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Controlled human exposure experiments with diesel exhaust particles (DEPs) and ozone serve to illustrate the important role pollutants play in modulating both allergic mechanisms and immune responses to affect the immunopathogenesis of airway diseases such as asthma. For DEP, evidence is stronger for the exacerbation of existing asthma rather than for the development of new disease. To the extent that this enhancement occurs, the augmentation of Th2-type immunity seems to be a common element. For ozone, neutrophilic inflammation, altered immune cell phenotype and function and oxidative stress are all marked responses that likely contribute to underlying immune-inflammatory features of asthma. Evidence is also emerging that unique gene signatures and epigenetic control of immune and inflammatory-based genes are playing important roles in the magnitude of the impact ozone is having on respiratory health. Indeed, the interplay between air pollutants such as DEP and ozone and asthma immunopathogenesis is an ongoing concern in terms of understanding how exposure to these agents can lead to worsening of disease. To this end, asthmatics may be pre-disposed to the deleterious effects of pollutants like ozone, having constitutively modified host defense functions and gene signatures. Although this review has utilized DEP and ozone as example pollutants, more research is needed to better understand the interplay between air pollution in general and asthma immumopathogenesis. (C) 2014 Elsevier B.V. All rights reserved.