The Journal of Allergy and Clinical Immunology
Volume 115, Issue 2 , Pages 221-228, February 2005

Biology of diesel exhaust effects on respiratory function

  • Marc Riedl, MD
  • ,
  • David Diaz-Sanchez, PhD

      Affiliations

    • Corresponding Author InformationReprint requests: David Diaz-Sanchez, PhD, Division of Clinical Immunology/Allergy, Department of Medicine, 52-175 Center for Health Sciences, UCLA School of Medicine, Los Angeles, CA 90095-1680.

From The Hart and Louis Lyon Laboratory, Division of Clinical Immunology and Allergy, Department of Medicine, David Geffen School of Medicine– University of California, Los Angeles

Received 22 November 2004; accepted 24 November 2004.

Los Angeles, Calif

This activity is available for CME credit. See page 32A for important information.

In recent decades, clinicians and scientists have witnessed a significant increase in the prevalence of allergic rhinitis and asthma. The factors underlying this phenomenon are clearly complex; however, this rapid increase in the burden of atopic disease has undeniably occurred in parallel with rapid industrialization and urbanization in many parts of the world. Consequently, more people are exposed to air pollutants than at any point in human history. Worldwide, increases in allergic respiratory disease have mainly been observed in urban communities. Epidemiologic and clinical investigations have suggested a strong link between particulate air pollution and detrimental health effects, including cardiopulmonary morbidity and mortality. The purpose of this review is to provide an evidence-based summary of the health effects of air pollutants on asthma, focusing on diesel exhaust particles (DEPs) as a model particulate air pollutant. An overview of observational and experimental studies linking DEPs and asthma will be provided, followed by consideration of the mechanisms underlying DEP-induced inflammation and a brief discussion of future research and clinical directions.

Key words: Air pollution, diesel exhaust particles, allergy, asthma, oxidative stress, respiratory effects

Abbreviations used: AHR, Airway hyperreactivity, BEC, Bronchial epithelial cell, DEP, Diesel exhaust particle, GST, Glutathione-S-transferase, ICAM-1, Intercellular adhesion molecule 1, KLH, Keyhole limpet hemocyanin, PM, Particulate matter, PM10, Particulate matter with diameter ≤10 μm, ROS, Reactive oxygen species

 

 Series editors: William T. Shearer, MD, PhD, Lanny J. Rosenwasser, MD, and Bruce S. Bochner, MDSupported by the UCLA Allergy, Asthma, and Immunologic Disease Center (grant AI-40945) funded by the National Institute of Allergy and Infectious Diseases and the National Institute of Environmental Health Sciences.Disclosure of potential conflict of interest: M. Riedl—none disclosed. D. Diaz-Sanchez—none disclosed.

PII: S0091-6749(04)03223-3

doi:10.1016/j.jaci.2004.11.047

The Journal of Allergy and Clinical Immunology
Volume 115, Issue 2 , Pages 221-228, February 2005