Impacts of low socioeconomic status and polycyclic aromatic hydrocarbons exposure on lung function among a community-based Chinese population.

Lung function is related to socioeconomic status (SES) and exposure to polycyclic aromatic hydrocarbons (PAHs). However, joint effect of SES and exposure to PAHs on lung function has been largely unknown. We aimed to investigate joint effects of SES and urinary OH-PAHs levels on lung function parameters. This study included 2739 Wuhan participants from the baseline survey of the Wuhan-Zhuhai (WHZH) Cohort Study (n=3053). They completed the questionnaire, physical examination and provided blood and urine samples. Twelve urinary monohydroxy-PAHs metabolites (OH-PAHs) and lung function were measured by gas chromatography-mass spectrometry and digital spirometers, respectively. Individuals with low educational levels and low or high levels of urinary ΣOH-PAHs had a 3.5% (95% CI: -5.4, -1.6%) or 4.2% (95% CI: -6.1, -2.3%) reduction in the ratio of forced expiratory volume in 1s to forced vital capacity (FEV1/FVC), respectively, and those with middle levels of education and high levels of urinary ΣOH-PAHs had a 2.1% (95% CI: -5.4, -1.6%) reduction in the FEV1/FVC ratio, rather than those with high levels of education and low levels of urinary ΣOH-PAHs. Individuals with low levels of education had a -3.0% (95% CI: -4.4, -1.6%) reduction in FEV1/FVC compared with individuals with high levels of education. Urinary OH-PAHs levels were marginally negatively related to FEV1 in all participants (p=0.073). The results indicated that there was a prominent effect of low levels of education and higher exposure to PAHs on lung function decline, indicating that it is a necessary to take measures to promote the education level and reduce exposure to environmental PAHs.

Hou J ，Sun H ，Ma J ，Zhou Y ，Xiao L ，Xu T ，Cheng J ，Chen W ，Yuan J ... -  《-》

Combined effect of urinary monohydroxylated polycyclic aromatic hydrocarbons and impaired lung function on diabetes.

Associations of type 2 diabetes with exposure to polycyclic aromatic hydrocarbons and reduced lung function have been reported. The aim of the present study was to investigate effect of reduced lung function and exposure to background PAHs on diabetes. A total of 2730 individuals were drawn from the Wuhan-Zhuhai (WHZH) Cohort Study (n=3053). Participants completed physical examination, measurement of lung function and urinary monohydroxylated polycyclic aromatic hydrocarbons (OH-PAHs). Risk factors for type 2 diabetes were identified by multiple logistic regression analysis, and the presence of additive interaction between levels of urinary OH-PAHs and lower lung function was evaluated by calculation of the relative excess risk due to interaction (RERI) and attributable proportion due to interaction (AP). Urinary OH-PAHs levels was positively associated with type 2 diabetes among individuals with impaired lung function (p<0.05). Forced expiratory volume in one second (FEV1, odd ratio (OR): 0.664, 95% confidence interval (CI): 0.491-0.900) and forced vital capacity (FVC, OR: 0.693, 95% CI: 0.537-0.893) were negatively associated with diabetes among individuals. Additive interaction of higher urinary levels of OH-PAHs and lower FVC (RERI: 0.679, 95% CI: 0.120-1.238); AP: 0.427, 95% CI: 0.072-0.782) was associated with diabetes. Exposure to background PAHs was related to diabetes among individuals with lower lung function. Urinary levels of OH-PAHs and reduced lung function had an additive effect on diabetes.

Hou J ，Sun H ，Xiao L ，Zhou Y ，Yin W ，Xu T ，Cheng J ，Chen W ，Yuan J ... -  《-》

Combined effect of central obesity and urinary PAH metabolites on lung function: A cross-sectional study in urban adults.

Central obesity and polycyclic aromatic hydrocarbons (PAHs) exposure were reported as independent risk factors for lung function decline. However, the interaction between central obesity and PAHs exposure on lung function is still unclear. To evaluate the impact of central obesity, urinary polycyclic aromatic hydrocarbon metabolites (OH-PAHs) and their combined effects on lung function in general population. Lung function and urinary OH-PAHs were measured for 3,749 participants from the Wuhan-Zhuhai cohort. Central obesity was evaluated by waist-to-hip ratio. Generalized linear regression was used to estimate combined effect of central obesity and OH-PAHs on lung function. Compared with participants without central obesity and with low urinary total OH-PAHs (∑OH-PAHs) level, those with central obesity and high urinary ∑OH-PAHs level had 59.4 mL and 61.0 mL reductions for forced vital capacity (FVC) and forced expiratory volume in 1s (FEV1), respectively (P < 0.05). The reductions were more evident in smokers and males. Additive interactions between central obesity and urinary ∑OH-PAHs on lung function were observed, especially on FEV1 (P < 0.05). Each 1-unit increase in log-transformed value of ∑OH-PAHs was associated with -34.4 ml (95% confidence interval [CI]: -66.9, -1.8) and -34.8 mL (-61.1, -8.5) changes in FVC and FEV1 among those without central obesity, while -21.4 ml (-49.9, 7.1) and -19.7 ml (-43.4, 4.0) changes among those with central obesity. Polycyclic aromatic hydrocarbons exposure has combined effect with central obesity on lung function parameters.

