Abstract Chronic inflammation induced by inhalation of airborne contaminants can contribute to cancer development. We have found that the anthracotic pigment in lungs of smokers is composed of nano-particulate carbon black (nCB), which accumulates in the antigen presenting cells (APCs) and promotes inflammation. Other occupational nCB exposures, such as coal-mining and carbon-black manufacturing, also raise the risk of chronic inflammatory lung diseases. No direct evidence establishes that nCB is a carcinogen; however, several cohort studies have shown a strong correlation between lung inflammation in carbon black industry workers and cancer. We examined whether nCB can promote non-small cell lung cancer (NSCLC) development. Using a novel non-Kras model of NSCLC, in which mice have airway epithelia-specific deletion of tumor suppressors Pten and Smad4 (Ptsd/d), we have found that intranasal challenge with nCB accelerates NSCLC progression. nCB exposure results in myeloid-derived suppressor recruitment and lactate accumulation to paralyze anti-tumor effects. Further, adoptive transfer of APCs from nCB exposed wild type mice (nCB-APC) to Ptsd/d mice showed increased incidences of lung tumor and metastasis, indicating a critical role for APCs in NSCLC progression. nCB-APC-induced immune suppression is in part mediated by expression of immunosuppressive enzymes and lactate production. Additionally, nCB-APCs express both pro-inflammatory and immunosuppressive cytokines to promote tumor growth. These findings suggest that nCB-APCs foster an immunosuppressive microenvironment, and indicate a mechanism responsible for environmental and occupational exposure to nCB in accelerating NSCLC progression.