Air pollutant gases have a significant association with respiratory
symptoms, including cough and wheeze. McLeod et al.
demonstrated that exposure to SO2 activated the transient receptor
potential vanilloid 1 (TRPV1) receptor in the nodose ganglia. This
effect was equivalent to increased sensitivity and cough as a response
to capsaicin [21]. Another study showed that there were
lower cough thresholds with enhanced exposure to O3 [22]. Belanger
et al. studied children with asthma exposed to indoor NO2 at concentrations
below the United States Environmental Protection Agency
(US EPA) outdoor standard of 53 ug/L [23]. Their results demonstrated
increased wheezing, polypnea, and chest distress in study
participants. In a cross-sectional study of 10-year-old children, elevated
PM10 and carbon dioxide (CO2) levels present during normal
daily activities were associated with a dry cough at night, wheezing,
and rhinitis in 654 children and acoustic rhinitis in 193 children
[24]. Schoolchildren who were exposed to CO2 (>1000 mg/L) had a
high risk of dry cough and rhinitis. A study of 352 infants showed
at that in the first year of life, the morbidity of persistent cough,
wheezing, and lower airway infection was 6.3%, 26.1% and 30.4%,
respectively [25]. With a 10 μg/m3 increment in ambient NO2 concentration,
the adjusted odds ratio of persistent cough was 1.40.
These study results indicate that when infants are exposed to outdoor
air pollution in the first year, the threat of persistent cough is enhanced.
Belanger et al. [26] indicated that each 5ug/L increment
(based on a threshold of 6 ug/L) in NO2 exposure was associated
with a dose-dependent increment in asthma severity including night
symptoms, rescue medication use, and wheezing. Children exposed
to indoor NO2 at levels below the US EPA outdoor standard (53 ug/
L) are at risk for enhanced asthma morbidity.