## 4 Discussion
Although the exposure time, exposure level, and population of the present study differed from those in the studies described above, Flt, Pyr, and BkF all contributed to nasal symptoms in adults in the present study. According to the present results, some PAHs appear to be associated with the occurrence of nasal symptoms; however, further studies are warranted to confirm this. The exact mechanisms by which inhaled PAHs lead to nasal symptoms remain unclear, while the adverse effects of PAHs are well known [35; 36; 37]. BaP exacerbated nasal congestion in an animal study [38]. Since the present results showing that BaP did not induce significant changes in nasal symptoms did not coincide with the findings of the animal study, its effects on nasal symptoms appear to differ between humans and animals [39; 40]. The underlying mechanisms by which PAHs induce rhinitis may be attributed to allergy and/or inflammation [30; 31; 32]. In a study on children 1-hydroxyrene, Pyr's metabolite, was associated with blood IgE levels [41], which plays an important role in allergic airway disease [42]. In another study on children, higher levels of PAHs significantly increased inflammatory cytokines such as IL-10, IL-18 and IL-22 [43]. PAHs may also cause rhinitis through oxidative stress. Cigarette smoke has been shown to promote the production of ROS and play a role in the pathogenesis of rhinitis [44; 45]. Therefore, further studies are needed to elucidate the mechanisms contributing to the effects of Flt, Pyr, and BkF on nasal symptoms. IcdP also showed an association with nasal symptoms in our results, but it was negative. This result is contrary to that of an animal experiment in Taiwan, which found that dose-related exposure to IcdP may increase the risk of allergic airway inflammation in mice [46]. However, the numbers of eosinophils, lymphocytes and neutrophils did not increase significantly when they used the lowest dose of 0.4 uM in their study. The different results may be due to the amount of exposure. Based on our data collected in Kanazawa, the average daily exposure of participants to IcdP was much less than 0.4 uM. Due to the lack of studies on the association of IcdP with the respiratory system, further studies are needed to clarify the reasons for this discrepancy. We also observed an association between NO\({}_{2}\), one of the covariates, and nasal symptoms, although this association was only observed for a delay of 5 days. A previous study demonstrated that no changes in nasal function were observed even in allergic rhinitis patients after exposure to 400 ppb of NO\({}_{2}\) for six hours [47], which is consistent with our results. Our results were also in line with another report of short-term exposure to NO\({}_{2}\), in which no airway inflammation was found in normal subjects, patients with chronic obstructive pulmonary disease, or patients with asthma [48]. In the previous study, they observed that PAHs, NO\({}_{2}\) and SO\({}_{2}\) are associated with cough, and their effects on the respiratory system may be delayed [33]. Therefore, our results indicate that NO\({}_{2}\) may also require a certain period until a change of nasal function occur. Our study may be the first longitudinal study targeting the association of specific PAHs with nasal symptoms among adults. An advantage of our study was the use of daily concentrations of different PAHs in combination with nasal symptoms, which allowed us to observe the association of these individual PAHs with nasal symptoms prevalence. In addition, repeated observation of participants over a two-month period was able to better reflect the response of the upper respiratory tract to changes in pollutant concentrations. But there were several limitations that need to be addressed. The number of participants enrolled in the present study was smaller than in previous studies. Furthermore, even though participants were requested to record their daily health status, some diary records were incomplete.