Asthma, which is primarily an allergic type of respiratory disease, ha
s increased in the U.S and Europe by 30% over the last decade. Air pol
lution may play a role in this rise, since during episodes of smog, ho
spital admissions due to asthma increase. Ambient air quality has gene
rally 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 throu
gh the introduction of closed ventilation systems and constant climate
control. Thus, although the direct health effects of acute and chroni
c air pollutant exposure are not in dispute, emphasis on the sources a
nd location of exposure is changing from outdoors to the home environm
ent and workplace. The few experimental studies which have investigate
d the interaction of air pollutants with allergic disease have shown t
hat exposure to O-3 or NO2 can increase levels of allergen-specific an
tibody and may augment allergic symptoms. These experiments are review
ed along with a study conducted in our laboratory which demonstrated t
he enhancing effect of NO2 exposure on immune responses and pulmonary
inflammation following sensitization and pulmonary challenge with hous
e dust mite allergen (HDM). In this study, rats exposed to 5 ppm NO2 f
or 3 h after each immunization had significantly higher levels of seru
m IgE and local IgA, IgG and IgE antibody than air controls. Lymphocyt
e activity in the spleen and local lymph nodes, and pulmonary inflamma
tory cells were also increased in NO2-exposed rats. The results show t
hat exposure to NO2 enhances immune responsiveness and the severity of
pulmonary inflammation following antigen challenge. Since allergic in
dividuals and most asthmatics also have increased immunity to these pr
oteins, the possibility that air pollutant exposure enhances immune re
sponses to allergens and thus exacerbates immune-mediated lung disease
exists.