along a congested London street for 2 h, a decline in FEV1 and pulmonary
neutrophilic inflammation indicated that these effects were
associated with exposure to organic carbon and ultrafine particles
[10]. Results from a study of 36 children with asthma who were
exposed to air pollution showed a longitudinal association between
PM2.5 from indoor and outdoor sources with cough and wheeze
symptoms [11]. This study using a hybrid model linked daily signs
of cough and wheeze with PM2.5 exposure; the odds ratios with an
standard deviation increase in PM2.5 from indoor sources were 1.24
(cough) and 1.63 (wheeze), respectively. Ozone (O3) levels correlated
with wheezing, and cough correlated with indoor PM2.5 from
ambient sources. Evidence from a cross-sectional study investigating
the prevalence of irritative symptoms and chronic respiratory
symptoms among 109 workers exposed to PM as a result of incense
burning in a temple in Taiwan, and 118 unexposed workers in a
control group, indicated that chronic cough was common in the exposure
group [12]. That study also found that working in a temple
increased the risk of acute irritative symptoms of the nose and throat.
A study of 108 Swedish mild steel welders exposed to respirable
dust (RD), manganese (Mn), and O3 showed that the welders frequently
demonstrated job-related symptoms including nasal
obstruction (33%), ocular symptoms (28%), and hacking cough (24%)
[13]. According to that study, the geometric average exposures to
RD and inhaled Mn were 1.3 mg/m3 and 0.08 mg/m3, respectively.
Over 50% of Mn concentrations surpassed the occupational exposure
limit in Sweden. In 7019 subjects in Switzerland tested at
baseline in 1991 and followed up in 2002 and who were exposed
to PM10 during the 12 months before each health evaluation, the
mean of exposure to PM10 in 2002 was no higher than that in 1991
[14].