Berkeley Exposure to dirty air is linked to decreased function of a gene that appears to increase the severity of asthma in children, according to a joint study by researchers at Stanford University and the University of California, Berkeley.
While air pollution is known to be a source of immediate inflammation, this new study provides one of the first pieces of direct evidence that explains how some ambient air pollutants could have long-term effects.
The findings, published in the October 2010 issue of the Journal of Allergy and Clinical Immunology, come from a study of 181 children with and without asthma in the California cities of Fresno and Palo Alto.
The researchers found that air pollution exposure suppressed the immune system's regulatory T cells (Treg), and that the decreased level of Treg function was linked to greater severity of asthma symptoms and lower lung capacity. Treg cells are responsible for putting the brakes on the immune system so that it doesn't react to non-pathogenic substances in the body that are associated with allergy and asthma. When Treg function is low, the cells fail to block the inflammatory responses that are the hallmark of asthma symptoms.
The findings have potential implications for altered birth outcomes associated with polluted air, much the same as those noted for the effects of cigarette smoke.
"When it came out that cigarettes can cause molecular changes, it meant the possibility that mothers who smoked could affect the DNA of their children during fetal development," said study lead author Dr. Kari Nadeau, pediatrician at Stanford's Lucile Packard Children's Hospital and an assistant professor of allergy and immunology at Stanford's School of Medicine. "Similarly, these new findings suggest the possibility of an inheritable effect from environmental pollution."
Forty-one participants came from the Fresno Asthmatic Children's Environment Study (FACES
|Contact: Sarah Yang|
University of California -- Berkeley