Tungsten is widely used in medical, industrial, and military applications. The environmental exposure to tungsten has increased over the past several years and few studies have addressed its potential toxicity.In this study, we evaluated the effects of chronic oral tungsten exposure (100 ppm) on renal in ammation in mice. We found that 30-or 90-day tungsten exposure led to the accumulation of LAMP1-positive lysosomes in renal tubular epithelial cells. In addition, the kidneys of mice exposed to tungsten showed interstitial in ltration of leukocytes, myeloid cells, and macrophages together with increased levels of proin ammatory cytokines and p50/p65-NFkB subunits. In proximal tubule epithelial cells (HK-2) in vitro, tungsten induced a similar in ammatory status characterized by increased mRNA levels of CSF1, IL34, CXCL2 and CXCL10 and NFkB activation. Moreover, tungsten exposure slowed HK-2 cell proliferation and enhanced reactive oxygen species generation. Conditioned media from HK-2 cells treated with tungsten induced an M1-proin ammatory polarization of RAW macrophages as evidenced by increased levels of iNOS and interleukin-6 and decreased levels of the M2-antiin ammatory marker CD206. These effects were not observed when RAW cells were exposed to conditioned media from HK-2 cells treated with tungsten and supplemented with the antioxidant N-acetylcysteine (NAC). Similarly, direct tungsten exposure induced M1-proin ammatory polarization of RAW cells that was prevented by NAC cotreatment. Altogether, our data suggest that prolonged tungsten exposure leads to oxidative injury in the kidney ultimately leading to chronic renal in ammation characterized by a proin ammatory status in kidney tubular epithelial cells and immune cell in ltration.