Airborne pollutants, both particulate and gaseous, represent a major environmental factor promoting allergic sensitization and disease expression. These adverse effects of particulate matter are highly dependent upon the nature and size of the particles, their content of chemicals and metals, and the subject's genetic makeup. Diesel exhaust and gases, in particular ozone, have been shown to exacerbate cellular inflammation and to act as mucosal adjuvants to skew the immune response to inhaled antigens toward a Th2-like phenotype. Growing evidence suggests that mechanisms of pollutant-induced amplification of the allergic reaction depend on oxidative stress that is under the control of susceptibility genes, as well as epigenetic mechanisms.
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