A joint study by researchers at Stanford University and the University of California, Berkeley has found direct evidence that air pollution can have long-term effects. The study involved 181 children with and without asthma in California. The findings, published in the October 2010 issue of The Journal of Allergy and Clinical Immunology, show that exposure to some air pollutants can suppress the immune system’s regulatory T cells (Treg), and that the decreased level of Treg function is linked to greater severity of asthma symptoms.

Treg cells prevent the immune system from reacting to non-pathenogenic substances in the body that are associated with allergy and asthma. When function is low, Treg cells fail to stop the inflammatory responses symptomatic of asthma attacks. The study also found that air pollution can affect the DNA of unborn children in the same way as cigarette smoke, suggesting the possibility of an “inheritable effect from environmental pollution”, says lead author of the study Dr Kari Nadeau, paediatrician at Stanford’s Lucile Packard Children’s Hospital.

In a longitudinal study led by principal investigator Dr Ira Trager, professor of epidemiology at UC Berkeley’s School of Public Health, and co-principal investigator S. Katharine Hammond, UC Berkely professor and chair of environmental health sciences, 41 children with asthma came from the Fresno Asthmatic Children’s Environmental Study (FACES), and 30 children without asthma from Fresno were also recruited. Fresno is nicknamed the asthma capital of California because its location in California’s Central Valley, in which hot air combined with high traffic activity and heavy agriculture to ensure that it has a high incidence of asthma: almost one in three children have asthma. The Fresno children were compared with 80 children from the low-pollution city of Palo Alto, California, and were all matched by age, gender and asthmatic status.

Daily air quality data came from the California Air resources Board monitoring stations, which showed that the Fresno children had an annual exposure 7 times greater than their Palo Alto counterparts to polycyclic aromatic hydrocarbons (PAH), byproducts of fossil fuels and found in vehicle exhaust.

The children were tested for breathing function, allergic sensitivity and Treg cells in their blood, and the findings showed that the Fresno children had lower levels of Treg function and more severe symptoms of asthma than the Palo Alto children. The authors correlated increased exposure to the pollutants with disabling of the gene that triggers Treg cell development, and few studies have traced this molecular pathway so completely.

"The link between diesel exhaust and asthma could simply have been that the particulates were irritating the lungs," said Nadeau. "What we found is that the problems are more systemic. This is one of the few papers to have linked from A to Z the increased exposure to ambient air pollution with suppressed Treg cell levels, changes in a key gene and increased severity of asthma symptoms."

The researchers also noted that Treg cells play an essential role in other autoimmune disorders, so the study’s implications could go way beyond asthma.

Other co-authors of the study are Dr. John Balmes, UC Berkeley professor of environmental health sciences; Elizabeth Noth and Boriana Pratt, UC Berkeley researchers at FACES; and Cameron McDonald-Hyman, research assistant at Stanford University's School of Medicine.
The National Institutes of Health, U.S. Environmental Protection Agency and the American Lung Association helped support this research.

First Published in October 2010

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