Ambient air pollution is a serious health hazard. Studies have demonstrated that short term and long term exposure to ambient air pollution leads to changes in inflammatory mediators in the lung and blood [169-178]. Children have been found to be at the highest risk of the detrimental health effects of ambient air pollution. Polycyclic aromatic hydrocarbons (PAHs) found in ambient air pollution can enhance IgE-mediated immune responses and are associated with exacerbation of asthma and, perhaps onset of atopy and asthma [169]. Overall, ambient air pollution inhalation can affect cell apoptosis, IgE, IL-8, IL-4, IL-6, TNF-D, oxidative stress metabolism, methylation of DNA, and DNA damage [175, 188]. Although there is much information related to the downstream responses to ambient air pollution exposure on immune cells in the lung and in the blood, there is little published data on how ambient air pollution could affect immune cells that serve as key regulators to the important early steps of allergen recognition and inflammatory immune responses [166]. Regulatory T cells (Treg) play an essential role in inhibition of the proximal pathways of allergic sensitization;for example, children born without regulatory T cells begin to develop severe atopy, including allergic asthma, at an early age [185-187]. The dysfunction of Treg is related to asthma exacerbations [189], severity of asthma [190-193], and could be one of the key features in asthma and atopy [166]. Treg have a pivotal place in the network of immunological interactions that makes them a possible common target for therapeutic interventions in asthma. Therefore, I propose to study the effects of ambient air exposure on Treg, and test the hypothesis that specific decreases in Treg function consequent to this exposure are a major component of the immunopathology of asthma.