Levels Of 1-hydroxypyrene Research Articles

Chemical exposure from the Hebei spirit oil spill accident and its long-term effects on mental health

While evidence indicates that exposure to oil spill incidents can affect mental health, it is unclear whether the mental health effects result from the incident itself or from exposure to associated chemicals. Oil contains chemicals that can impact mental health and these chemicals may have long-term effects due to their persistence in the environment. To address the gap in current knowledge, we conducted cross-sectional and prospective analyses of data from adults who participated in the Health Effects of the Hebei Spirit Oil Spill study. To assess chemical exposure from oil spills, we used indirect exposure indicators such as distance from the contaminated oil band to residences and duration of clean-up work, along with direct exposure indicators such as urine metabolite concentrations of volatile organic compounds and polycyclic aromatic hydrocarbons. Mental health assessments covered posttraumatic stress disorder (PTSD), depression, state anxiety, and trait anxiety. In the cross-sectional analyses, all four mental health issues were found to be associated with proximity to the oil band (p-value<0.05) and showed a positive association with clean-up work duration (p-value<0.05). Cox regression analysis revealed that higher urinary t, t-muconic acid levels were associated with an increased risk of depression (Hazard Ratio [HR] = 1.55, 95 % Confidence Interval [CI] = 1.05–2.28), and elevated 1-hydroxypyrene levels increased the risk of PTSD (HR = 1.60, 95 % CI = 1.03–2.48). Additionally, higher urinary 2-naphthol levels were associated with increased state anxiety (HR = 1.39, 95 % CI = 1.00–1.93) and trait anxiety (HR = 1.64, 95 % CI = 1.15–2.32). These associations persisted even after controlling for distance and duration variables related to psychosocial exposure. Our findings suggest that environmental disaster response plans should prioritize minimizing chemical exposure while also considering the duration and nature of the mental health impacts.

Generating high spatial resolution exposure estimates from sparse regulatory monitoring data

Random Forest algorithms have extensively been used to estimate ambient air pollutant concentrations. However, the accuracy of model-predicted estimates can suffer from extrapolation problems associated with limited measurement data to train the machine learning algorithms. In this study, we developed and evaluated two approaches, incorporating low-cost sensor data, that enhanced the extrapolating ability of random-forest models in areas with sparse monitoring data. Rochester, NY is the area of a pregnancy-cohort study. Daily PM2.5 concentrations from the NAMS/SLAMS sites were obtained and used as the response variable in the model, with satellite data, meteorological, and land-use variables included as predictors. To improve the base random-forest models, we used PM2.5 measurements from a pre-existing low-cost sensors network, and then conducted a two-step backward selection to gradually eliminate variables with potential emission heterogeneity from the base models. We then introduced the regression-enhanced random forest method into the model development. Finally, contemporaneous urinary 1-hydroxypyrene was used to evaluate the PM2.5 predictions generated from the two approaches. The two-step approach increased the average external validation R2 from 0.49 to 0.65, and decreased the RMSE from 3.56 μg/m3 to 2.96 μg/m3. For the regression-enhanced random forest models, the average R2 of the external validation was 0.54, and the RMSE was 3.40 μg/m3. We also observed significant and comparable relationships between urinary 1-hydroxypyrene levels and PM2.5 predictions from both improved models. This PM2.5 model estimation strategy could improve the extrapolating ability of random forest models in areas with sparse monitoring data.

Associationof polycyclic aromatic hydrocarbons with systemic inflammation and metabolic syndrome and its components.

