Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most
asthma exacerbations that result in hospitalization are associated with viral
upper respiratory tract infections. Such
infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of
nuclear factor-kappaB (
NF-Kappa B). However, a more recently appreciated cause of
asthma exacerbation is exposure to
pollutants, including
ozone and various components of
particulate matter (PM), including transition metals,
diesel exhaust, and biologicals such as
endotoxin. Although the role of air toxics in
asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of
asthma are also prominent air toxics (
metal ions and organic residues). These agents have been observed to activate
NF-Kappa B. Reviewed in this article are the actions of specific
air pollutants on airway
inflammation in humans and potential common response pathways for
ozone, PM, and several air toxics.