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To quantify the association of polycyclic aromatic hydrocarbons (PAHs) and the polygenic risk score (PRS) with lung function decline, we developed a repeated-measures study with 4681 observations from baseline and 6-year follow-up of the Wuhan-Zhuhai cohort. Lung function and urinary monohydroxylated PAH metabolites (OH-PAHs) were measured for each observation. The PRS was derived from 246 lung function-associated genetic variants weighted by the effect size of the decreasing ratio of forced expiratory volume in 1 s by forced vital capacity (FEV1/FVC). Linear mixed models were used to estimate the longitudinal exposure-response relationships between OH-PAHs and lung function, and to evaluate the interactions between OH-PAHs and PRS on the longitudinal change of lung function. We found that each 1-unit increase in log-transformed values of 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxyphenanthrene, 1-hydroxypyrene, low molecular weight OH-PAHs (ΣLMW-OH-PAHs), and total OH-PAHs (ΣOH-PAHs) was associated with an annual change in FEV1/FVC of -0.140, -0.112, -0.260, -0.300, -0.159, -0.220, -0.145, -0.156, and -0.177 %/year, respectively. Interactions on the annual decline of FEV1/FVC were detected between ΣLMW-OH-PAHs and PRS (-0.010 %/year, 95% confidence interval -0.018 to -0.001, P int  = 0.0228), and between ΣOH-PAHs and PRS (-0.010 %/year, -0.018 to -0.001, P int  = 0.0203). These results indicated that specific and total urinary OH-PAHs were associated with the longitudinal FEV1/FVC decline, and ΣLMW-OH-PAHs as well as ΣOH-PAHs interacted with PRS on the annual decline of FEV1/FVC., 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 © 2023. Published by Elsevier Ltd.)

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants that pose detrimental effects on human health, and the exploration of the associations of PAHs exposure with long non-coding RNA (lncRNA) may provide novel clues to the underlying mechanisms. In the present study, we detected 10 urinary PAHs metabolites by GC-MS and plasma lncRNAs levels by Human LncRNA Array v4 among 230 participants from two panels (160 in the Shiyan panel and 70 in the Wuhan-Zhuhai panel). We applied linear regression models to assess the associations between PAHs metabolites and lncRNAs separately in each panel and combined the results using fixed-effect meta-analysis. To explore the potential origin of PAHs-related lncRNAs in plasma, we estimated their tissue-specificity and associations between lncRNAs levels in plasma and leukocytes. Leukocytes mRNA sequencing data and RNA binding proteins were utilized to explore implicated pathways of identified lncRNAs. We found that urinary 1-hydroxyphenanthrene (1-OH-Phe) was inversely associated with 8 lncRNAs and positively associated with 1 lncRNA, as well as 9-hydroxyphenanthrene (9-OH-Phe) was inversely associated with 11 lncRNAs (FDR < 0.1). Tissue specificity analysis using Genome Tissue Expression database suggested that several identified lncRNAs might specifically express in organs targeted by PAHs exposure (lung, liver, heart, kidney, and brain). Besides, plasma levels of 1-OH-Phe related ENSG00000260616 and 9-OH-Phe related STARD4-AS1 were inversely associated with their intra-leukocytes levels (P value < 0.05). Notably, STARD4-AS1 was positively associated with the expression levels of its neighboring protein-coding gene (CAMK4 and STARD4) in leukocytes and were involved in pathways related to cellular response to DNA damage, which we further confirmed using DNA damage biomarker, 8-hydroxydeoxyguanosine. Functional analysis also revealed vital pathways related to cytokine-mediated signaling and glucose homeostasis. Our findings provided novel insights into plausible biological mechanisms underlying the adverse effects of PAHs exposure., 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 © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

As a polycyclic aromatic hydrocarbon, environmental exposure to phenanthrene is widespread worldwide. The potential effects and mechanism of phenanthrene exposure on fasting plasma glucose (FPG) have not been well determined. In this study, we aim to explore the effects of phenanthrene exposure and AMER3 variants on fasting plasma glucose (FPG) through a longitudinal epidemiological study. Repeated measurements of five urinary hydroxyphenanthrene (OHPh) for 5739 participants with 7083 observations from the Wuhan-Zhuhai cohort were performed to analyze the relationships between total OHPh (ΣOHPh) and FPG using linear mixed models and restricted cubic spline functions. Then, we genotyped 2777 participants (4104 observations) using the Infinium OmniZhongHua-8 BeadChip and included all 14 single nucleotide polymorphisms (SNPs) within the AMER3 gene to analyze the interaction of the AMER3 on the relationship between ΣOHPh and FPG. We observed a U-shaped relationship between ΣOHPh and FPG, and the turning point of ΣOHPh was 2.512 μg/mmol Cr. When lower than the turning point, ΣOHPh was negatively associated with FPG, while higher than the turning point, ΣOHPh was positively associated with FPG. Furthermore, we observed interactions (P int <0.05) between two common variants (rs72854995 and rs72854999) of the AMER3 and ΣOHPh on FPG change: the U-shaped relationship was still observed in the GG genotype groups but not in the allele A carriers. Our results suggested that the AMER3 gene can modify the U-shaped relationship between phenanthrenes exposure and FPG, which showed a new gene-environment interaction and will provide a new perspective on the relationship between phenanthrene exposure and FPG., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Background: The adverse effects of polycyclic aromatic hydrocarbon (PAHs), a group of common environmental pollutants, on mental health are unclear. This study is developed to evaluate the potential association of urinary PAH metabolites with depression in US adults., Methods: Measurement of 8 urinary PAH metabolites and assessment of depression