This study aimed to evaluate the relationship of polycyclic aromatic hydrocarbon (PAH) exposure with metabolic syndrome (MetS) and its components and to explore the potential mechanism. Participants from the National Health and Nutrition Examination Survey (NHANES 2001-2016) were included. A total of 6532 adults and 1237 adolescents were included in the present analysis. For adults, the odds ratios (ORs) and 95% CIs for each one-unit increase in the log-transformed level of 1-hydroxynaphthalene (1-OHNa), 2-hydroxynaphthalene (2-OHNa), 3-hydroxyfluorene (3-OHFlu), 2-hydroxyfluorene (2-OHFlu), 1-hydroxyphenanthrene (1-OHPh), 1-hydroxypyrene (1-OHP), 2- and 3-hydroxyphenanthrene (2&3-OHPh), and total urinary PAH metabolites (∑OH-PAHs) with MetS were 1.11 (1.03-1.20), 1.18 (1.07-1.29), 1.10 (1.01-1.12), 1.18 (1.07-1.30), 1.17 (1.03-1.33), 1.09 (1.01-1.22), 1.24 (1.09-1.40), and 1.17 (1.06-1.29), respectively. They were 1.61 (1.21-2.14) for 2-OHNa, 1.27 (1.01-1.60) for 2-OHFlu, 1.53 (1.15-2.03) for 1-OHPh, and 1.61 (1.20-2.15) for ∑OH-PAHs among adolescents. C-reactive protein was not only positively associated with urinary PAH metabolites, but also positively related to MetS, and it mediated 10.23% to 20.21% for urinary PAH metabolites and MetS among adults. PAH exposure is associated with a higher prevalence of MetS or MetS components among adults and adolescents. Systemic inflammation partly mediated the association among adults.

Exposure to polycyclic aromatic hydrocarbons assessed by biomonitoring of firefighters during fire operations in Germany.

Firefighters are exposed to a variety of hazardous substances including carcinogens such as polycyclic aromatic hydrocarbons (PAH) during firefighting. In order to minimize the uptake of such substances into the body, firefighters wear personal protective equipment. Only few data exist from real-life firefighting missions and under common although highly variable exposure scenarios such as fighting fires in residential buildings, outdoor, and vehicle fires. The aim of this study is to assess the levels of 1-Hydroxypyrene (1-OHP) as marker for incorporated PAH during firefighting operations in Germany using biomonitoring methods. We analyzed urine samples for 1-OHP from 77 firefighters who reported firefighting operations (with and without creatinine adjustment). Urine samples were collected before (baseline) and, where applicable, after firefighting operations at three time points subsequent (2-4, 6-8, and 12h). Compared to the baseline measurements, mean 1-OHP concentrations after firefighting missions were doubled (0.14 vs. 0.31μg/L urine, 0.13μg/g vs. 0.27μg/g creatinine) and this increase was observed 2-4h after firefighting. Firefighting in residential buildings (N=54) and of outdoor and vehicle fires (N=17) occurred most frequently, whereas blazes, vegetation fires, and fires in underground facilities (N=6) were rarely encountered. For residential building fires, a 3-fold increase in mean 1-OPH concentrations was observed, whereas no increase could be observed for outdoor and vehicle fires. The highest increase was observed for firefighters with interior attack missions (0.11μg/L vs. 0.48μg/L 1-OHP) despite the use of self-contained breathing apparatus (SCBA). During the suppression of outdoor or vehicle fires using SCBA, again, no increase was observed. Although PAH are taken up during certain firefighting missions, the 1-OHP levels almost entirely remained (in 64 of the 77 reported missions) within the normal range of the German general population, i.e., below the reference levels (95th percentiles) of smokers (0.73μg/g creatinine) and non-smokers (0.30μg/g creatine). Under study conditions, properly applied protective clothing and wearing of SCBA led to a significant reduction of PAH exposure levels. But there are individual situations in which PAH are increasingly incorporated since the incorporation depends on several factors and can be extremely variable. In contrast to many workplaces with high occupational exposure levels, firefighters are not exposed to PAH on a daily basis. Nevertheless, the possibility of an individual increased cancer risk for a particular firefighter cannot completely be ruled out.

Effects of H19/SAHH/DNMT1 on the oxidative DNA damage related to benzo[a]pyrene exposure.

