Environmental impacts on immune responses in atopy and asthma

Despite the improvement of air quality in the U.S. since the enhancement of the Clean Air Act in 1990, exposures to outdoor and indoor air pollution remain a significant risk factor for both the development of asthma and the triggering of asthma symptoms.   Clinical studies have shown that significant asthma exacerbations were attributable to air pollution exposure, as a result of living in densely populated cities with elevated ambient fine particulate matter (PM_2.5) and ozone (O₃). In their review, Miller and Peden highlight new data on the effects of pollutant exposure on the innate and adaptive immune responses, genetic and epigenetic modifiers of response to pollutants, and potential interventions to mitigate these effects (J Allergy Clin Immunol 2014; 134(5): 1001-1008).

Several studies have determined that the effects of air pollution are heightened during the prenatal period.  This suggests that there is greater vulnerability of the growing lungs and the developing immune system, thus predisposing towards more airway inflammation later in life.  Similarly, studies suggest that factors such as chronic low-grade inflammation associated with obesity and stress may predispose towards asthma. Furthermore, the authors describe evidence that the mechanism behind these effects alter the innate and adaptive immunity, inducing a heightened immune response. Another emerging area of investigation is the effects of the environment on oxidative stress genes such as glutathione S-transferase (GST) genes as well as genes associated with Toll-like receptors of the innate immune system. Newer mechanistic lines of investigation focus on epigenetic regulation, and identifying asthma genes whose imprinting may be disrupted by environmental exposures.

Pollutant induced asthma exacerbations are less frequent in patients that use inhaled corticosteroids, suggestive that interventions that target acute inflammatory responses are beneficial, however future studies are required to test the efficacy of interventions in this population. Actively minimizing both indoor and outdoor pollutants and government air care regulations could decrease pollutant impacts on allergic lung disease.

Question for the authors:

How has the improved air quality over recent decades relate to the incidence of pollution related asthma exacerbations? 

In studies of both the Atlanta and Beijing Olympic Games, interventions that decreased automotive and point-source combustion were associated with decreased asthma morbidity. Future studies are needed to investigate more thoroughly whether improvements in air quality contribute to fewer asthma exacerbations.   This remains a difficult challenge to show as even the best designed epidemiological studies are unable to prove causality.