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Polycyclic aromatic hydrocarbons (PAHs) can interfere with testosterone levels, and low levels of testosterone are associated with increased cardiovascular events. To explore the role of testosterone in PAHs exposure and cardiovascular health, we used data from the 2011–2016 National Health and Nutrition Examination Survey (NHANES) and a longitudinal database of 332 male coke oven workers from China. The urine PAHs, tobacco metabolites and plasma testosterone levels of coke oven workers were measured. There were inverse associations between serum (plasma) testosterone concentrations and the risk of dysarteriotony and dyslipidemia among the NHANES participants and coke oven workers. The results of the cross-lagged panel analysis among workers showed that the decrease in testosterone preceded the increase in diastolic blood pressure (DBP), and the absolute value of the path coefficient from baseline testosterone to follow-up DBP (β 2 = −8.162, P = 0.077) was significantly larger than the absolute value of the path coefficient from baseline DBP to follow-up testosterone (β 1 = −0.001, P = 0.781). Results from the half-longitudinal mediation analysis showed that baseline hydroxyfluorene predicted significant decreases in plasma testosterone from baseline to follow-up (path a: 0.71, 95% CI: 1.26, −0.16), whereas plasma testosterone at baseline also predicted significant increments in DBP from baseline to follow-up (path b: 9.22, 95% CI: 17.24, −1.19). The indirect effect of PAHs on DBP via plasma testosterone level was marginally significant (test for indirect effects a*b (P = 0.08)). In conclusion, testosterone level is a longitudinal precursor to increased DBP and plays an essential role in the association between PAHs exposure and damage to the cardiovascular system. Coke oven workers with low plasma testosterone levels are more likely to experience adverse changes in blood pressure and lipid levels after exposure to PAHs. [Display omitted] • Temporal order between testosterone and DBP was analysed by cross-lagged panel. • Mediation relationship was analysed by half-longitudinal mediation analysis. • The decrease in testosterone preceded DBP increase. • Testosterone mediates PAHs-induced DBP increase. [ABSTRACT FROM AUTHOR]

Background: Multiple factors, including co-exposure between lifestyle and environmental risks, are important in susceptibility to oxidative DNA damage. However, the underlying mechanism is not fully understood. This study was undertaken to evaluate whether Cytochrome P4501A1 (CYP1A1) methylation can mediate the co-exposure effect between smoking and occupational polycyclic aromatic hydrocarbons (PAH) in development of oxidative DNA damage.Methods: We explored the associations between smoking and occupational PAH co-exposure effect, CYP1A1 methylation and oxidative DNA damage among 500 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (1-hydroxypyrene, 1-OHP; 2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; and 9-hydroxyphenanthren, 9-PHE) and a marker of oxidative DNA damage (8-hydroxy- 2'- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. CYP1A1 methylation was measured by pyrosequencing. Finally, mediation analysis was performed to investigate whether CYP1A1 methylation mediated smoking and occupational PAH co-exposure effect on oxidative DNA damage.Results: We observed significant associations of smoking and 1-OHP co-exposure with CYP1A1 hypomethylation (OR: 1.87, 95% CI: 1.01-3.47) and high 8-OHdG (OR: 2.13, 95% CI: 1.14-3.97). There was a significant relationship between CYP1A1 hypomethylation and high 8-OHdG (1st vs. 3rd tertile = 1.58, 95% CI: 1.01-2.47, P for trend = 0.046). In addition, mediation analysis suggested CYP1A1 hypomethylation could explain 13.6% of effect of high 8-OHdG related to smoking and 1-OHP co-exposure.Conclusions: Our findings suggested that the co-exposure effect of smoking and occupational PAH could increase the risk of oxidative DNA damage by a mechanism partly involving CYP1A1 hypomethylation. [ABSTRACT FROM AUTHOR]

