Last Updated: 2003-12-30 13:59:59 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Exposure to airborne endotoxin, a bacterial substance commonly found in both indoor and outdoor air, appears to increase the risk of asthma attacks in patients who are already sensitive to house dust, according to the results of a new study. This "sensitizing" effect seen with endotoxin is similar to what has been reported with ozone exposure.

"We know that asthmatics can have asthma attacks triggered by various environmental exposures, but we don't always know why certain circumstances precipitate asthma attacks when there are no clear-cut exposures to the allergens they are sensitized to," lead author Dr. Brian A. Boehlecke said in a statement.

In the new study, Boehlecke, from the University of North Carolina at Chapel Hill, and colleagues exposed 14 subjects with allergic asthma with dust mite allergen after being exposed for several hours to air with and without endotoxin.

Endotoxin is composed of a complex of fat and sugar molecules, which is released through the outer wall of bacteria when they die. Once released, these endotoxins find their way into air and dust.

The researchers found that exposure to airborne endotoxin increased airway responsiveness to dust mite allergen. Specifically, the amount of allergen needed to produce a predefined drop in the ability to expel air from the lungs was much lower when the subjects were exposed to endotoxin first, they report in the Journal of Allergy and Clinical Immunology.

The results suggest that "airborne irritants such as ozone and endotoxin, which can cause airway inflammation, may interact synergistically with other causes of airway problems, including allergens, to make asthma worse," Dr. Boehlecke noted.

"So in folks who are already allergic, if they are inhaling pollutants that can further exacerbate their inflammation, it may aggravate the symptoms they normally would have," he continued. "In other words, they may experience a worsening of their symptoms."

SOURCE: Journal of Allergy Clinical Immunology, December 2003.

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