Korean J Asthma Allergy Clin Immunol.  2004 Sep;24(3):269-281.

Diesel Exhaust Particles and Asthma

Abstract

It has been demonstrated that particulate air pollutants, such as diesel exhaust particles (DEP), are related to allergic respiratory disorders including asthma and allergic rhinitis by extensive epidemiological studies. To perform environmental control with good cost-effective performance, it is crucial to elucidate the cellular and molecular mechanisms of effects of particulate pollutants. In vivo and in vitro studies so far strongly suggest that DEP may induce both anti- and pro-inflammatory compounds by activating their transcription. In conjunction with allergen, diesel exhaust particles can act as an adjuvant to enhance IgE antibody responses, and induce T-helper 2 (Th2) cytokine, chemokine and adhesion molecule expression. Studies have elucidated that DEP activate several signaling pathways such as mitogen-activated protein kinases and transcription factors especially NFkappaB, and these effects are thought to be via production of reactive oxygen species. Antioxidants reduce the allergic inflammatory effects of diesel exhaust particles in vitro and in mice. Therefore, host responses to DEP might be regulated by balance between antioxidants and proinflammatory responses. Recent human studies highlighted a possibility of chemoprevention against DEP-induced health effect in susceptible people.

MeSH Terms

Animals
Antibody Formation
Antioxidants
Asthma*
Chemoprevention
Humans
Immunoglobulin E
Mice
Mitogen-Activated Protein Kinases
Particulate Matter
Reactive Oxygen Species
Rhinitis
Transcription Factors
Vehicle Emissions*
Antioxidants
Immunoglobulin E
Mitogen-Activated Protein Kinases
Particulate Matter
Reactive Oxygen Species
Transcription Factors
Vehicle Emissions