There is evidence that chronic exposure to high levels of ambient particulate pollutants (PM) is associated with chronic airflow obstruction, but how this occurs is not known. We exposed rat tracheal explants to Ottawa Urban Air Particles (ECH93) or Diesel Exhaust Particles (DEP). After 7 days in air organ culture, both types of PM increased explant procollagen and TGF₁ gene expression and markedly increased tissue hydroxyproline. For both types of particle, NF-B inhibitor SN50 completely blocked increased gene expression. With EHC93, procollagen expression was inhibited by the oxidant scavenger, tetramethylthiourea, and by the iron chelator, deferoxamine, but TGF₁ expression was not inhibited by deferoxamine. Inhibitors of extracellular signal related kinase (ERK) and p38 kinase did not affect EHC93-induced gene expression. With DEP, tetramethylthiourea and deferoxamine had no effect, but ERK and p38 inhibitors completely blocked effects on procollagen and TGF₁ . Fetuin, an inhibitor of TGF receptor binding, prevented increases in procollagen gene expression. We conclude that two common types of PM can directly induce expression of genes involved in fibrogenesis and actual airway wall fibrosis through NF-B and TGF-mediated mechanisms. PM-induced airway wall remodeling may play an important role in producing airflow obstruction in individuals living in high PM regions.