were available for 9625 adults in the National Health and Nutritional Examination Survey 2005-2016. Multiple logistic regression models and weighted quantile sum (WQS) regression models were applied to evaluate the association between urinary PAH metabolites and depression., Results: Among 9625 individuals with a weighted geometric mean age of 42.63 years, 801 participants suffered from depression. Significant positive dose-response relationships were observed between specific urinary PAH metabolites and the risk of depression after adjusting for potential confounders. Urinary 1-hydroxynaphthalene was positively and dose-dependently associated with the risk of depression among total participants (odds ratio: 1.188; 95% confidence interval: 1.096-1.288). In addition, each 1-unit increase of ln-transformed urinary 1-hydroxynaphthalene, 2-hydroxynaphthalene, 3-hydroxyfluorene, 2-hydroxyfluorene, 1-hydroxyphenanthrene, 2&3-hydroxyphenanthrene, 1-hydroxypyrene, and total PAH metabolites was associated with a 23.3%, 32.6%, 23.3%, 29.4%, 30.8%, 22.8%, 29.4%, and 31.7% increment in the risk of depression in smokers, respectively (all P and P trend  < 0.05). Of note, the positive WQS index was also significantly associated with the increased risk of depression in smokers (1.122, 1.059-1.188)., Conclusion: Exposure to PAHs may elevate the risk of depression among US adults. More studies are warranted to investigate the underlying mechanism by which PAHs induce the development of depression., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Objective: We aim to analyze the effects of polycyclic aromatic hydrocarbons (PAHs) exposure and genetic predisposition on blood lipid through a longitudinal epidemiological study., Methods: We enrolled 4,356 observations who participated at baseline (n = 2,435) and 6-year follow-up (n = 1,921) from Wuhan-Zhuhai cohort. Ten urinary PAHs metabolites and blood lipid (i.e., total cholesterol [TC], triglycerides [TG], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) were measured at both baseline and follow-up. The polygenic risk scores (PRS) of blood lipid were constructed by the corresponding genome-wide association studies. Linear mixed models were fit to identify associations between urinary PAHs metabolites, blood lipid, and lipid-PRSs in the repeated-measure analysis. Besides, longitudinal relationships of blood lipid with urinary PAHs metabolites and respective lipid-PRSs were examined by using linear regression models., Results: Compared with subjects who had persistently low urinary total hydroxyphenanthrene (ΣOHPh), those with persistently high levels had an average increase of 0.137 mmol/l for TC and 0.129 mmol/l for LDL-C over 6 years. Each 1-unit increase of TC-, TG-, LDL-C-, and HDL-C-specific PRS were associated with an average increase of 0.438 mmol/l for TC, 0.264 mmol/l for TG, 0.198 mmol/l for LDL-C, and 0.043 mmol/l for HDL-C over 6 years, respectively. Compared with subjects who had low genetic risk and persistently low ΣOHPh, subjects with high LDL-specific PRS and persistently high ΣOHPh had an average increase of 0.652 mmol/l for LDL-C., Conclusions: Our results suggest that high-level ΣOHPh exposure is associated with an average increase of LDL-C over 6 years, and those relationships can be aggravated by a higher LDL-C-genetic risk. No significant relationships were observed between other PAHs metabolites (including hydroxynaphthalene, hydroxyfluorene, and hydroxypyrene) and blood lipid changes over 6 years. Our findings emphasize the importance of preventing PAHs exposure, particularly among those with a higher genetic predisposition of hyperlipidemia., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

We aim to investigate the long-term adverse effects of polycyclic aromatic hydrocarbons (PAHs) exposure on heart rate variability (HRV) reduction, and to assess the potential role of transforming growth factor-β1 (TGF-β1) in such relationship. We enrolled 2985 adult residents with 4100 observations who participated at baseline and 6-years follow-up from Wuhan-Zhuhai cohort. Ten detectable urinary PAHs metabolites and two HRV indices were repeatedly measured at baseline and follow-up; and plasma TGF-β1 levels were also determined for all subjects. We observed that both total urinary low molecular weight PAHs (ΣLWM OH-PAH) and total urinary high molecular weight PAHs (ΣHWM OH-PAH) were negatively associated with HRV reductions (P < 0.05). Subjects with persistent high levels of ΣHWM OH-PAH had a significant reduction in HRV over 6 years, and the incensement of TGF-β1 could aggravate above adverse effects in a dose-response manner. All kinds of PAHs were positively associated with plasma TGF-β1 elevation, which in turn, were negatively related to HRV indices. Increased TGF-β1 significant mediated 1.34-3.62% of PAHs-associated HRV reduction. Our findings demonstrated that long-term high levels of PAHs exposure could cause HRV reductions, and TGF-β1 may play an essential role in such association., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with heart rate variability (HRV) reduction, a widely used marker of cardiovascular autonomic dysfunction. The role of DNA methylation in the relationship between PAHs exposure and decreased HRV is largely unknown. This study aims to explore epigenome-wide DNA methylation changes associated with PAHs exposure and further evaluate their associations with HRV alternations among non-current smokers. We measured 10 mono-hydroxylated PAHs (OH-PAHs) in urine and DNA methylation levels in blood leukocytes among participants from three panels of Chinese non-current smokers (152 in WHZH, 99 in SY, and 53 in COW). We conducted linear regression analyses between DNA methylation and OH-PAHs metabolites with adjustment for age, gender, body mass index, drinking, blood cell counts, and surrogate variables in each panel separately, and combined the results by using inverse-variance weighted fixed-effect meta-analysis to obtain estimates of effect size. The median value of total OH-PAHs ranged from 