Does traffic exhaust contribute to the development of asthma and allergic sensitization in children: findings from recent cohort studies

There is a strong body of evidence that traffic-related air pollutants aggravate asthmatic symptoms. Short-term exposure to air pollutants has been associated with e.g. peak flow values [1], daily symptoms [2], anti-asthmatic medication [3], emergency visits [4] and hospital admissions [5]. However, exposure to traffic exhaust may also induce onset of asthma and asthma-like symptoms in healthy individuals. Oxidative stress has been suggested as the major, underlying mechanism behind many of the toxic reactions induced by air pollutants [6]. Childhood asthma is associated with decreased levels of various components in the antioxidant defences [7]. Reactive oxygen species (ROS) and free radicals are generated by traffic related pollutants such as nitrogen dioxide (NO2) and particulates. Reduced glutathione, ascorbic acid, uric acid, tocopherol and other antioxidants in the airways counteract the effects of ROS. Oxidative stress arises when the neutralising antioxidant defence is overwhelmed. An inflammatory response involves an endogenous production of additional ROS and further inflammation. High levels of ROS cause a depletion of local antioxidants and lead to widespread inflammatory reactions also outside the target tissues.There is increasing evidence mainly from experimental studies that exposure to diesel exhaust particles also has immunologic effects influencing the development of allergic sensitization. Several animal and human in vivo and in vitro studies strongly suggest that diesel exhaust particles act as adjuvants and augment the allergic reaction [8]. Combined exposure to diesel exhaust particles and antigen could switch the immune response towards IgE [9]. A recent animal study indicated that exposure to diesel exhaust particles induces epigenetic changes [10]. Concomitant exposure to ambient diesel exhaust particles and antigen in mice altered the methylation of T helper genes. Changes in the methylation affect the differentiation of the T helper cells