Common airborne substance makes asthmatics more sensitive to house dust mites: study
Exposure to endotoxin, a bacterial substance found commonly in outdoor and indoor air, makes mite-allergic asthmatics more sensitive to house dust and may place them at increased risk of asthma attack.
The new research findings from the University of North Carolina at Chapel Hill School of Medicine are consistent with previous UNC studies showing exposure to ozone to make asthmatics more sensitive to allergens, the environmental triggers of allergic reactions. Both ozone and endotoxin are not allergens; however, they can cause portions of the respiratory tract to become inflamed.
The study is published this week in the online December issue of the Journal of Allergy and Clinical Immunology.
Endotoxin is a complex of lipids (fats) and sugar molecules thats released through the outer cell wall of common bacteria. When the bacteria die, the cell wall collapses and endotoxin is released into the environment, finding its way into the air and dust.
“We know that asthmatics can have asthma attacks triggered by various environmental exposures, but we dont always know why certain circumstances precipitate asthma attacks when there are no clear-cut exposures to the allergens they are sensitized to,” said Dr. Brian A. Boehlecke, lead author of the report, professor of medicine in UNCs pulmonary medicine division and member of UNCs Center for Environmental Medicine, Asthma and Lung Biology.
“Now it appears that various 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,” he said.
The new study involved 14 participants with mild asthma for whom skin testing showed allergies to house dust mites, one of the most common airborne allergens. Study participants inhaled relatively low levels of endotoxin over four hours that approximated those levels found in some homes and office buildings.
Following this exposure, participants underwent an “allergen challenge test.” This inhalation test identifies the dose that causes their airways to constrict a specified degree. That dose, once determined for each person, is called their provocation dose, said study co-author Dr. Neil Alexis, assistant professor of pediatrics in the division of allergy, immunology and environmental medicine and a UNC center member.
“We found that when allergic individuals breathe endotoxin prior to their allergen challenge, they in fact became more sensitive to the allergen challenge. They were provoked at a lower concentration of allergen compared to previously inhaling air without endotoxin,” he said.
The findings have implications for air pollution exposure, “in particular those pollutants that cause airway inflammation, which endotoxin does and which ozone does,” Alexis said. “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. In other words, they may experience a worsening of their symptoms.”
Further UNC studies will examine if endotoxin, ozone and other airborne agents share common interactive mechanisms that may increase allergen sensitivity and disease severity in people with asthma.
“There is also the possibility of finding drugs to block that interaction and prevent the worsening of asthma,” Boehlecke said. Along with Alexis and Boehlecke, UNC co-authors were Drs. Milan Hazucha, Robert Jacobs, Parker Reist, Philip A. Bromberg and David Peden.
Funding for the research came from the Center for Indoor Air Research and the National Institutes of Health.
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