated. Main Outcome Measures: Ocular fin dings, clinical course, treatment measures, and histopathologic studies. Results : Of 48 patients, 31 (64.6%) had chronic symptomatology, whereas 17 (35.4%)-e xperienced delayed-onset lesions. Visual acuity at referral ranged from hand mo tions to 20/20. Ocular surface changes included chronic blepharitis and decrease d tear meniscus in all patients, limbal ischemia (81.3%), and conjunctival vasc ular abnormalities (50%). Corneal signs in order of frequency were: scar or opa city (87.5%), neovascularization (70.8%), thinning (58.3%), lipoid deposits ( 52.1%), amyloid deposits (43.8%), and epithelial defects and irregularity (31. 3%). Many patients received conservative treatment; others underwent allograft stem cell transplantation (20 eyes of 17 patients), penetrating keratoplasty (12 eyes of 12 patients), and lamellar keratoplasty (4 eyes of 3 patients). Conjunc tival specimens were evaluated by light microscopy. Decreased goblet cell densit y, attenuated or thickened epithelium, scarring in the substantia propria associ ated with plasmacytic and lymphocytic infiltration, and dilated lymphatic vessel s were noted. Excised corneal buttons disclosed absence of epithelium and Bowman ’s layer, fibrovascular pannus, stromal scarring, and vascularization. Conclusi ons: Mustard gas causes chronic and delayed destructive lesions in the ocular su rface and cornea, leading to progressive visual deterioration and ocular irritat ion. The pathophysiologic features of these changes are not clearly identified. Excised conjunctival and corneal specimens revealed a mixed inflammatory respons e without any specific features. Based on the clinical appearance of the lesions and the histopathologic findings, an immune-mediated component seems possible. Purpose: To report the clinical features of 93 eyes of 48 pa-tients with chro nic and delayed-onset mustard gas keratitis. Clinicopathologic correlation in 5 eyes and a review of related literature are presented. Design: Retrospective, n on comparative case series. Participants : Forty-eight Iranian survivors of Iraqi chemical warfare with chronic or delayed-onset mustard gas keratitis. Methods: We reviewed the symptoms, clinical findings, course, and treatment of our patients and reviewed the literature. In 5 patients, histopathologic features of Main Outcome Measures: Ocular fin dings, clinical course, treatment measures, and histopathologic studies. Results: Of 48 patients, 31 (64.6%) had chronic symptomatology, 17 (35.4%) - e xperienced delayed-onset lesions. Visual acuity at referral ranged from hand mo tions to 20/20. Ocular surface changes included chronic blepharitis and decrease d tear meniscus in all patients, limbal i Corneal signs in the order of frequency were: scar or opa city (87.5%), neovascularization (70.8%), thinning (58.3%), lipoid deposits (52.1% ), amyloid deposits (43.8%), and epithelial defects and irregularity (31.3%). Many patients received conservative treatment; others underwent allograft stem cell transplantation (20 eyes of 17 patients), penetrating keratoplasty (12 eyes of 12 patients) , and lamellar keratoplasty (4 eyes of 3 patients). Conjunc tival specimens were evaluated by light microscopy. Decreased goblet cell densit y, attenuated or thickened epithelium, scarring in the substantia propria associated with a plasmacytic and lymphocytic infiltration, and dilated lymphatic vessel s were noted. Excised corneal buttons disclosed absence of epithelium and Bowman’s layer, fibrovascular pannus, stromal scarring, and vascularization. Conclusi ons: Mustard gas causes chronic and delayed destructive lesions in the ocular surface and cornea, leading to progressive visual deterioration and ocular irritat ion. The pathophysiologic features of these changes are not identified identified. the histopathologic findings, an immune-mediated component seems possible.