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Air Pollutants Alone May Cause Asthma Attacks

Date:
November 11, 2003
Source:
University Of California - Los Angeles
Summary:
UCLA researchers have shown for the first time that diesel exhaust particles alone may be enough to induce acute asthma attacks. A new testing method used in an animal model helped researchers better isolate the effect of diesel exhaust particles, a component of air pollution, on asthma.

UCLA researchers have shown for the first time that diesel exhaust particles alone may be enough to induce acute asthma attacks. A new testing method used in an animal model helped researchers better isolate the effect of diesel exhaust particles, a component of air pollution, on asthma.

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"Previously, we thought that air pollution alone was not enough to incite acute asthma attacks, but [that an attack] also required the presence of allergens such as pollen or house dust mites to establish airway inflammation and allergic responses in the airways," said Dr. Andre Nel, the study's principal investigator and a professor of medicine in the division of clinical immunology and allergy at UCLA's David Geffen School of Medicine. "However, this new experimental study shows that we need to pay closer attention to the intrinsic abilities of the air pollutant particles to induce asthma."

The study, which appears in the November 2003 issue of the Journal of Allergy and Clinical Immunology, will enhance research methods and lead to a better epidemiological understanding of how sudden surges in air pollution levels induce acute asthma attacks. Researchers at the Mayo Clinic in Scottsdale, AZ, collaborated with UCLA researchers on the study.

Asthma affects 15 to 20 million people in the United States, with the largest increase in cases seen among school-age children. Asthma is a chronic inflammatory disease of the small airways in the lung and can trigger acute episodes of airway tightening and wheezing. Researchers first gave mice a surrogate allergen, which would be similar to exposing humans to an allergen such as pollen. After several days, researchers administered aerosolized diesel particles to the mice, simulating the inhalation of air-pollution particles. This quickly resulted in an acute asthma-like condition. From a research standpoint, this is the first time that the asthma attack-prompting effects of diesel particles have been separated from the potent effects of allergens.

According to researchers, the test showed that if an initial exposure to an allergen was downscaled into a weakened allergic response, the aerosolized diesel exhaust particles could induce an asthma-like condition. Researchers next tested the aerosolized diesel particles on genetically modified mice that had chronic airway inflammation, even in the absence of an allergen. The diesel particles also caused acute asthma attacks in this setting.

According to Nel, the ability of the diesel particles to cause asthma flares after the initial allergen effect has diminished, and even in the absence an allergen, demonstrated that air pollution may play a larger role than previously thought in acute asthmatic events.

Acute asthma attacks are difficult to reproduce in a research setting. Previous animal models in which diesel exhaust particles were used took weeks to induce an asthma-like condition. In these cases, it was difficult to decipher the extent to which pollutant particles, allergens or other factors contributed to the airway inflammation.

This study introduces new and more rapid screening models that better isolate the biological mechanisms behind an acute asthma attack. This technological advancement may allow researchers to develop an explanation for acute asthma flares that occur within hours after a single pollution event. Nel noted that this would also be helpful in testing the effectiveness of asthma medications in relation to air pollution.

During the next phase of the study, researchers will more closely examine the mechanisms by which air pollution induces airway inflammation and will determine if the responses to pollutants that occurred in mice also occur in humans. Researchers will also employ new particle concentrator technology, developed by Dr. Constantinos Sioutas at the University of Southern California, to collect real-life ambient particles in the Los Angeles basin to reproduce the effects of diesel-exhaust particle inhalation in animals, said Nel.

This study builds on the growing body of research on airborne pollution at the UCLA's David Geffen School of Medicine and the Southern California Particle Center and Supersite at UCLA. Another recent study by these researchers and their colleagues, published in the journal Environmental Health Perspectives, linked real-life ambient particles, collected by particle concentrators in the Los Angeles basin, to cell damage. That study also highlighted the fact that the smallest particles, known as ultrafine particles, penetrate most deeply into tissue and cause the most damage.

The current study was funded by the National Institutes of Health and the Environmental Protection Agency.

Other study authors include Dr. Minqi Hao and Dr. Meying Wang of the division of immunology and allergy in the department of medicine at UCLA Medical Center; and Stephania Cormier and James J. Lee of the division of pulmonary medicine in the department of medicine at the Mayo Clinic in Scottsdale, AZ.


Story Source:

The above story is based on materials provided by University Of California - Los Angeles. Note: Materials may be edited for content and length.


Cite This Page:

University Of California - Los Angeles. "Air Pollutants Alone May Cause Asthma Attacks." ScienceDaily. ScienceDaily, 11 November 2003. <www.sciencedaily.com/releases/2003/11/031111065914.htm>.
University Of California - Los Angeles. (2003, November 11). Air Pollutants Alone May Cause Asthma Attacks. ScienceDaily. Retrieved December 22, 2014 from www.sciencedaily.com/releases/2003/11/031111065914.htm
University Of California - Los Angeles. "Air Pollutants Alone May Cause Asthma Attacks." ScienceDaily. www.sciencedaily.com/releases/2003/11/031111065914.htm (accessed December 22, 2014).

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