Background: Exposure to polycyclic aromatic hydrocarbons (PAH) and tobacco smoke is associated with epithelial damage and reduced lung function. Club cell secretory protein (CC16) is a known biomarker for lung epithelial cells. However, the potential relationships between PAH and tobacco smoke exposure, CC16 levels, and reduced lung function remain unclear.Objectives: This longitudinal study aimed to explore the potential role of CC16 in the association of tobacco smoke and PAH co-exposure with lung function.Methods: We enrolled 313 workers from a coking plant in China in 2014 and followed them up in 2019. The concentrations of PAH and nicotine metabolites in urine were determined using high-performance liquid chromatography (HPLC) with a fluorescence detector and HPLC-tandem mass spectrometry, respectively. The plasma CC16 concentration was determined using an enzyme-linked immunosorbent assay.Results: An analysis of the generalized estimating equation showed that each 1-unit increase in log-transformation of the last tertile of trans-3'-hydroxycotinine (3HC) was associated with a 3.30 ng/ml decrease in CC16. Restricted cubic spline analysis revealed a significant nonlinear dose-effect association between cotinine (COT) and CC16 (Pnonlinear = 0.018). In the low- CC16 subgroup, we found a significant association between total nicotine metabolites and forced vital capacity (FVC%) (β: 1.45, 95% CI: 2.87, -0.03), and the associations of nicotine (NIC), COT, and 3HC with FVC% were all of marginal significance. High levels of total hydroxyl polycyclic aromatic hydrocarbons (ΣOH-PAH) and NIC in the urine had an interactive effect on the decline of CC16 (P < 0.05). Cross-lagged panel analysis indicated that the decrease in CC16 preceded the decrease in FVC%. CC16 mediated the association between elevated nicotine metabolites and decreased FVC% in the low- CC16 subgroup.Conclusions: CC16 plays an essential role in the association of PAH and tobacco smoke exposure with reduced lung function. Coke oven workers with low plasma CC16 levels are more likely to experience decreased lung function after tobacco smoke exposure. [ABSTRACT FROM AUTHOR]

The prevalence of hypertension may be affected by environmental pollution and personal behavior. We aimed to evaluate the interaction effects of secondhand smoke exposure and overweight on hypertension. In this cross-sectional study, a total of 627 workers from a coking plant in China and 1011 individuals from the NHANES database in the United States from 2013 to 2016 were selected as the research participants. The concentrations of 11 urinary polycyclic aromatic hydrocarbons (PAHs) metabolites and 3 tobacco metabolites were measured. An interaction effect was tested in the modified Poisson regression models. For smokers among Chinese coke oven workers, the only statistically significant positive association was with hypertension in the highest tertile of nicotine metabolized ratio (NMR) (PR: 1.539, 95% CI: 1.013–2.337). Nonsmoking Chinese workers with 3rd tertile urinary nicotine levels were associated with a 114.8% significantly increased prevalence of hypertension (PR: 2.148, 95% CI: 1.025–4.500) compared to nonsmokers 1st tertile with nicotine levels. Association between tobacco exposure and hypertension is possibly modified by PAHs exposure (PR: 2.335, 95% CI: 0.933–5.841). Nonsmokers in the NHANES database with high urinary nicotine levels were associated with a 17.3% significantly increased prevalence of hypertension (PR: 1.173, 95% CI: 1.028–1.338) compared to those with low nicotine levels. We observed that overweight people with high nicotine levels had a significantly higher likelihood of hypertension than no overweight people with low nicotine levels among nonsmoking Chinese coke oven workers and NHANES participants (PR = 4.686, 95% CI: 1.488–14.754; PR = 1.251, 95% CI: 1.039–1.506). Tobacco exposure and overweight are important risk factors for hypertension, and secondhand smoke exposure and overweight have an interactive effect on the incidence of hypertension in nonsmoking Chinese coke oven workers and NHANES participants. [Display omitted] • Nicotine metabolized ratio can increase prevalence of hypertension among smokers. • Nicotine can increase the prevalence of hypertension among nonsmokers. • PAHs may have modified the association between tobacco exposure and hypertension. • There is an interaction between overweight and high nicotine levels in nonsmokers. [ABSTRACT FROM AUTHOR]

