Data from epidemiological studies have shown that allergic conditions have
increased over the last 30-40 years, particularly in developed countries, d
espite a decrease in the severity of grass pollen seasons. Other epidemiolo
gical studies suggest an interaction between allergic diseases and traffic
pollution, and laboratory findings indicate that diesel exhaust particles e
nhance sensitivity to allergens. In an in vitro study, we found evidence to
suggest that cigarette smoke may render the airway epithelium more suscept
ible to adverse effects of allergens. Evidence from other studies indicates
that O-3 and NO2, with or without SO2, can enhance the airway allergic res
ponse in susceptible individuals such as those with asthma and rhinitis. St
udies investigating cellular and subcellular mechanisms suggest that pollut
ants are likely to influence the actions and interactions of a variety of c
ells, and lead to the synthesis of proinflammatory mediators that modulate
the activity and functions of inflammatory cells.