<p>Rheumatoid arthritis (RA) is a systemic autoimmune disease with substantial extraarticular morbidity and mortality, particularly from rheumatoid arthritis–associated interstitial lung disease (RA-ILD). Although advances in disease-modifying therapies have improved joint outcomes and overall survival, RA-ILD remains a major contributor to premature death. Emerging evidence supports the mucosal origins hypothesis, which proposes that RA-related autoimmunity may be initiated at extraarticular sites, particularly the lungs following inhalational exposures. This narrative review synthesizes the current body of literature linking various inhaled exposures, including cigarette smoking, particulate matter, gaseous air pollutants, silica, coal dust, military-related exposures and pesticides, to RA and RA-ILD risk. Cigarette smoking is the most well-established environmental risk factor for RA, demonstrating strong dose-dependent associations with disease risk, severity, and the development and progression of RA-ILD, especially in genetically susceptible individuals. Evidence for other airborne pollutants is mixed, with particulate matter and nitrogen dioxide showing emerging but inconsistent associations with RA and limited data for RA-ILD. Occupational exposures such as silica and coal dust demonstrate stronger links, particularly for seropositive RA. Translational models further support sex-specific immune and fibrotic responses to inhaled irritants. Collectively, current data suggest that inhaled environmental exposures may contribute to the pathogenesis of RA and RA-ILD, highlighting the lungs as a critical interface between environmental risk and autoimmunity and underscoring the need for prospective studies to clarify causality and prevention strategies.</p>