Individuals with abnormal fasting plasma glucose (FPG) may be more susceptible to lung diseases associated with environmental pollutants. A cross-sectional survey of 629 workers in 2017 and a panel study of 304 workers from 2014 to 2019 were performed in China. The results showed that elevated total hydroxylated polycyclic aromatic hydrocarbon (ΣOH-PAH) concentration was associated with lower the percentage of predicted forced vital capacity (FVC%) among high-FPG workers (β for the cross-sectional analysis: −1.78%, 95%CI: −2.92%, −0.64%; β for the panel study: −1.10%, 95%CI: −2.19%, −0.02%). The absolute value of the cross-lagged path coefficient from FPG to FVC% (β 2 = −0.096) was significantly greater than that from FVC% to FPG (β 1 = 0.037). Our results suggest that FPG abnormalities may precede the lung function decline induced by PAH exposure and that high-FPG and high ΣOH-PAH levels have an interactive effect on lung function decline. [Display omitted] • The association between PAH and lung function was influenced by FPG. • Causal relationship in temporal order was analyzed by cross-lagged panel analyses. • Fasting glucose abnormalities precede FVC% decline. • FPG and PAH had interaction effects on the decline in lung function. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a cluster of interrelated risk factors, which increase the risk of cardiovascular disease (CVD) and cancer. The prevalence of MetS might be affected by environmental pollution and individual's poor lifestyles. In this cross-sectional study, we aimed to evaluate the interactions effect of PAHs exposure and poor lifestyles on MetS among coke oven workers. We measured the concentrations of 11 urinary PAH metabolites among 682 coke oven workers by HPLC-MS. China adult blood lipid abnormality prevention guide (2016) was employed for diagnosing MetS. An interaction effect was tested in the modified Poisson regression models. The results showed that the urinary level of 1-NAP (P for trend = 0.043) and 2-FLU (P for trend = 0.037) had significant dose-response relationships with increased PR of MetS. For 1-NAP, statistically significant positive association was with low HDL among individuals (P for trend = 0.003). Besides, smoking was associated with a significantly increased risk of prevalence ratio of MetS (PR = 1.07; 95% CI 1.00–1.13), high triglycerides (PR = 1.13; 95% CI 1.05–1.20) and low HDL (PR = 1.07; 95% CI 1.01–1.14). Smokers who with high levels of 1-NAP and 2-FLU had higher prevalence ratio of MetS compared with non-smokers who with low levels of 1-NAP [PR (95% CI): 1.17 (1.06–1.29); P for trend = 0.002] and 2-FLU [PR (95% CI): 1.17 (1.06–1.29); P for trend = 0.004]. Our findings suggested PAHs exposure increased the prevalence ratio of MetS and this effect can be modified by smoking status. Image 1 • Relationship of PAH exposure and MetS was analysed by modified Poisson regression. • PAHs exposure can increase the prevalence ratio of MetS in coke oven workers. • Smoking modifies the prevalence ratio of MetS induced by PAHs exposure. [ABSTRACT FROM AUTHOR]

Purpose: Smoking is a major risk factor for the group 3 PH. NT-proBNP is a biomarker for risk stratification in PH. This study aims to investigate the effects of smoking status and smoking index (SI) on group 3 PH and to evaluate the value of SI and SI combined with NT-proBNP in early diagnosis and prediction of disease severity., Patients and Methods: Four hundred patients with group 3 PH at the First Hospital of Shanxi Medical University between January 2020 and December 2021 were enrolled and divided into two groups: mild (30 mmHg ≤ pulmonary artery systolic pressure (PASP)≤50 mmHg) and non-mild (PASP >50 mmHg). The effect of smoking on group 3 PH was analyzed using univariate analysis, and logistic analysis was conducted to evaluate the risk of group 3 PH according to smoking status and SI. Spearman correlation coefficient was used to test the correlation between SI and the index of group 3 PH severity. The predictive value of SI was evaluated using a receiver operating characteristic (ROC) curve., Results: Correlation and logistic analyses showed that SI was associated with PH severity. Smoking status (P =0.009) and SI ( P =0.039) were independent risk factors for non-mild group 3 PH, and ROC showed that the predictive value of SI (AUC:0.596) for non-mild PH was better than that of the recognized pro-brain natriuretic peptide (NT-proBNP) (AUC:0.586). SI can be used as a single predictive marker. SI and NT-proBNP can be formulated as prediction models for screening non-mild clinical cases (AUC:0.628)., Conclusion: SI is a potentially ideal non-invasive predictive marker for group 3 PH. SI and NT-proBNP could be used to develop a prediction model for screening non-mild PH cases. This can greatly improve the predictive specificity of the established PH marker, NT-proBNP., Competing Interests: The authors report no conflicts of interest in this work., (© 2024 Sun et al.)

