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Diesel exhaust particles (DEP) are a complex environmental pollutant and a major component of urban particulate matter air pollution. They consist of a carbonaceous core with thousands of adsorbed organic compounds, including polycyclic aromatic hydrocarbons (PAHs), and trace metals. In clinical research, particularly at the University of California, Los Angeles (UCLA), DEP is utilized as a standardized nasal challenge agent to investigate the pathophysiology of airway inflammation. DEP acts as a potent pro-inflammatory stimulus and an immunological adjuvant that enhances Th2-mediated immune responses, increases immunoglobulin E (IgE) production, and induces oxidative stress in the nasal mucosa. This model is used to study the mechanisms by which air pollution exacerbates allergic rhinitis and asthma in susceptible individuals.
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