miR‐221, an oncogenic microRNA, can promote cell proliferation and is highly expressed in various types of tumors. However, the role of exosomal miR‐221 in benzene‐caused carcinogenesis remains elusive. Our study was designed to investi- gate whether exosomes secreted by the hydroquinone (HQ; an active metabolite of benzene)‐transformed malignant cells can transmit miR‐221 to normal recipient cells and its possible effects on cell viability. Our investigation revealed that expres- sion levels of miR‐221 were significantly increased in HQ‐transformed malignant cells relative to normal controls. Furthermore, exposure of control cells to exosomes that were derived from HQ‐transformed malignant cells increased miR‐ 221 levels and promoted their proliferation. Analyses of the biological potency of exosomes derived from HQ‐transformed malignant cells in which miR‐221 levels were decreased using an inhibitor, showed that both miR‐221 levels and prolifera- tion of recipient cells were decreased, but still were higher than those of normal 16HBE cells. Our study indicates that exosomal miR‐221 derived from HQ‐ transformed malignant human bronchial epithelial cells is involved in the prolifera- tion of recipient cells.