Occupationally encountered mineral dusts such as asbestos, silica, silicates (talc, mica), and metals can produce a distinctive pattern of fibrosis and distortion of the small airways, particularly the distal membranous bronchioles (MB) and the respiratory bronchioles (RB). Recent reports show that the same types of changes, accompanied by considerable muscle hyperplasia, are found in individuals living in regions with high levels of particulate air pollutants (PM). Models and actual measurements suggest that these changes occur because the small airways are sites of high particle deposition, and inhaled and deposited particulates, including PM, enter the airway walls. Studies from our laboratory using a tracheal explant model have shown that, for many types of particles, entry into the airway wall causes expression of mediators that lead to airway wall fibrosis and airway wall smooth muscle hyperplasia, probably through oxidant mechanisms. These reactions are intrinsic properties of the particles and do not require exogenous inflammatory cells. There is considerable evidence that individuals with occupational exposure to a wide variety of mineral dusts, as well as individuals with chronic exposure to high levels of PM, develop chronic airflow obstruction. The type of small airway remodeling seen in particle-induced bronchiolitis appears to be one cause of chronic airflow obstruction in this setting.