0.92 × 10 -2 in SY panel (62.6% men) to 13.82 × 10 -2  μmol/mmol creatinine in COW panel (43.4% men). The results showed that methylation levels of cg18223625 (COL20A1) and cg07805771 (SLC16A1) were significantly or marginally significantly associated with urinary 2-hydroxynaphthalene [β(SE) = 0.431(0.074) and 0.354(0.068), FDR = 0.016 and 0.056, respectively], while methylation level of cg09235308 (PLEC1) was positively associated with urinary total OH-PAHs [β(SE) = 0.478(0.079), FDR = 0.004]. Hypermethylations of cg18223625, cg07805771, and cg09235308 were inversely associated with HRV indices among the WHZH and COW non-current smokers. However, we did not observe significant epigenome-wide associations for the other 9 urinary OH-PAHs. These findings provide new evidence that PAHs exposure is linked to differential DNA methylation, which may help better understand the influences of PAHs exposure on HRV alternations., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Polycyclic aromatic hydrocarbons (PAHs) have been reported to cause various health damages. However, some PAH derivatives are still used as agents, and some of them have hypoglycemic effects. Till now, few studies explored the relationship between urinary PAH metabolites and fasting plasma glucose (FPG). In this study, A total of 2682 non-smokers in the second follow-up of the Wuhan-Zhuhai cohort were included to explore the relationship between urinary PAH metabolites and FPG. FPG related epigenome-wide association study (EWAS) was conducted among 212 never smokers, and the mediation analysis was performed to find potential mediator cytosine-phosphoguanine (CpG) sites in the above relationship. The concentration of total urinary PAH metabolites was 3.60 (2.37, 5.85) μg/mmol Cr. The urinary PAH metabolites were negatively associated with FPG. Each 1-U increase in ln-transformed levels of 1-hydroxynaphthalene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, or 2- hydroxyphenanthrene was associated with 0.008-, 0.007-, 0.010-, or 0.010- unit decreased in ln-transformed levels of FPG, respectively (all p < 0.05). We found 28 new CpG sites related to FPG (FDR <0.05) through EWAS. Mediation analysis found that cg11350141 on AMER3 mediated 41.91% of the negative association of total urinary PAH metabolites with FPG. These results provide a new clue for the development of hypoglycemic agents., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Previous studies found that exposure to polycyclic aromatic hydrocarbons (PAHs) was associated with type 2 diabetes (T2D) prevalence. However, the potential mechanism is still unclear. In this study, we investigated 3031 Chinese urban adults to discover the relationship between PAH exposure and plasma Interleukin-22 (IL-22) and potential role of IL-22 in the association between PAH and fasting plasma glucose (FPG) or risk of T2D. After adjustment for potential confounders, significant dose-response relationships were observed between several urinary PAH metabolites with FPG and the prevalence of T2D. Each 1-U increase in ln-transformed value of 2-hydroxynaphthalene (2-OHNa), 2-hydroxyphenanthrene (2-OHPh), 3-hydroxyphenanthrene (3-OHPh), 4-hydroxyphenanthrene (4-OHPh), 9-hydroxyphenanthrene (9-OHPh), 1-hydroxypyrene (1-OHP) or total PAH metabolites was significantly associated with a 0.053, 0.026, 0.037, 0.045, 0.051, 0.041 or 0.047 unit decrease in IL-22 level, respectively. In addition, plasma IL-22 level was negatively associated with FPG and prevalence of T2D in a dose-dependent manner. Mediation analysis showed that IL-22 mediated 8.48 %, 3.87 %, 6.64 %, 6.47 %, and 8.67 % of the associations between urinary 2-OHNa, 1-OHPh, 3-OHPh, 4-OHPh, and 9-OHPh with the prevalence of T2D, respectively. These results indicated that urinary PAHs metabolites were inversely associated with plasma levels of IL-22, but positively related to FPG and the T2D prevalence. Downregulation of IL-22 might play a significant role in mediating PAHs exposure-associated risk increasement of T2D., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Polycyclic aromatic hydrocarbon (PAH) exposure has been considered a risk factor for cardiovascular diseases (CVD), whereas possible mechanisms for this association have not been fully understood. This study focused on exploring the potential effect of oxidatively damaged DNA on the relationships between PAH exposure and the 10-year atherosclerotic CVD (ASCVD) risk. Urinary levels of monohydroxy PAH metabolites (OH-PAHs) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG, the typical biomarker for oxidatively damaged DNA) were measured among 3052 subjects in the baseline of the Wuhan-Zhuhai cohort. The relationships between urinary OH-PAHs, 8-oxodG and 10-year risk of ASCVD were analyzed by linear mixed models and logistic regression models, respectively. The mediation analysis was further applied to explore the role of 8-oxodG in the relationship between urinary OH-PAHs and 10-year ASCVD risk. After controlling for potential confounders, the log-transformed level of total urinary low molecular weight OH-PAHs (∑LMW OH-PAHs) was significantly associated with an elevated risk of 10-year ASCVD [odds ratio (OR) = 1.222, 95% confidence interval (CI): 1.065-1.402]. More specifically, significantly positive dose-response relationships between total urinary hydroxynaphthalene (∑OHNa), hydroxyfluorene (∑OHFlu), hydroxyphenanthrene (∑OHPh) and 10-year ASCVD risk were observed (all P for trend <0.05). We also found positive relationships between urinary OH-PAH levels and 8-oxodG, as well as between urinary 8-oxodG levels and 10-year risk of ASCVD. Moreover, mediation analyses indicated that urinary 8-oxodG mediated 14.49%, 12.62% and 10.55% of the associations between urinary ∑LMW OH-PAHs, ∑OHNa, ∑OHFlu and 10-year ASCVD risk, respectively. These findings suggest that the oxidatively damaged DNA pathway may be a possible mechanism underlying PAH-associated ASCVD risk elevation., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) is related to decreased lung function. However, whether oxidative damage is involved in this relationship remains unclear. This study was aimed to explore the potential mediating role of oxidative DNA or lipid damage in the association between PAH exposure and lung function., Methods: The urinary levels of monohydroxy polycyclic aromatic hydrocarbon metabolites (OH-PAHs) and lung function parameters were measured among 3367 participants from the baseline of the Wuhan-Zhuhai cohort. