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Associations between inhaled doses of PM2.5-bound polycyclic aromatic hydrocarbons and fractional exhaled nitric oxide
- Li, Tian, Wang, Yao, Hou, Jian, Zheng, Dan, Wang, Guiyang, Hu, Chen, Xu, Tian, Cheng, Juan, Yin, Wenjun, Mao, Xiang, Wang, Lin, He, Zhenyu, Yuan, Jing
- Chemosphere 2019 v.218 pp. 992-1001
- acute exposure, air, biomarkers, breathing, nitric oxide, particulates, polycyclic aromatic hydrocarbons, regression analysis, students, China
- Exposure to fine particulate matter (PM2.5) is linked to various respiratory outcomes. However, the associations of concentrations of PM2.5-bound polycyclic aromatic hydrocarbons (PM2.5-bound PAHs) with airway inflammatory indices remains unclear. To assess effects of short-term exposure to PM2.5-bound PAHs on fractional exhaled nitric oxide (FeNO), we conducted a pilot study with repeated measures. We recruited 20 postgraduate students in Wuhan city, China, and repeatedly measured outdoor and indoor (including dormitories, offices and laboratories) PM2.5-bound PAHs concentrations, urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) and FeNO levels in the four seasons. Subsequently, we estimated inhaled doses of PM2.5-bound PAHs based on the micro-environmental PM2.5-bound PAHs concentrations, time-activity patterns and referred inhalation rates. We assessed the association of inhaled doses of PM2.5-bound PAHs with FeNO using linear mixed-effects regression models. We found the positive associations of urinary ∑OH-PAHs levels with inhaled doses of indoor PM2.5-bound PAHs (including dormitories and offices) (all p < 0.05). A one-unit increase in inhaled doses of PM2.5-bound PAHs or in urinary concentrations of ∑OH-PAHs was corresponded to a maximum FeNO increase of 13.5% (95% CI: 5.4, 22.2) at lag2 day or of 6.8% (95% CI: 3.4, 10.2) at lag1 day. Inhaled doses of PM2.5-bound PAHs or urinary OH-PAHs was positively related to increased FeNO, they may be accepted as a short-term biomarker of exposure to PAHs in air. Exposure to PM2.5-bound PAHs in indoor air may contribute more to the body burden of PAHs than outdoor air, and exhibited stronger effect on increased FeNO rather than urinary OH-PAHs.