Abstract

Associations and dose-response relationships between different kinds of urine polycyclic aromatic hydrocarbons (PAHs) metabolites and lung functions in general American adults were unknown. Data from the National Health and Nutrition Examination Survey database of the 2009-2012 cycles were used. The independent variables were urine PAHs adjusted for urine creatinine, including 1-hydroxynaphthalene (1-NAP), 2-hydroxynaphthalene (2-NAP), 3-hydroxyfluorene (3-FLU), 2-hydroxyfluorene (2-FLU), 3-hydroxyphenanthrene (3-PHE), 1-hydroxyphenanthrene (1-PHE), 2-hydroxyphenanthrene (2-PHE), 1-hydroxypyrene (1-PYR), and 9-hydroxyfluorene (9-FLU). The dependent variables were lung function indices including the forced vital capacity (FVC), the 1st second of a forceful exhalation (FEV1), the ratio of FEV1/FVC, the forced expiratory flow rate 25-75% (FEF25%-75%), and the fractional exhaled nitric oxide (FENO). Multivariate linear regression analyses and the restricted cubic splines were used. Except for 1-PHE and 9-FLU, FEF25%-75% decreased in quartile (Q) 4 of all the remaining seven PAHs; FEV1 decreased in Q4 of 2-NAP, 3-PHE, 2-PHE, and 9-FLU, with β (SE) of -121.89 (45.46), -105.21 (33.57), -143.67 (40.60), and -127.71 (37.14), respectively. FVC decreased only in Q3 of 9-FLU, with β (SE) of -142.24 (56.54); FEV1/FVC decreased in Q4 of all PAHs except for 2-FLU. Besides, FENO decreased in Q4 of all PAHs in smokers, while in non-smokers, the results were opposite. The dose-response relationships were non-linear. In conclusion, we found that urine PAHs may relate to the changes in lung functions. Besides, smoking status had a significant influence on FENO; FENO decreased in smokers while increased in non-smokers, suggesting that PAHs exposure may relate to airway inflammation.

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