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-isoprostane (8-iso-PGF2α) were determined to evaluate the individuals' oxidative DNA and lipid damage degrees, respectively. Linear mixed models were used to investigate the associations of urinary OH-PAHs, 8-OHdG and 8-iso-PGF2α with lung function parameters. Mediation analysis was further conducted to assess the potential role of oxidative damage in the association between urinary OH-PAHs and lung function., Results: Each one-percentage increase in the sum of urinary OH-PAHs, high-molecular-weight or low-molecular-weight OH-PAHs (ƩOH-PAHs, ƩHMW OH-PAH or ƩLMW OH-PAHs, respectively) was associated with a 0.2152-, 0.2076- or 0.1985- ml decrease in FEV 1 , and a 0.1891-, 0.2195- or 0.1634- ml decrease in FVC, respectively. Additionally, significantly positive dose-response relationships of ƩOH-PAHs, ƩHMW OH-PAH and ƩLMW OH-PAHs with urinary 8-OHdG or 8-iso-PGF2α, as well as an inverse dose-response relationship between urinary 8-OHdG and FVC, were observed (all P for trend < 0.05). Mediation analysis indicated that urinary 8-OHdG mediated 14.22% of the association between ƩHMW OH-PAH and FVC., Conclusion: Higher levels of oxidative DNA damage might be involved in the decreased levels of FVC caused by high-molecular-weight PAH exposure.

Urinary polycyclic aromatic hydrocarbon (PAH) metabolites, biomarkers of internal PAH exposure, are commonly used to explore the effects of PAH on human health. However, the correlation between environmental PAH exposure and the species or levels of urinary PAH metabolites remains unclear. We collected detailed information on PAH exposure sources, including cigarette smoking, cooking, traffic and diet habits via structured questionnaires, and determined 12 urinary monohydroxylated PAH metabolites (OH-PAHs) among 4092 participants from the Wuhan-Zhuhai cohort. Linear mixed models and generalized linear models were conducted to explore the associations of urinary metabolite levels with single or multiple PAH exposure sources. We also calculated the standardized regression coefficients to further compare the contributions of different sources to urinary OH-PAH levels. Our results showed that increasing levels of urinary 1-, 2-hydroxynaphthalene (1-, 2- OHNa) and 2-hydroxyfluorene (2-OHFlu) were significantly correlated with tobacco smoking (all P < 0.01). The concentrations of 1-, 2- OHNa and 9-hydroxyfluorene (9-OHFlu) were positively correlated with dietary intake (all P < 0.05). Individuals who spent a long time in traffic showed elevated levels of 9-OHFlu and 1-hydroxyphenanthrene (1-OHPh) compared with individuals who spent a short time in traffic (all P < 0.05). Self-cooking was associated only with elevated 1-hydroxypyrene (1-OHP) levels. Moreover, good kitchen ventilation resulted in significantly decreased urinary low-molecular-weight OH-PAH levels. These findings suggested that cigarette smoking, self-cooking, high dietary PAH intake and a long time spent in traffic were associated with increased levels of specific urinary PAH metabolites, and good kitchen ventilation effectively reduced the exposure to low-molecular-weight PAHs in self-cooking participants., (Copyright © 2019 Elsevier Ltd. 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.)

Few studies have compared the biological effects of PM 2.5 from coal combustion, gasoline exhaust and urban ambient air, and the roles of polycyclic aromatic hydrocarbons (PAHs) and metals playing in the process remain unclear. In this study, PM 2.5 samples from coal combustion, gasoline exhaust and urban ambient air were analyzed for 16 PAHs and 23 metals. Cytotoxic and inflammatory effects of different PM 2.5 were evaluated on differentiated THP-1 and A549 cells, respectively. We found that the coal combustion PM 2.5 samples induced stronger cytotoxic and inflammatory effects (p < 0.05). Pearson's correlation and principal component analysis showed that the PAHs containing four or more benzenoid rings and specific metals of cadmium, thallium, zinc and lead were positively related to the biological effects. Our results suggested that coal combustion PM 2.5 might be a more serious health hazard. Specific PAHs and metals might be account for the PM 2.5 induced biological effects., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: 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., Objectives: To evaluate the impact of central obesity, urinary polycyclic aromatic hydrocarbon metabolites (OH-PAHs) and their combined effects on lung function in general population., Methods: 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., Results: 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 (FEV 1 ), 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 FEV 1 (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 FEV 1 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., Conclusion: Polycyclic aromatic hydrocarbons exposure has combined effect with central obesity on lung function parameters., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with metabolic diseases. However, relationships between PAH exposures and dyslipidemias have not been well addressed., Objectives: To investigate associations between urinary PAH metabolite concentrations and dyslipidemias in the general population., Methods: Twelve urinary PAH metabolites and four serum lipid profiles were measured in 3640 Chinese adults from the Wuhan-Zhuhai cohort. Dyslipidemias, including hyper-total cholesterol (HyperTC), hyper-triglyceride (HyperTG), hyper-low density lipoprotein cholesterol (HyperLDL-C), and hypo-high density lipoprotein