There is growing evidence that fossil fuel combustion products act as adjuvants in the immune system and may lead to enhancement of allergic inflammation. Through this mechanism, particulate air pollutants may be an important contributor to the increased prevalence and morbidity of asthma and allergic rhinitis. In this communication we focus on the role of diesel exhaust particles (DEPs) in skewing the immune response towards IgE production and induction of allergic inflammation. We review experimental studies in animals and humans showing that DEPs enhance IgE production by a variety of mechanisms, including effects on cytokine and chemokine production, as well as activation of macrophages and other mucosal cell types. We discuss metabolic and cellular activation pathways linked to chemicals such as polycyclic aromatic hydrocarbons contained in DEPs and demonstrate how these molecular events may impact cytokine, chemokine, and accessory molecule expression in the immune system.