Web edition: February 25, 2013
Print edition: March 23, 2013; Vol.183 #6 (p. 19)
SAN ANTONIO — Bad actors in air pollution may contribute to asthma and allergy by subverting protective cells in the body that tone down immune reactions, researchers report. The pollution components also seem to rev up overactive immune warriors — already linked to allergies — that need no such prompting.
The airborne culprits are polycyclic aromatic hydrocarbons, or PAHs, the products of incomplete burning of fuel in diesel engines, furnaces, wood fires, wildfires and even barbeque grills. Air pollution has been tied to asthma and allergy in past research, but the link between PAHs and these immune problems is still unclear.
In the new report, researchers show that children exposed to high levels of PAHs had poorly functioning T-regulatory cells, or T-regs, which normally ratchet down immune-caused inflammation as needed. “T-regs are peacekeeper cells,” says Kari Nadeau, a physician and biochemist at Stanford University, who presented the findings February 23 at a meeting of the American Academy of Allergy, Asthma and Immunology. “But in asthma, T-regs are impaired.”
The team also found that kids exposed to a lot of PAHs made excess amounts of an antibody called immunoglobulin E, or IgE. The IgE antibody normally helps the body fight parasites. But in developed countries, where parasitic infections are largely a thing of the past, IgE has become better known for its role in allergy. The body often cranks out IgE as part of a misguided immune reaction against noninfectious substances in the environment. IgE also shows up in asthma, which can be triggered by allergy.
To study the effect of air pollution on these immune players, Nadeau and her colleagues obtained blood tests, lung function readings and health information from 153 children, median age 14, in Fresno, Calif. The researchers used airborne PAH sampling to estimate exposure to PAHs, and chose Fresno because of its relatively high air pollution levels. Children with high exposure to PAHs, based on air sampling in and around their homes, made high amounts of IgE and had lower T-reg function than children exposed to low levels. High PAH exposure during the most recent three months was linked to 51 percent higher risk of being diagnosed with asthma.
“I think this is a very interesting and thought-provoking study,” says Todd Rambasek, an allergist at Ohio University in Athens. He notes that other studies had linked air pollution with asthma and allergy but failed to discern between PAH and ozone or particulate matter that could contribute to the conditions.
Nadeau also reported that consistent PAH exposure coincided with changes in a gene called Foxp3. As reported in Nature in 2010, Foxp3 seems to be a master regulator of T-reg populations in the body. Unfortunately, Nadeau says, the changes observed in the Foxp3 gene seem irreversible and widespread.
The asthma rate is 22 percent among children in Fresno, Nadeau says, compared with 12 percent in the United States as a whole. Up to 70 percent of people in Fresno have an allergy, she notes, more than double the average lifetime risk of having an allergy in California. The new study adds PAHs to a known pollution problem in the area: In 2012, the American Lung Association ranked Fresno fifth-worst among California cities for overall particulate pollution and fourth-worst for ozone.
E. Noth et al. A spatial-temporal regression model to predict daily outdoor residential PAH concentrations in an epidemiological study in Fresno, CA. Atmospheric Environment. Vol. 45, May 2011, p. 2394. doi:10.1016/j.atmosenv.2011.02.014. [Go to]
A. Walker et al. Exposure to polycyclic aromatic hydrocarbons is associated with higher levels of total IgE, decreased function of T regulatory cells and an increase of asthma occurrence in children. Abstract #197. American Academy of Allergy, Asthma and Immunology meeting. San Antonio, Texas, February 22-26, 2013.
Y. Zheng et al. Role of conserved non-coding DNA elements in the Foxp3 gene in regulatory T cell fate. Nature. Vol. 463, February 11, 2010, p. 808. doi:10.1038/nature08750. [Go to]