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Mexico (Castillejos, Gold et al. 1992), with atopic status being an additional risk factor
(Jorres, Nowak et al. 1996). In children with moderate to severe asthma attending surnmer
camps over three years, air pollution levels (predominantly ozone) were associated with acute
asthma exacerbations, chest symptoms and a reduction in lung function (Thurston, Lippmann
et al.1997).
Increased absences in school and kindergarten or playschool attendances have also been
associated with an increase in particulate matter -
which was more pronounced in six to nine
year olds than older age groups (Pope, Schwartz et al. lgg2: Ransom and pope lgg2). There
has also been an association with rises in levels of pollutants on prolonging episodes of
infection (Bates 1995). Increased levels of pollutants have also been associated with an
increased risk of developing upper respiratory tract infections and symptoms in children
(Jaakkola, Paunio et al. 1991, Ostro, 1999 #657), particularly with high concentrations of
SOz, and moderate levels of NOz and particulate matter (von Mutius, Sherrill et al. 1995).
Clearly, it would be helpful to confirm these findings using more specific experiments to
determine a dose response and the mechanism of damage which causes disease. This has been
done in a few animal models which have demonstrated the development of infectious and
allergic lung disease with increased severity when exposure to air pollutants (ozone, NO2,
SOz). These pollutants increased damage in infection and inflammation in mouse and guinea
pig populations predominantly but also in a dog and a monkey model (Gilmour 1995;
Miyabara, Takano et al. 1998; Ng, Kokot et al. 1998; Selgrade 200O; Whitekus, Li et al.
2002). While it is more problematic to confirm a dose response in humans, it has been
possible to do nasal challenges with allergen, with or without the addition of diesel exhaust
particles, showing exaggerated responses in the presence of the particles @iaz-Sanchez, Tsien
et al. 1996; Diaz-Sanchez, Jyrala et al. 2000; Bastain, Gilliland et al, 2003; Gilliland, Li et al.
2004).It is now thought that oxidant stress is the mechanism that underlies the toxic effect of
most forms of air pollution (Nel, Diaz-Sanchez et al. 2001; Kelly 2003; Kelly and Sandstrom
2004; Gauderman 2006). The lung is actually well equipped to deal with oxidative stress as
the lung lining fluid is rich in enzymatic and low molecular weight non-enzymatic
antioxidants. In addition, there are intracellular defences with glutathione based enzymes that
use a variety of the products of oxidative stress as substrates and therefore prevent their build-
up. However individuals have differing genotypes of this enzqe family, which appear to
make them more or less susceptible to damage from air pollutants, including active or passive
smoke inhalation (Miyabara, Yanagisawa et al. 1998; Mudway and Kelly 2000; Gilliland,
Rappaport et aL.2002; Bastain, Gilliland et aI.2003; Gilliland, Li et al. 2004).
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