Exposure to fine
particulate matter (PM2.5) and
ozone (O3) may lead to
inflammation and oxidative damage in the oral cavity, which is hypothesized to contribute to the worsening of airway
inflammation and
asthma symptoms. In this panel study of 43 asthmatic children aged 5-13 years old, each child had 4
clinic visits with a 2-week interval between two consecutive visits. At each visit, saliva samples were collected and subsequently analyzed for
interleukin 6 (IL-6) and
eosinophil cationic protein (ECP) as
biomarkers of
inflammation and
malondialdehyde (MDA) as a
biomarker of oxidative stress in the oral cavity. At each visit, children were measured for fractional exhaled
nitric oxide (FeNO) as a marker of
pulmonary inflammation.
Asthma symptoms of these children were measured using the Childhood
Asthma Control Test (C-ACT). We found that an interquartile range (IQR) increase in 24-h average personal exposure to PM2.5 measured 1 and 2 days prior was associated with increased salivary
IL-6 concentration by 3.0% (95%CI: 0.2%-6.0%) and 4.2% (0.7%-8.0%), respectively. However, we did not find a clear association between personal O3 exposure and any of the salivary
biomarkers, except for a negative association between salivary MDA and O3 exposure measured 1 day prior. An IQR increase in salivary
IL-6 concentration was associated with significantly increased FeNO by 28.8% (4.3%-53.4%). In addition, we found that increasing salivary
IL-6 concentrations were associated with decreased individual and total C-ACT scores, indicating the worsening of
asthma symptoms. We estimated that 13.2%-22.2% of the associations of PM2.5 exposure measured 1 day prior with FeNO and C-ACT scores were mediated by salivary
IL-6. These findings suggest that the induction of
inflammation in the oral cavity may have played a role in linking air pollution exposure with the worsening of airway
inflammation and
asthma symptoms.