The question of whether the emerging nano-material, nanosized carbon black (CB) could influence the lung damage-induced by radiation exposure in cancer patients or in acute nuclear accident population remains incompletely uncovered. Therefore, our study investigated potential health risk from environmental low-dose CB exposure level (0.1 mg/kg/d, once per three days, for 12 weeks) via nasal instillation using a lung fibrosis mouse model induced by radiation. Compared to either CB or radiation single exposure, low-dose CB plus radiation exposure showed an aggravated risk of lung damage in mice, which was embodied in more increased collagen, reactive oxygen species (ROS) concentrations, and inflammation cytokines levels including IL-1β and TNF-α, as well as promoted epithelial-mesenchymal transition (EMT) progress through increasing relative biomarkers such as N-cadherin and α-SMA. Mechanistically, CB triggered the cGAS-STING signaling pathway to aggravation of radiation-induced lung injury. Furthermore, knocking down the GAS or STING expression would suppress the EMT process and inflammation reaction, resulting in significantly attenuating the combination effects of low-dose CB plus radiation on lung damage. Overall, our study indicates that environmental CB exposure may increase the lung damage in certain special population cannot be ignored. It sheds light on possible molecular mechanisms from cGAS-STING inflammation perspective and providing valuable basic understanding for future study on radiation-induced lung damage. Synopsis State of exposure of environmentally relevant nanosized carbon black may exacerbate the lung injury among cancer patients undergoing radiotherapy.