Asthma is now recognized to be a chronic inflammatory disease that affects
the whole lung. Incidence appears to be increasing despite improved treatme
nt regimens. There is substantial epidemiological evidence suggesting a rel
ationship between the incidence and severity of asthma ( e. g., hospitaliza
tions) and exposure to increased levels of air pollution, especially fine a
nd ultrafine particulate material, in susceptible individuals. There have b
een a few studies in animal models that support this concept, but additiona
l animal studies to test this hypothesis are needed. However, such studies
must be performed with awareness of the strengths and weaknesses of the cur
rently available animal models. For studies in mice, the most commonly used
animal, a broad spectrum of molecular and immunological tools is available
, particularly to study the balance between Th1 and Th2 responses, and inbr
ed strains may be useful for genetic dissection of susceptibility to the di
sease. However, the mouse is a poor model for bronchoconstriction or locali
zed immune responses that characterize the human disease. In contrast, alle
rgic lung diseases in dogs and cats may more accurately model the human con
dition, but fewer tools are available for characterization of the mechanism
s. Finally, economic issues as well as reagent availability limit the utili
ty of horses, sheep, and primates.