The mechanisms that long noncoding RNA (lncRNA) H19 binding to S-adenosylhomocysteine hydrolase (SAHH) interacted with DNA methyltransferase 1 (DNMT1) and then regulated DNA damage caused by polycyclic aromatic hydrocarbons (PAHs) remain unclear. A total of 146 occupational workers in a Chinese coke-oven plant in 2014 were included in the final analyses. We used high-performance liquid chromatography mass spectrometry (HPLC-MS) equipped to detect urine biomarkers of PAHs exposure, including 2-hydroxynaphthalene (2-NAP), 2-hydroxyfluorene (2-FLU), 9-hydroxyphenanthrene (9-PHE) and 1-hydroxypyrene (1-OHP). The levels of SAM and SAH in plasma were detected by HPLC-ultraviolet. By constructing various BEAS-2B cell models exposed to 16μM benzo[a]pyrene (BaP) for 24h, toxicological parameters reflecting distinct mechanisms were evaluated. We documented that urinary 1-hydroxypyrene (1-OHP) levels were positively associated with blood H19 RNA expression (OR: 1.51, 95% CI: 1.03-2.19), but opposite to plasma SAHH activity (OR: 0.63, 95% CI: 0.41-0.98) in coke oven workers. Moreover, by constructing various BEAS-2B cell models exposed to benzo[a]pyrene (BaP), we investigated that H19 binding to SAHH exaggerated DNMT1 expressions and activity. Suppression of H19 enhanced the interaction of SAHH and DNMT1 in BaP-treated cells, decreased eight-oxoguanine DNA glycosylase 1 (OGG1) methylation, reduced oxidative DNA damage and lessened S phase arrest. However, SAHH or DNMT1 single knockdown and SAHH/DNMT1 double knockdown showed the opposite trend. A H19/SAHH/DNMT1 axis was involved in OGG1 methylation, oxidative DNA damage and cell cycle arrest by carcinogen BaP.

Genetic polymorphism impact superoxide dismutase and glutathione peroxidase activity in charcoal workers.

Incomplete combustion of wood releases toxic chemicals. Exposure to these chemicals during charcoal production can modulate redox status of cellular system which may further lead to genomic instability and of antioxidant enzymes. Genetic polymorphism may alter the functioning properties of these enzymes and modulate the response to oxidative stress. In this study, we analyzed the link between genetic polymorphism and enzyme activity for antioxidant enzymes: MnSOD and GPx-1 in charcoal workers and control population. This study included 77 charcoal workers and 79 demographically matched healthy control subjects. This association was studied using multiple linear regression, adjusted for confounding factors viz. age, consumption habits and exposure duration. SOD activity was lower for TT genotype (3.47 ± 0.66; 5.92 ± 1.08) versus CC genotype (3.47 ± 0.66; 6.67 ± 1.60) in control and charcoal workers respectively. Significant lower GPx-1 activity was found in leu/leu genotype (7.25 ± 0.38; 3.59 ± 0.57) when compared to pro/pro genotype (7.78 ± 0.59; 4.28 ± 0.71) and pro/leu genotype (8.48 ± 0.34; 4.30 ± 0.76) in control population and charcoal workers respectively. A significant difference in the levels of 1-Hydroxypyrene (biomarker of exposure) and SOD and GPx-1 activity (biomarkers of oxidative stress) was evident in exposed group in comparison to the control one. Collectively, our findings suggested that PAH influenced the mode of action of SOD and GPx-1 which were impacted by polymorphism in SOD and GPx-1 gene. Hence, polymorphism of MnSOD and GPx-1 genes were found to play a modulatory role in human susceptibility to oxidative damage induced by wood smoke in charcoal workers.

Four-year population exposure study: Implications for the effectiveness of e-waste control and biomarkers of e-waste pollution

