The effects of air pollution have been described some years ago as significantly harmful in children with elevated IgE and bronchial hyper-responsiveness. Airborne particulate of a size of less than 10 μm (PM10), sulfur dioxide, black smoke, and nitrogen dioxide provoked lower airways symptoms in these patients (wheezing
and dyspnea), as well as a decrease in peak expiratory flow greater than 10% while
particulate amounts increased.
PM10, nitrogen dioxide, and carbon monoxide showed a considerable correlation with emergency assistance in children, but not in adults. In children under 5 years, peak carbon monoxide level was predictive of hospitalization because of asthma attack.
Going from an epidemiological to a bio-immunological approach, one of the risk factors that could explain the increasing prevalence of atopic diseases in industrialized countries has been the exposure to diesel exhaust particles, recognized as enhancer of IgE-dependent allergic inflammation, and the consequent
symptoms of asthma and rhinitis. Once again, a recent revision cannot be conclusive in considering these particles as a significant risk factor for having atopic diseases.
About indoor pollution, there is no doubt that tobacco smoke constitutes the key factor to be considered, since it has been implicated in the development of asthma in children and non-smoking adults exposed. About those smoking actively, the RR for incidental asthma was reported as high as 3.9 (95% CI 1.7–8.5).