cholesterol (HypoHDL-C) were classified according to the levels of serum lipids. Multiple logistic regression models were used to estimate the associations between urinary PAH metabolites and the prevalence of dyslipidemias. The effects of PAH exposure routes on dyslipidemias were further estimated by stratified analysis., Results: We found positive exposure-response relationships between urinary PAH metabolites and the prevalence of dyslipidemias. Compared with the lowest tertile of urinary PAH metabolites, increased risk of HyperTC were observed in those in the highest tertiles; The odds ratios (ORs) and 95% confidence intervals were 1.23 (1.03, 1.47), 1.44 (1.21, 1.71), 1.19 (1.01, 1.42), and 1.43 (1.20, 1.71) for 1-OHNa, 9-OHFlu, 1-OHPh, and 4-OHPh, respectively. Participants in the highest tertiles of 1-OHNa and 2-OHFlu had higher risk for HyperLDL-C, and the ORs were 1.21 (1.01, 1.45) and 1.18 (0.98, 1.42), respectively. Among smokers, only urinary 1-OHNa was associated with increased risk of HyperTC (1.36, 1.08-1.73) and HyperLDL-C (1.33, 1.01-1.74). While the increasing urinary levels of 9-OHFlu, 1-OHPh, and 4-OHPh were significantly associated with increased risk of HyperTC among non-smokers. In addition, the associations between urinary PAH metabolites and dyslipidemias were more pronounced among non-smokers who are cooked for themselves and had long-term traffic exposure., Conclusion: Elevated urinary PAH metabolites were associated with increased risks of HyperTC and HyperLDL-C. The source of PAH exposure could modify PAH species that affect dyslipidemias., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The relations of polycyclic aromatic hydrocarbons (PAHs) exposure with platelet indices remain unclear. Based on the baseline data from the Wuhan-Zhuhai Cohort Study, we used generalized linear model, multivariate logistic regression analysis and restricted cubic splines (RCS) to assess linear and nonlinear relationship of PAHs exposure with platelet indices. The results showed that among Wuhan individuals, there were the non-linear relations between total hydroxynaphthalene (ΣOHNa) and mean platelet volume (MPV) or ratio of mean platelet volume to platelet count (MPVP), total hydrophenanthrene (ΣOHPh) and MPV or platelet distribution width (PDW), the sum concentration of urinary monohydroxylated metabolites of PAHs (ΣOH-PAHs) and ratio of platelet count to lymphocyte count (PLR) or MPVP, 1-hydropyrene (1-OHP) and PLR or PDW. But among Zhuhai individuals, neither linear nor non-linear relations were found between each of OH-PAHs or ΣOH-PAHs and platelet indices. The findings indicate that serum MPV and MPVP may be independent biomarkers of effects of exposing to environmental PAHs on human bodies., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Exposure to polycyclic aromatic hydrocarbons (PAHs) is linked with increased risk of diabetes, whereas socioeconomic status (SES) may contribute to the development of diabetes. However, the mechanisms underlying the relationships between them are unclear. We used structural equation modeling (SEM) to identify mediating factors in the associations of PAHs exposure, low SES with diabetes risk. Data were collected from 2751 Wuhan participants at baseline from the Wuhan-Zhuhai Cohort Study (n = 3053). They answered the questionnaires regarding socio-demographic, participated physical examinations and provided urine samples for measurements of urinary monohydroxy-polycyclic aromatic hydrocarbons (OH-PAHs) levels. SEM was used to identify the mediating factors (such as hypertension, body mass index (BMI), triglycerides (TG) and total cholesterol (TCHO)) in the associations of low SES or PAHs exposure with diabetes risk. We observed that partial effect of PAHs exposure (β = 0.281, p = 0.034), BMI (β = 0.182, p = 0.000), TG (β = 0.358, p = 0.000), TCHO (β = 0.203, p = 0.009) or hypertension (β = 0.385, p = 0.000) on diabetes was directive. Moreover, low SES also exhibited a directive effect on PAHs exposure (β = -0.084, p = 0.000), BMI (β = 0.301, p = 0.000), hypertension (β = 0.134, p = 0.003) and TG (β = 0.087, p = 0.001). PAHs exposure directly affected TCHO levels (β = 0.080, p = 0.002) and TG (β = 0.076, p = 0.017). The proportion of the effect of PAHs exposure on diabetes mediated by TG and TCHO was 15.6%. The proportion of the effect of low SES on diabetes mediated by BMI, hypertension and TG was 89.1%. The results suggested that low SES increased diabetes risk, which may be partially explained by BMI, hypertension and triglycerides, and exposure to high levels of PAHs may have indirect contribution to increased risk for diabetes with dyslipidemia., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Polycyclic Aromatic Hydrocarbons (PAHs) exposure was related with metabolic syndrome (MetS) and heart rate variability (HRV) reduction, and HRV was also affected by cardiometabolic traits. However, the role of cardiometabolic traits in the associations from PAHs exposures to HRV was largely unknown. We conducted this study to investigate whether the relationship between PAHs exposure and HRV reduction was mediated by cardiometabolic traits. Levels of urinary polycyclic aromatic hydrocarbons metabolites (OH-PAHs), 10min-HRV, and metabolic traits were accurately measured for 2476 participants from Wuhan-Zhuhai (WHZH) cohort. Single mediator and multiple mediator models were used to evaluate the mediation effects of cadiometabolic traits. The concentrations of ΣOH-PAHs ranged from 4.20 to 8.63 mg/mmol Cr. When compared with the lowest tertile, ΣOH-PAHs in the highest tertile were significantly related with 20% (95% confidence interval [95%CI]:1%, 40%), 35% (95%CI: 14%, 56%), 22% (95%CI: 1%, 44%), and 38% (95%CI: 9%, 68%) decreases in very low frequency (VLF), low frequency (LF), high frequency (HF), and total power (TP) for participants with MetS, respectively. No statistically significant associations between ΣOH-PAHs and HRV indices were observed for participants without MetS. Similar results were found when we investigated