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Air pollutants alone may cause severe asthma attacks



Researchers have found that diesel exhaust particles alone may be enough to induce acute asthma attacks.

UNIVERSITY OF California at Los Angeles 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.

"Previously, we thought that air pollution alone was not strong enough to incite acute asthma attacks, but [that an attack] also required the presence of allergens such as the 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 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.

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, the researchers administered aerosolised diesel particles to the mice, simulating the experience of 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 aerosolised 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 major technological advancement may allow the researchers to develop an explanation for acute asthma flares that occur within hours after a single notable 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, the asthma 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.

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