leukoderma." 3 Depigmentation from chemicals may be associated with an initial instance of allergic contact dermatitis and appears to be due to the activation of melanocyte-specific autoimmunity, as also seen in non-chemically-induced vitiligo. 3 Pantoprazole and rabeprazole, which are members of a highly sensitizing group of chemicals, may cause an airborne pattern of contact dermatitis. 1,4 This inflammation can subsequently lead to the Koebner phenomenon, which can result in the occurrence of vitiligo in people with genetic susceptibility. Our case serves as an additional example of chemical-induced vitiligo, either direct exposure or airborne allergic contact dermatitis to PPIs. The actual mechanism of melanocyte loss in our patient is thought to be PPIs initially absorbed into skin by airborne exposure, leading to sensitization and then melanocyte loss by cytotoxic and autoreactive CD8+ T cells. Previous study 2 reported a potential melanogenesis-inhibitory effect of PPIs by reducing melanin content and tyrosinase activity levels in melanocytes and by inhibiting H+/K + -ATPase at the melanocytic cytoplasmic membrane. However, these explanations cannot explain PPI-induced vitiligo fully because the key pathogenesis in vitiligo is the loss of melanocytes rather than decreased melanin production. Herein, we suggest that PPIs most likely lead to the apoptosis of melanocytes by modifying the pH gradient and enhancing oxidative stress in melanocytes, possibly resulting in melanocyte-specific autoimmunity. 5 In summary, this case highlights the first report of PPI-induced vitiligo from occupational exposure and the potential of PPIs to augment melanocyte-specific autoimmunity.