the relationships between OH-PAHs and HRV indices by three groups of OH-PAHs (including total hydroxynaphthalene [ΣOHNa], total hydroxy fluorene [ΣOHFlu], and total hydroxyphenanthrene [ΣOHPh] metabolites). Further, mediation analysis suggested that cardiometabolic traits, including fasting glucose (GLU), high density lipoprotein (HDL), and blood pressure partially mediated the relationship from ΣOH-PAHs to HRV reduction. GLU was the strongest mediator, with mediation percentages of 15.70% for VLF, 14.70% for LF, 43.03% for HF, and 5.61% for TP. Our study found that the relationships between OH-PAHs and HRV reduction differed among participants with and without MetS, and these relationships were found to be partially mediated by cardiometabolic traits, especially fasting glucose. Further studies are encouraged to validate our findings and investigate potential mechanisms., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Aging is related to an increased risk of morbidity and mortality and is affected by environmental factors. Exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse health outcomes; but the association of such exposure with DNA methylation aging, a novel aging marker, is unclear., Objectives: Our aim was to investigate the association of PAH exposure with methylation aging., Methods: We trained and validated a methylation age predictor suitable for Chinese populations using whole blood methylation data in 989 Chinese and 160 Caucasians. We defined two aging indicators: δage, as methylation age minus chronological age; and aging rate, the ratio of methylation to chronological age. The association of PAH exposure with aging indicators was evaluated using linear regressions in three panels of healthy Chinese participants ( N =539, among the aforementioned 989 Chinese participants) whose exposure levels were assessed by 10 urinary monohydroxy-PAH metabolites., Results: We developed a methylation age predictor providing accurate predictions in both Chinese individuals and Caucasian persons (R=0.94-0.96, RMSE=3.8-4.3). Among the 10 urinary metabolites that we measured, 1-hydroxypyrene and 9-hydroxyphenanthrene were associated with methylation aging independently of other OH-PAHs and risk factors; 1-unit increase in 1-hydroxypyrene was associated with a 0.53-y increase in Δage [95% confidence interval (CI): 0.18, 0.88; false discovery rate (FDR) FDR =0.004] and 1.17% increase in aging rate (95% CI: 0.36, 1.98; FDR =0.02), whereas for 9-hydroxyphenanthrene, the increase was 0.54-y for Δage (95% CI: 0.17, 0.91; FDR =0.004), and 1.15% for aging rate (95% CI: 0.31, 1.99; FDR =0.02). The association direction was consistent across the three Chinese panels with the association magnitude correlating with the panels' exposure levels; the association was validated by methylation data of purified leukocytes. Several cytosine-phosphoguanines, including those located on FHL2 and ELOVL2 , were found associated with both aging indicators and monohydroxy-PAH levels., Conclusions: We developed a methylation age predictor specific for Chinese populations but also accurate for Caucasian populations. Our findings suggest that exposure to PAHs may be associated with an adverse impact on human aging and epigenetic alterations in Chinese populations. https://doi.org/10.1289/EHP2773.

Polycyclic aromatic hydrocarbons (PAHs) exposure was reported to be associated with childhood asthma. However, the quantitative relationship between PAHs exposure and adult asthma and possible inflammatory pathways are less clear. We aimed to investigate potential associations between urinary PAHs metabolites and adult asthma. We enrolled 507 adult asthma cases and 536 matched controls. The concentrations of 12 urinary PAHs metabolites and plasma cytokines of interleukin (IL)-9 and eotaxin were measured. Potential associations between urinary PAHs metabolites and adult asthma were analyzed by logistic regression. The relationships between urinary PAHs metabolites and plasma cytokines were determined by generalized linear regression. After adjusted for covariates, each 1-unit-increase in natural log-transformed concentrations of 2-hydroxyfluorene (2-OHFLU), 4- hydroxyphenanthrene (4-OHPHE), 1-OHPHE, 2-OHPHE, 1-Hydroxypyrene (1-OHPYR) and ∑OH-PAHs were significantly associated with elevated risk of adult asthma with odds ratios of 2.04, 2.38, 2.04, 1.26, 2.35 and 1.34, respectively. And the associations were more pronounced in the subjects who were female, younger than 45 years, smoker and had history of occupational dust exposure. No associations were observed between urinary PAHs metabolites levels and expressions of IL-9 and eotaxin. Our results demonstrated that elevated urinary PAHs metabolites levels were associated with increased risk of asthma in adults.

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., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background: Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear., Objectives: To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association., Methods: A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling., Results: The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194-2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139-1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008-2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151-2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05)., Conclusions: Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with lung function decline. However, the underlying mechanisms for the association remain unclear., Objectives: To explore potential role of a lung epithelial biomarker, Club cell secretory protein (CC16), in associations between PAH exposures and lung function decline., Methods: 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., Results: 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 FEV 1 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., Conclusions: 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., (Copyright © 2017. Published by Elsevier Ltd.)