E-waste pollution has emerged as a significant environmental concern. To assess the impact of e-waste control on human pollutant exposure risk and identify appropriate biomarkers to classify e-waste pollution levels, we performed longitudinal population exposure monitoring research in an e-waste recycling area in China after e-waste control. The urinary levels of oxidative stress markers and typical pollutants emitted during e-waste recycling, including heavy metals, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs), were continuously monitored in the surrounding population (including 275 children and 485 adults) from 2016 to 2019 using high-performance liquid chromatography-tandem mass spectrometry and inductively coupled plasma–mass spectrometry. The results showed that exposure to PAHs, VOCs and heavy metals was significantly associated with oxidative stress levels in urine. After e-waste control, the exposure levels of most PAHs and VOCs and a few heavy metals in the population significantly decreased. Interestingly, the level of 8-hydroxy-2′-deoxyguanosine (a biomarker of oxidative DNA damage) in children significantly decreased by 17.6 %, from 9.45 μg/g CRE in 2017 to 7.79 μg/g CRE in 2019 (p < 0.01). Thus, implementing e-waste control measures effectively reduced the human exposure risk to e-waste pollutants. Urinary tin (Sn), s-phenylmercapturic acid (PMA), 2-&3-hydroxyfluorene (2-&3-OHF), 3-hydroxyphenanthrene (3-OHPhe), and 1-hydroxypyrene (1-OHP) levels decreased significantly and monotonically over time (p < 0.01). The levels of urinary Sn and PMA in combination with 1-OHP, 2-&3-OHF, or 3-OHPhe as biomarkers demonstrated an excellent ability to classify e-waste pollution. These biomarkers will facilitate evaluations of the effectiveness of the governmental pollution regulations and policy measures. Additionally, children were generally exposed to higher levels of heavy metals and VOCs and suffered higher levels of oxidative stress damage than adults, suggesting that children are more vulnerable to e-waste pollution. This work will provide a reference for e-waste management and control.

Urinary PAHs metabolites in Karakoram Highway's heavy traffic vehicle (HTV) drivers: evidence of exposure and health risk.

The current study features PAHs exposure on Karakoram Highway, a route of utmost importance in Pakistan. The drivers of heavy traffic vehicles (HTV) on Karakoram Highway spend long hours amid dense traffic and therefore, inevitably inhale huge amount of PAH carcinogens. The urinary metabolites of PAHs in such drivers (meeting selection criteria n = 48) and a control group (n = 49) were comparatively profiled. The higher urinary biomarkers among ninety-six percent HTV drivers were evident of PAHs exposure. We observed elevated concentrations of urinary benzo[a]pyrene metabolites (3-OH-BaP = 3.53 ± 0.62ngg-1 creatinine and 9-OH-BaP = 3.69 ± 0.74ngg-1 creatinine) in HTV driver's samples compared to controls (0.85 ± 0.08 and 0.31 ± 0.03ngg-1 creatinine, respectively). Interestingly, urinary benzo[a]pyrene metabolites were detected in almost similar amount among HTV drivers irrespective of their working hours. A distinct smoking effect was manifested with rising urinary levels of 1-hydroxypyrene, 2-hydroxyphenanthrene, and 3-hydroxybenzo[a]pyrene with corresponding increase in driving hours per day. These metabolites exhibited characteristic exposures to low molecular weight volatile PAHs that are commonly found in vehicular exhaust. The elevated PAH body burden was directly linked to the nature of their job and the route-long environmental pollution on Karakoram Highway. Additionally, the poor economic status and smoking also increased HTV driver's health vulnerability and significantly declined their health capacity. There was conclusive evidence that HTV drivers were exposed to PAHs during a ride on Karakoram Highway, back and forth, an aspect not reported earlier.

Children's exposure to polycyclic aromatic hydrocarbon (PAHs): a review on urinary 1-hydroxypyrene and associated health effects.

This article reviewed the published studies on theenvironmental exposure to polycyclic aromatic hydrocarbons (PAHs) among children and assessed the urinary 1-hydroxypyrene (1-OHP) level as a biomarker of exposure to PAHs. The current knowledge of the potential health effects of increased 1-OHP in children was reviewed. Additionally, the influence of genetic polymorphism on the urinary 1-OHP level was discussed in this review. The assembled data showed that children who are attending schools or living close to industrial and polluted urban areas might have greater exposure to higher concentrations of PAHs with a higher level of urinary 1-OHP when compared to those children living in rural areas. Urinary 1-OHP may be a reliable biomarker for determining the genotoxic effects, oxidative stress and inflammation caused by exposure to PAHs. Strong research evidence indicated that the total body burden of PAHs should be evaluated by biomonitoring of 1-OHP in line with other urinary PAHs metabolites (with 2-3 rings) to evaluate recent total exposure to PAHs. Overall, the study suggests implementing a mitigation plan to combat air pollution to provide a cleaner environment for children.