This study intends to examine the association of urinary monohydroxyl PAHs (OH-PAHs) concentration and occupational stress in coal miners. We sampled 671 underground coal miners from Datong, China, assessed their occupational stress using the Occupational Stress Inventory-Revised edition (OSI-R), and categorized them into the high stress miners and controls based on that. We determined urinary OH-PAHs concentration using ultrahigh performance liquid chromatography-tandem mass spectrometry, and analyzed its association with occupational stress using multiple linear regression, covariate balancing generalized propensity score (CBGPS), and Bayesian kernel machine regression (BKMR). The low molecular weight (LMW) OH-PAHs in quartile or homologue was significantly positively associated with Occupational Role Questionnaire (ORQ) and Personal Strain Questionnaire (PSQ) score, but was not associated with Personal Resources Questionnaire (PRQ) score. The OH-PAHs concentration was positively associated with ORQ and PSQ scores in coal miners, particularly the LMW OH-PAHs. Non-association was found in the OH-PAHs with PRQ score., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Multiple factors, including co-exposure between lifestyle and environmental risks, are important in susceptibility to oxidative DNA damage. However, the underlying mechanism is not fully understood. This study was undertaken to evaluate whether Cytochrome P4501A1 (CYP1A1) methylation can mediate the co-exposure effect between smoking and occupational polycyclic aromatic hydrocarbons (PAH) in development of oxidative DNA damage., Methods: We explored the associations between smoking and occupational PAH co-exposure effect, CYP1A1 methylation and oxidative DNA damage among 500 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (1-hydroxypyrene, 1-OHP; 2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; and 9-hydroxyphenanthren, 9-PHE) and a marker of oxidative DNA damage (8-hydroxy- 2'- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. CYP1A1 methylation was measured by pyrosequencing. Finally, mediation analysis was performed to investigate whether CYP1A1 methylation mediated smoking and occupational PAH co-exposure effect on oxidative DNA damage., Results: We observed significant associations of smoking and 1-OHP co-exposure with CYP1A1 hypomethylation (OR: 1.87, 95% CI: 1.01-3.47) and high 8-OHdG (OR: 2.13, 95% CI: 1.14-3.97). There was a significant relationship between CYP1A1 hypomethylation and high 8-OHdG (1st vs. 3rd tertile = 1.58, 95% CI: 1.01-2.47, P for trend = 0.046). In addition, mediation analysis suggested CYP1A1 hypomethylation could explain 13.6% of effect of high 8-OHdG related to smoking and 1-OHP co-exposure., Conclusions: Our findings suggested that the co-exposure effect of smoking and occupational PAH could increase the risk of oxidative DNA damage by a mechanism partly involving CYP1A1 hypomethylation.

Background: Naphthalene is the simplest polycyclic aromatic hydrocarbon (PAH). It is easily emitted into the atmosphere, posing a significant risk to human health. However, limited studies have described the impact of naphthalene exposure on birth outcomes. In this study, we investigated the association between the maternal urinary metabolites of naphthalene, 2-hydroxynaphthalene (2-OH NAP), and birth outcomes., Method: In the present study, four urinary PAH metabolites were measured in 263 pregnant women during late pregnancy. Multiple linear regression analysis was used to analyze the relationship between the concentrations of 2-OH NAP and birth outcomes, and restricted cubic spline models were further used to examine the shapes of the dose-response association., Result: General linear models showed that prenatal urinary 2-OH NAP was associated with lower birth weight (BW) (- 4.38% for the high vs. low exposure group of 2-OH NAP; p for trend = 0.049) and higher cephalization index (CI) (4.30% for the high vs. low exposure group of 2-OH NAP; p for trend = 0.038). These associations were linear and significant when 2-OH NAP was modeled as a continuous variable in restricted cubic spline models (P linear  = 0.0293 for 2-OH NAP and BW; P linear  = 0.0326 for 2-OH NAP and CI). Multiple linear regression data indicated that each 1 ln-unit increase in 2-OH NAP was significantly associated with a 2.09 g/cm increase in the CI. The associations among 2-OH NAP, BW, and CI were also observed in a subset of participants residing close to arterial traffic., Conclusion: Our data indicated that prenatal exposure to naphthalene had an adverse effect on fetal birth outcomes, especially the brain development index. Reduced exposure to naphthalene may improve newborn health outcomes. In Taiyuan, naphthalene may result from traffic pollution.

Polycyclic aromatic hydrocarbons (PAH) are well-known to be carcinogenic and the mechanisms that it contributes to oxidative DNA damage and aryl hydrocarbon receptor (AhR)-dependent induction are also well understood. However, little is known about the associations between PAH exposure, AhR expression, and oxidative DNA damage. We investigated their associations of AhR expression and oxidative DNA damage related to PAH exposure among 310 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; 9-hydroxyphenanthren, 9-PHE; and 1-hydroxypyrene, 1-OHP) and a marker of oxidative damage (8-hydroxy- 2'- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. AhR expression in venous blood was measured by reverse transcription -polymerase chain reaction. The results showed that increasing levels of urinary 1-OHP was positively associated with high 8-OHdG (OR (95% CI) was 4.01 (1.41-11.45) for 4th quartile, compared with 1st quartile, P for trend = 0.013). The similar associations were also found between urinary 1-OHP and high-AhR expressions (4th vs. 1st quartile = 3.50, 95% CI: 1.24-9.87, P for trend = 0.029). A significant association between AhR expression and high 8-OHdG was also found (4th vs. 1st quartile = 2.44, 95% CI: 1.05-5.70, P for trend = 0.027). In addition, mediation analysis showed the AhR expression could explain 35.9% of the association of oxidative DNA damage related to PAH exposure. Our findings implicated that the association between PAH exposure and oxidative DNA damage may be mediated by AhR expression among Chinese occupational workers., (Copyright © 2018 Elsevier Ltd. All rights reserved.)