It is well known that particulate matter suspended in the earth's atmosphere generated by tobacco smoke, automobile exhaust, industrial processes, and forest fires has been identified as a major risk factor for chronic lung disease. Particulate matter can be divided into large, intermediate, and fine particulates. When inhaled, large particulates develop sufficient momentum to leave the flowing stream of inhaled air and deposit by impaction in the nose, mouth, nasopharynx, larynx, trachea, and central bronchi. Intermediate-sized particulates that develop less momentum deposit in the smaller bronchi and larger bronchioles, and the finest particulates that develop the least momentum make it to the distal gas-exchanging tissue, where gas moves solely by diffusion. On the basis of Einstein's classic work on Brownian motion that showed particles suspended in a gas diffuse much more slowly than the gas in which they are suspended, we postulate that the small airways that accommodate the shift from bulk airflow to diffusion become the major site for deposition of fine particles, resulting in a host immune response. Much remains to be learned about the interaction between the deposition of fine particulates and the host immune and tissue responses; the purpose of this review is to examine the hypothesis that the smallest conducting airways and proximal gas-exchanging tissue are the primary sites for the deposition of the finest particulates inhaled into the lungs.
Keywords: chronic obstructive pulmonary disease; host response; particulate matter; small airways disease; tertiary lymphoid follicles.