Combined effects of exposure to polycyclic aromatic hydrocarbons and metals on oxidative stress among healthy adults in Caofeidian, China

Exposure to polycyclic aromatic hydrocarbons (PAHs) and metals is associated with many adverse effects on human health, accompanied by oxidative stress. This study aimed to investigate the effects of co-exposure to PAHs and metals on oxidative stress in healthy adults. A preliminary longitudinal panel study was conducted between 2017 and 2018 in 45 healthy college students in Caofeidian, China. Six urinary monohydroxylated-PAHs (OH-PAHs), ten metals, 8-hydroxydeoxyguanosine (8-OHdG), and 8-iso-prostaglandin-F2α (8-iso-PGF2α) were measured. Linear mixed effects (LME) models and Bayesian kernel machine regression (BKMR) models were used to explore the associations of urinary OH-PAHs and metals with 8-OHdG and 8-iso-PGF2α. LME models showed that most urinary OH-PAHs and metals were positively associated with 8-OHdG and 8-iso-PGF2α. For example, a one-unit increase in the ln-transformed level of 1-hydroxypyrene (1-OHPyr) and vanadium (V) was associated with an increase of 143.8% (95% CI: 105.7 – 188.9%) and 105.8% (95% CI: 79.2–136.4%) in 8-OHdG; 8-iso-PGF2α increased by 118.9% (95% CI: 99.2–140.5%) and 83.9% (95% CI: 67.2–102.2%) with a one-unit increase in the ln-transformed level of 3-hydroxyphenanthrene (3-OHPhe) and aluminum (Al). BKMR models indicated the overall positive associations of the mixture of six OH-PAHs, ten metals, or six OH-PAHs and ten metals with 8-OHdG and 8-iso-PGF2α. Urinary 1-OHPyr and V were identified as the major contributors to the increased urinary 8-OHdG levels, while urinary 3-OHPhe and Al were the most vital contributors to the increased urinary 8-iso-PGF2α levels. The results revealed the longitudinal dose-response relationships of urinary OH-PAHs and metals with oxidative stress among healthy adults in Caofeidian; this finding serves as an evidence regarding the early health hazard caused by exposure to PAHs and metals and has implications for the environmental management of PAH and metal emissions in this area.

1-Hydroxypyrene mediates renal fibrosis through aryl hydrocarbon receptor signalling pathway.

In chronic kidney disease (CKD), patients inevitably reach end-stage renal disease and require renal transplant. Evidence suggests that CKD is associated with metabolite disorders. However, the molecular pathways targeted by metabolites remain enigmatic. Here, we describe roles of 1-hydroxypyrene in mediating renal fibrosis. We analysed 5406 urine and serum samples from patients with Stage 1-5 CKD using metabolomics, and 1-hydroxypyrene was identified and validated using longitudinal and drug intervention cohorts as well as 5/6 nephrectomised and adenine-induced rats. We identified correlations between the urine and serum levels of 1-hydroxypyrene and the estimated GFR in patients with CKD onset and progression. Moreover, increased 1-hydroxypyrene levels in serum and kidney tissues correlated with decreased renal function in two rat models. Up-regulated mRNA expression of aryl hydrocarbon receptor and its target genes, including CYP1A1, CYP1A2 and CYP1B1, were observed in patients and rats with progressive CKD. Further we showed up-regulated mRNA expression of aryl hydrocarbon receptor and its three target genes, plus up-regulated nuclear aryl hydrocarbon receptor protein levels in mice and HK-2 cells treated with 1-hydroxypyrene, which caused accumulation of extracellular matrix components. Treatment with aryl hydrocarbon receptor short hairpin RNA or flavonoids inhibited mRNA expression of aryl hydrocarbon receptor and its target genes in 1-hydroxypyrene-induced HK-2 cells and mice. Metabolite 1-hydroxypyrene was demonstrated to mediate renal fibrosis through activation of the aryl hydrocarbon receptor signalling pathway. Targeting aryl hydrocarbon receptor may be an alternative therapeutic strategy for CKD progression.