Previous studies have reported an association of exposure to polycyclic aromatic hydrocarbons (PAHs) with lung function decline or cardiovascular diseases, or reduced lung function with 10-year cardiovascular (CV) risk. We analyzed risk factors for the 10-year Framingham CV risk using multiple logistic regression, and examined the mediational effect of reduced lung function on the association between exposure to PAHs and FRS using the post-exploratory structural equation modeling. Participants (n = 2268) were drawn from the Wuhan residents at baseline from the Wuhan-Zhuhai Cohort Study. They completed the physical examination, measurements of lung function and urinary monohydroxylated-PAHs (OH-PAHs). In all individuals, we found a dose-response relationship of PAHs exposure, forced expiratory volume in 1s (FEV1) or forced vital capacity (FVC) with the 10-year CV risk. The proportions of FEV1 and FVC mediation effects in association of PAH exposure with the10-year CV risk were 35% and 24%, respectively. The findings indicated that PAHs exposure or reduced lung function increased the 10-year CV risk. Impaired lung function may partly contribute to increase in the 10-year CV risk regarding exposure to PAHs., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Some studies have shown an association between obesity or exposure to polycyclic aromatic hydrocarbons (PAHs) and the risk of diabetes. This study aimed to investigate the interaction of obesity and urinary monohydroxy-PAHs (OH-PAHs) on diabetes. Individuals (n = 2716) were drawn from the baseline survey of the Wuhan-Zhuhai Cohort Study. They completed the physical examination, measurements of lung function, biochemical indices and urinary OH-PAHs levels. Additive effect of obesity and urinary ΣOH-PAHs levels on diabetes was assessed by calculating the relative excess risk due to interaction (RERI) and the attributable proportion (AP) due to interaction. Several urinary OH-PAHs were positively associated with diabetes in individuals with central obesity or normal weight (p < 0.05 for all). Among individuals with poor lung function, the RERI between urinary ΣOH-PAHs and waist circumstance (WC, RERI: 0.866, 95% CI: -0.431, 2.164, p = 0.192) or waist-to-height ratio (WHtR, RERI: 1.091, 95% CI: -0.124, 2.305, p = 0.078) was found; the AP due to the interaction between urinary ΣOH-PAHs and WC or WHtR was 0.383 (95% CI: -0.07, 0.80, p = 0.086) or 0.465 (95% CI: 0.019, 0.912, p = 0.04). The results indicated that central obesity may enhance the effect of exposure to background PAHs on diabetes in individuals with poor lung function., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Association of exposure to polycyclic aromatic hydrocarbons (PAHs) with increased urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation has been reported in occupational population and children. However, studies on the association between them in general population are limited. A total of 1864 eligible subjects from the baseline Wuhan participants of the Wuhan-Zhuhai Cohort Study (n = 3053) were included in this study, after excluding individuals with certain disease and missing data on urinary monohydroxy PAHs (OH-PAHs) and 8-OHdG levels. Urinary monohydroxy PAHs and 8-OHdG levels were measured by gas chromatography-mass spectrometry and high performance liquid chromatography-electrochemical detection, respectively. Association of urinary OH-PAHs with urinary 8-OHdG was analyzed by multiple linear regression analysis. We found a dose-dependent relationship between urinary PAHs metabolites and urinary 8-OHdG (p < 0.05 for all). Furthermore, more evidence for the association of total concentrations of urinary OH-PAHs with 8-OHdG levels were observed in individuals with normal body mass index or central obesity (p < 0.01 for all). There was a dose-dependent relationship between urinary OH-PAHs levels and urinary 8-OHdG levels among a general Chinese population. Exposure to background PAHs may have a greater influence on urinary 8-OHdG levels in individuals with central obesity., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

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., (Copyright © 2016 Elsevier B.V. All rights reserved.)

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., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Rationale: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with adverse effects on the respiratory system. However, the association between internal levels of PAH metabolites and lung function levels remains unclear., Objectives: We investigated the relationships between urinary PAH metabolite concentrations and lung function levels in a general Chinese population., Methods: Lung function and 12 urinary PAH metabolites were measured in 2,747 participants from the Wuhan-Zhuhai cohort in China. Associations between urinary PAH metabolites and lung function were analyzed by linear mixed models. We also investigated associations among urinary PAH metabolite concentrations, traffic exposure time, and dietary PAH exposure., Measurements and Main Results: We found significant associations between increased levels of urinary PAH metabolites and reduced lung function. Each 1-U increase in log-transformed levels of 2-hydroxynaphthalene, 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 3-hydroxyphenanthrene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxypyrene, or total urinary PAH metabolites was associated with a 23.79-, 19.36-, 41.76-, 36.87-, 33.47-, 27.37-, 39.53-, 34.35-, 25.03-, or 37.13-ml reduction in FEV1, respectively (all P < 0.05). Each 1-U increase in 2-hydroxynaphthalene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, or total urinary PAH metabolites was associated with a 24.39-, 33.90-, 27.15-, 28.56-, 27.46-, or 27.99-ml reduction in FVC, respectively (all P < 0.05). The total urinary PAH metabolites concentration was positively associated with both traffic exposure time and dietary PAH exposure among nonsmokers., Conclusions: Total and specific urinary PAH metabolites were associated with lung function reduction in a general Chinese population. Further studies are needed to investigate the potential mechanism by which PAHs induces lung function reduction.