Mu G ，Zhou Y ，Ma J ，Guo Y ，Xiao L ，Zhou M ，Cao L ，Li W ，Wang B ，Yuan J ，Chen W ... -  《-》

Urinary polycyclic aromatic hydrocarbon metabolites, Club cell secretory protein and lung function.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with lung function decline. However, the underlying mechanisms for the association remain unclear. To explore potential role of a lung epithelial biomarker, Club cell secretory protein (CC16), in associations between PAH exposures and lung function decline. We investigated 3384 adults from the Wuhan-Zhuhai cohort, and followed up at three years after first examination. Linear mixed models was used to quantify dose-response relationships between urinary monohydroxylated PAH metabolites (OH-PAHs) and lung function, as well as OH-PAHs and plasma CC16. Mediation analysis was conducted to investigate role of CC16 in the association between OH-PAHs and lung function. We also estimated the relationships between OH-PAHs and lung function change in three years among participants with different levels of CC16. Each 1-unit increase of log-transformed total urinary high and low molecular weight OH-PAHs (∑HMW OH-PAH and ∑LMW OH-PAHs) were associated with a 22.59 and 25.25ml reduction of FEV1 respectively, while∑HMW OH-PAH was associated with a 30.38ml reduction of FVC. Moreover, these negative associations between OH-PAHs and lung function levels were significant only among low CC16 group (<15.83ng/ml). CC16 concentration decreased monotonically with increased high molecular weight OH-PAHs (∑HMW OH-PAHs) when ∑HMW OH-PAH concentration was over 0.67μg/mmol Cr. CC16 mediated 22.13% of the association between ∑HMW OH-PAH and FVC among individuals with higher ∑HMW OH-PAH. After three years of follow-up, subjects with low level of plasma CC16 had a significant decline of FVC when exposed to high level of ∑HMW OH-PAH. CC16 play an important role in the association between high molecular weight PAHs and FVC. Individuals with low plasma CC16 level might suffer a decline in lung function when exposed to high level of high molecular weight PAHs.

Zhou Y ，Mu G ，Liu Y ，Xiao L ，Ma J ，Wang B ，Shi T ，Tan A ，Yuan J ，Chen W ... -  《-》

Polycyclic aromatic hydrocarbons exposure and lung function decline among coke-oven workers: A four-year follow-up study.

This study aimed to investigate quantitative relationships of urinary PAH metabolites with lung function declines among coke-oven workers. We performed a prospective investigation involving 1243 workers with follow-up periods from 2010 to 2014. Their lung function measurements, including forced vital capacity (FVC), forced expiratory volume in one second (FEV1), the percentage of predicted FVC (FVC%) and FEV1 (FEV1%), FEV1/FVC ratio, and forced expiratory flow between 25% and 75% of vital capacity (FEF25-75), were detected in both baseline (2010) and follow-up study (2014). We also detected the urinary concentrations of 12 PAH metabolites in the baseline study. The relationships between the baseline urinary PAH metabolites and 4-year lung function declines were analyzed by multivariate linear regressions, with adjustment for potential confounders. We found that the baseline concentrations of urinary 1-hydroxynaphthalene (1-OHNa), 2-OHNa, 2-hydroxyfluorene (2-OHFlu), 9-OHFlu, 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, and ΣOH-PAHs were significantly associated with accelerated decline in FEV1/FVC [all β>0 and false discovery rate (FDR) P<0.05]. Additionally, the baseline levels of urinary 1-OHNa, 1-OHPh, 2-OHPh, 9-OHPh, 1-hydroxypyrene (1-OHP), and ΣOH-PAHs were associated with significantly deeper decline in FEF25-75 (all β>0 and FDR P<0.10). When using backward selection to adjustment for 10 urinary PAH metabolites, the most significant determiner for FEV1/FVC decline was 1-OHNa among nonsmokers and 9-OHFlu among smokers, and the significant determiner for FEF25-75 decline was 9-OHPh among nonsmokers and 1-OHP among smokers. This longitudinal study revealed that higher baseline exposure levels of PAHs could lead to greater decline in lung function over a 4-year follow-up.

Wang S ，Bai Y ，Deng Q ，Chen Z ，Dai J ，Li X ，Zhang W ，Zhang X ，He M ，Wu T ，Guo H ... -  《-》