Associations of Bitumen Fumes with Lymphocyte Subsets and Cytokines Expression in the Peripheral Blood of Exposed Workers

The present study aimed to investigate the distribution of lymphocyte subsets and cytokines expression in the peripheral blood of bitumen fumes-exposed workers. In this study, 129 workers from molding and roasting workshops were recruited as the exposed group and 99 office and quality inspection staff were chosen as the control. The polycyclic aromatic hydrocarbons (PAHs) levels of bitumen fumes in individual and fixed-point air samples and the urinary levels of 1-hydroxypyrene (1-OH-P), 1-hydroxynaphthols (1-OH-N) and 2-hydroxynaphthols (2-OH-N) in workers were measured using High Performance Liquid Chromatography. The lymphocyte subsets and serum cytokines concentrations were analyzed by flow cytometry and cytometric bead array, respectively. The median values of PAHs were 0.08 mg/m3 for permissible concentration-time weighted average and 0.12 mg/m3 for permissible concentration-short term exposure (PC-STEL) in molding and roasting workshops, which were higher than that in the control area (< 0.01 mg/m3). Multivariate linear regression models were used to adjust for influential covariates, including age, gender, work age, smoking status, and alcohol consumptions. After adjusting for these covariates, we compared levels of urinary PAHs metabolites, the percentages of lymphocyte subsets, and serum cytokines concentrations between the two groups. The 1-OH-P, 1-OH-N, and 2-OH-N levels in the urine of bitumen fumes exposed workers were significantly higher than that in the controls (P < 0.05). Compared with the control group, the percentage of the natural killer (NK) cell (CD56+ cell) was significantly increased in the exposed group (P < 0.001). There was a significant decrease in the percentages of CD3+ T cell, CD4+ T cell, and CD8+ T cell in the exposed group compared to the control (P < 0.001). The serum levels of interleukin-1β (IL-1β) and IL-6 in bitumen fumes exposed workers were significantly higher than that of the controls (P < 0.05). Moreover, positive correlations were observed between the serum levels of IL-1β, IL-6, and urinary 1-OH-P levels in bitumen fumes-exposed workers, respectively (P < 0.05). There were no significant differences in the serum levels of IL-8, tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-1β (MIP-1β) and monocyte chemotactic protein-1 (MCP-1) between the exposed group and the control group (P > 0.05). Our study suggested that low dose of bitumen fumes exposure could decrease the percentage of T cell, increase the percentage of NK cell and stimulate the release of serum IL-1β and IL-6 in the peripheral blood of exposed workers. The serum levels of IL-1β and IL-6 were positive correlated with the urinary 1-OH-P levels in bitumen fumes exposed workers. These results may inform the search for potential effective biomarkers and provide evidences for early health monitoring in workers occupationally exposed to bitumen fumes.

Investigation of Ambient Polycyclic Aromatic Hydrocarbons in a Populated Middle Eastern City

Characteristics, sources and health risks of atmospheric PM10-bound polycyclic aromatic hydrocarbons (PAHs) on residents living in different regions of Ahvaz, Southwest Iran were investigated during 2016–2017. 84 samples were taken from the different regions: (S1) industrial; (S2) high traffic and (S3) residential sites in Ahvaz metropolitan. Urinary samples were collected from people who came to the east health center of Ahvaz. Urinary 1-hydroxypyrene and PAHs levels were analyzed by Gas Chromatography with Mass Spectrometry (GC/MS). Exposure and risk assessment (Incremental Lifetime Cancer Risk (ILCR), Lifetime Average Daily Dose (LADD) and hazard index (HI)) of these pollutants were estimated, using USEPA’s exposure parameters. Results of this study showed that in the air of residential and industrial areas observed the lowest and the highest level of PAHs, respectively. High molecular weight compounds (2–4rings), contributed to 85% of ∑PAHs mass in the atmospheric PM10-bound samples. Industrial processing and petroleum refining, were identified to be major outdoor resources of PAHs. Based on the result of this study, the highest and the lowest concentration of PAHs metabolites were observed in the industrial and residential areas. Average urinary 1-hydroxypyrene levels of S1, S2 and S3 regions were 0.4735; 1.311 and 1.4942 ng/dL, respectively. The values of ILCR in cold (0.06913) and warm (0.052854) seasons were higher than EPA which, was significantly correlated with the concentration of PAHs. In conclusion, increasing exposure concentration of polycyclic aromatic hydrocarbons would have a significant potential for increased ILCR and risk of health endpoint. ILCR in different areas was significantly higher than standard. Our results show that the air quality of Ahvaz city was in an unfavorable condition and increasing exposure concentration of PAHs would have a significant potential for increased ILCR and risk of diseases.

