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Exposure to Polycyclic aromatic hydrocarbons (PAHs) has been associated with inflammatory responses. Fractional exhaled nitric oxide (FeNO) and exhaled carbon monoxide (eCO) are both important inflammatory mediators especially in airways. However, few studies have investigated associations of PAH exposures with FeNO or eCO. Therefore, we aimed to quantify the associations of urinary PAH metabolites with FeNO and eCO levels, and investigate their potential effect modifiers by linear mixed models among 4133 participants from the Wuhan-Zhuhai cohort in China. We further performed stratified analyses to estimate effect modification. We found significant associations of increased urinary PAH metabolites with elevated eCO and FeNO. Among all participants, each 1% increase of 1-hydroxynaphthalene, 2-hydroxynaphthalene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 3-hydroxyphenanthrene, and total PAH metabolites was significantly associated with a 12.6% (95% confidence interval: 9.3%, 15.9%), 9.7% (6.5%, 12.9%), 7.5% (4.1%, 10.9%), 3.2% (0.2%, 6.2%), 2.7% (0.1%, 5.3%), and 6.5% (2.7%, 10.4%) increased eCO level, respectively; while each 1% increase of urinary 1-hydroxynaphthalene, 9-hydroxyphenanthrene, 3-hydroxyphenanthrene, and 2-hydroxyphenanthrene was associated with a − 3.0% (− 5.8%, − 0.2%), 2.9% (0.3%, 5.6%), 3.2% (1.0%, 5.4%), and 4.5% (2.2%, 6.9%) change of FeNO level, respectively. Positive associations between certain urinary PAH metabolites and eCO were observed among both ever-smokers and non-smokers, and the associations were stronger among ever-smokers than that among non-smokers. Increased urinary PAH metabolites were associated with decreased FeNO among ever-smokers and elevated FeNO levels among non-smokers. Our findings suggest that PAH exposures may impair airway through inducing inflammatory response, especially among ever-smokers. [ABSTRACT FROM AUTHOR]

Background: Short-term effects of fine particulate matter (PM 2.5 ) exposure on lung function have been reported. However, few studies have assessed PM 2.5 exposure on the personal level, and the mechanism underlying the effects of PM 2.5 exposure on lung function remains less clear., Objectives: To evaluate the association between personal PM 2.5 exposure and lung function alteration in general population and to explore the roles of systematic inflammation and oxidative damage in this association., Methods: A total of 7685 lung function tests were completed among 4697 urban adults in Wuhan, China. Plasma C-reactive protein (CRP), urinary 8-iso-prostaglandin-F 2α (8-iso-PGF 2α ) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were measured. Personal PM 2.5 exposure levels were estimated using an estimation model from the actual measurements of individual PM 2.5 levels in 191 participants. Mixed linear models were used to evaluate the association between personal PM 2.5 exposure and lung function. Mediation analyses were conducted to investigate the roles of CRP, 8-iso-PGF 2α and 8-OHdG in above associations., Results: After adjusting for confounders, each 10 μg/m 3 increase in the previous-day personal PM 2.5 exposure was associated with 2.94 mL, 2.02 mL and 16.14 mL/s decreases in forced vital capacity (FVC), forced expiration volume in 1 s (FEV 1 ) and peak expiratory flow, respectively. The associations were more obvious among never smokers compared with current smokers. Cumulative 7-day exposure to PM 2.5 led to the strongest adverse effects on lung function. Among never smokers with high PM 2.5 exposure levels, a positive relationship was observed between personal PM 2.5 level and urinary 8-iso-PGF 2α , and 8-iso-PGF 2α meditated 4.69% and 12.30% of the association between the 7-day moving PM 2.5 concentration and FVC and FEV 1 , respectively. We did not observe a significant positive association between PM 2.5 exposure and plasma CRP or urinary 8-OHdG., Conclusion: Short-term personal exposure to PM 2.5 is associated with reduced pulmonary ventilation function. Urinary 8-iso-PGF 2α partly mediates these associations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Fine particulate matter (PM 2.5 ) exposure has been associated with lung function decline, but impact of PM 2.5 constituents especially for polycyclic aromatic hydrocarbons (PAHs) on lung function is unclear among community population. We enrolled 224 Chinese participants who participated in two study periods (2014-2015 and 2017-2018) of the Wuhan-Zhuhai cohort as a panel, and quantified the associations of personal PM 2.5 and sixteen PM 2.5 -bound PAHs with lung function levels as well as lung function change in three years by linear mixed models. Diagnostic ratios were calculated to identify potential sources of PM 2.5 -bound PAHs in Wuhan and Zhuhai separately. In single-constituent models, we found that each one interquartile-range increase of naphthalene, acenaphthene, fluoranthene and pyrene were associated with 26.82, 60.99, 45.25 and 23.37 mL decline in FVC respectively; while fluoranthene and pyrene were associated with 27.43 and 15.49 mL decline in FEV 1 respectively. Similar results were observed in consitituent-PM 2.5 joint models and single-constituent residual models. Persistently long-term high levels of three HMW-PAHs (benzo[a]anthracene, dibenzo[a,h]anthracene, and benzo[ghi]perylene) were associated with 214.65, 226.13, and 265.00 mL decline in FVC decline in three years, compared with persistently low exposure level groups. The associations were different between Wuhan and Zhuhai. The results of diagnostic ratios suggested the differences in PAH emissions between two cities. Our findings provide evidence that both short- and long-term PM 2.5 -bound PAH exposures might affect lung function., (Copyright © 2019 Elsevier B.V. All rights reserved.)