Interaction of air pollutants and pulmonary allergic responses in experimental animals.

Asthma, which is primarily an allergic type of respiratory disease, has increased in the U.S. and Europe by 30% over the last decade. Air pollution may play a role in this rise, since during episodes of smog, hospital admissions due to asthma increase. Ambient air quality has generally improved since the Clean Air Act was implemented in 1971 however, and has led some investigators to suggest that the increased risk of asthma is associated with a deterioration of indoor air quality through the introduction of closed ventilation systems and constant climate control. Thus, although the direct health effects of acute and chronic air pollutant exposure are not in dispute, emphasis on the sources and location of exposure is changing from outdoors to the home environment and workplace. The few experimental studies which have investigated the interaction of air pollutants with allergic disease have shown that exposure to O3 or NO2 can increase levels of allergen-specific antibody and may augment allergic symptoms. These experiments are reviewed along with a study conducted in our laboratory which demonstrated the enhancing effect of NO2 exposure on immune responses and pulmonary inflammation following sensitization and pulmonary challenge with house dust mite allergen (HDM). In this study, rats exposed to 5 ppm NO2 for 3 h after each immunization had significantly higher levels of serum IgE and local IgA, IgG and IgE antibody than air controls. Lymphocyte activity in the spleen and local lymph nodes, and pulmonary inflammatory cells were also increased in NO2-exposed rats. The results show that exposure to NO2 enhances immune responsiveness and the severity of pulmonary inflammation following antigen challenge. Since allergic individuals and most asthmatics also have increased immunity to these proteins, the possibility that air pollutant exposure enhances immune responses to allergens and thus exacerbates immune-mediated lung disease exists.