The incidence of diabetes is increasing rapidly in Chinese population, and it has been postulated that environmental factors may play a role in the etiology of diabetes. Therefore, we aimed to investigate the association between PAHs exposure and risk of diabetes in a community-based population of 2824 participants with completed questionnaires, measurements of biochemical indices, and urinary PAHs metabolites. We found that elevated urinary PAHs metabolites were associated, in a dose-dependent manner, with increased risk of diabetes. Particularly, these associations were more evident in subjects who were female, less than 55 years old, nonsmokers, and normal weight. In addition, there was a modest improvement in diabetes discrimination of prediction models when incorporating certain PAHs metabolites into conventional risk factors (CRF). Overall, our data suggested that there may be a dose-dependent relationship between PAHs metabolites and risk of diabetes among general Chinese population., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objectives: To investigate the effects of the urinary metabolite profiles of background exposure to the atmospheric pollutants polycyclic aromatic hydrocarbon (PAH) and Framingham risk score (FRS), which assesses an individual's cardiovascular disease risk, on heart rate variability (HRV)., Methods: The study conducted from April to May 2011 in Wuhan, China, included 1978 adult residents with completed questionnaires, physical examinations, blood and urine samples, and 5-min HRV indices (including SD of all normal to normal intervals (SDNN), root mean square successive difference (rMSSD), low frequency (LF), high frequency (HF) and their ratio (LF/HF), and total power) obtained from 3-channel Holter monitor. 12 urinary PAH metabolites were measured by gas chromatography-mass spectrometry. FRS was calculated by age, sex, lipid profiles, blood pressure, diabetes and smoking status. Linear regression models were constructed after adjusting for potential confounders., Results: Elevated total concentration of hydroxynaphthalene (ΣOHNa) was significantly associated, in a dose-responsive manner, with decreased SDNN and LF/HF (ptrend=0.014 and 0.007, respectively); elevated total concentration of hydroxyfluorene (ΣOHFlu) was significantly associated with reduced SDNN, LF and LF/HF (ptrend=0.027, 0.003, and <0.0001, respectively); and elevated total concentration of all PAH metabolites (ΣOH-PAHs) was associated with decreased LF and LF/HF (ptrend=0.005 and <0.0001, respectively). Moreover, increasing quartiles of FRS were significantly associated with decreased HRV indices, except LF/HF (all ptrend<0.0001). Interestingly, individuals in low-risk subgroups had greater decreases in SDNN, LF and LF/HF in relation to ΣOH-PAHs, ΣOHNa and ΣOHFlu than those in high-risk subgroups (all p<0.05)., Conclusions: Environmental PAH exposure may differentially affect HRV based on individual coronary risk profiles.

The article presents the study conducted on interaction of RARB variant with polycyclic aromatic hydrocarbon exposure on lung function. Topics of discussion includes studies suggest that genetic variants may imapct the association of air pollutants with respiratory results. Epidemiological studies also presents the relation between polycyclic aromatic hydrocarbon in air pollution on the altered lung function.

The role of silica in the causation of lung cancer is an ongoing debate. In order to explore whether observed association between silica exposure and lung cancer is confounded by exposure to other occupational carcinogens, we updated a previously nested case-control study among a cohort of male workers in 29 Chinese mines and factories on the basis of an extended follow-up. Five hundred and eleven lung cancer cases and 1,879 matched controls were selected. Exposure to respirable silica as well as relevant occupational confounders were quantitatively assessed based on historical industrial hygiene data. The relationship between exposure to silica and lung cancer was analyzed by conditional logistic regression analysis adjusted for exposure to arsenic, polycyclic aromatic hydrocarbons (PAHs), radon, and smoking. In a crude analysis adjusted for smoking only, a significant trend of increasing risk of lung cancer with exposure to silica was found for tin, iron/copper miners, and pottery workers. But after adjustment for relevant occupational confounders, no relationship between silica and lung cancer can be observed. Instead, there is a significant association between lung cancer mortality and cumulative exposure to inorganic arsenic (OR = 1.86, 95% CI: 1.14, 3.04 for each mg/m3-year increase) and carcinogenic PAHs (OR = 1.35, 95% CI: 1.08, 1.69 for each 100 μg/m3-year increase). This analysis does not provide any evidence to show that exposure to silica causes lung cancer in the absence of confounding factors. [ABSTRACT FROM AUTHOR]

Adverse effects of fine particulate matter (particulate matter ≤2.5 μm aerodynamic diameter, PM 2.5) and PM 2.5 -bound polycyclic aromatic hydrocarbons (PAHs) on blood lipid profiles remain uncertain. We designed a panel study with repeated measures. In this panel study, we enrolled 215 adult residents who participated in two study periods from the Wuhan-Zhuhai cohort. Personal 24-h PM 2.5 , sixteen kinds of 24-h PM 2.5 -bound PAHs, and blood lipid profiles were repeatedly measured across two study periods. We observed that an interquartile-range increase in four-ring or five-ring PAHs was linked with a 0.112 and 0.108 mmol/l increase in triglyceride, respectively in single-constituent models. These associations remained robust in both constituent-PM 2.5 joint models and single-constituent residual models. Additionally, we observed that the significant relationships of four/five-ring PAHs with triglycerides were stronger among females, non-smokers, and participants without hypertension and diabetes. Bayesian kernel machine regression models further revealed that combining sixteen kinds of PM 2.5 -bound PAHs as a mixture of pollutants could result in a cumulative toxic effect on total cholesterol and triglycerides. No significant relationships were observed between personal PM 2.5 exposure and blood lipid changes. Our findings suggest that exposure to PM 2.5 -bound PAHs may adversely affect lipid metabolism, which provides new evidence for formulating pollution abatement strategies for cardiovascular health. [Display omitted] • 4-/5-ring atmospheric PAHs exposure is positively associated with TG. • Combining 16 kinds of PAHs results in a cumulative toxic effect on TC and TG. • Females or non-smokers were more susceptible to atmospheric PAHs exposure. [ABSTRACT FROM AUTHOR]