Human health risks estimations from polycyclic aromatic hydrocarbons in serum and their hydroxylated metabolites in paired urine samples

Polycyclic aromatic hydrocarbons (PAHs) are compounds with two or more benzene rings whose hydroxylated metabolites (OH-PAHs) are excreted in urine. Human PAH exposure is therefore commonly estimated based on urinary OH-PAH concentrations. However, no study has compared PAH exposure estimates based on urinary OH-PAHs to measurements of PAH levels in blood samples. Estimates of PAH exposure based solely on urinary OH-PAHs may thus be subject to substantial error. To test this hypothesis, paired measurements of parent PAHs in serum and OH-PAHs in urine samples from 480 participants in Guangzhou, a typical developed city in southern China, were used to investigate differences in the estimates of human PAH exposure obtained by sampling different biological matrices. The median PAH concentration in serum was 4.05 ng mL−1, which was lower than that of OH-PAHs in urine (8.33 ng mL−1). However, serum pyrene levels were significantly higher than urinary levels of its metabolite 1-hydroxypyrene. Concentrations of parent PAHs in serum were not significantly correlated with those of their metabolites in urine with the exception of phenanthrene, which exhibited a significant negative correlation. Over 28% of the participants had carcinogenic risk values above the acceptable cancer risk level of 10−6. Overall, estimated human exposure and health risks based on urinary 1-hydroxypyrene levels were only 13.6% of those based on serum pyrene measurements, indicating that estimates based solely on urine sampling may substantially understate health risks due to PAH exposure.

26030 The impact of allergic sensitization and smoking on the association between urinary polycyclic aromatic hydrocarbons and the symptoms of atopic triad in the US population

Polycyclic aromatic hydrocarbons (PAHs) exposure is well known for its negative health effects. To investigate the relationship between PAHs and atopic triad as well as the impact of allergic sensitization and smoking on these connections, binary multivariable logistic regression was performed using National Heath and Nutritional Examination Survey 2005-2006 dataset. 2242 participants were included and nine urinary PAHs, 1-hydroxynaphthol (NAP), 2-NAP, 2-hydroxyfluorene (FLU), 3-FLU, 9-FLU, 1-hydroxylphenanthrene (PHE), 2-PHE, 3-PHE, 1-hydroxypyrene (PYR) levels were log transformed.

Associations between exposure to polycyclic aromatic hydrocarbons and metabolic syndrome in U.S. adolescents: Cross-sectional results from the National Health and Nutrition Examination Survey (2003–2016) data

BackgroundThe metabolic syndrome is a constellation of risk factors, including abdominal obesity, hypertension, dyslipidemia, and hyperglycemia. Polycyclic aromatic hydrocarbons (PAHs) constitute a group of chemicals that are formed during the incomplete combustion of coal, oil and gas, garbage, and other organic substances. In the occupational exposure population, PAHs exposure increased the prevalence ratio of metabolic syndrome. However, the effect of PAHs on prevalence of metabolic syndrome in adolescents has not been reported. Because of the propensity for childhood metabolic risk to track into adulthood, there is a great need to identify risk factors for childhood metabolic syndrome. MethodUsing data from the 2003–2016 National Health and Nutrition Examination Survey. We defined metabolic syndrome using a modified version of the National Cholesterol Education Program Adult Treatment Panel Ⅲ definition for adolescents. Weighted logistic regression was used to calculate the odds ratio and 95 % confidence intervals for each biomarker. In addition, we applied the weighted quantile sum (WQS) regressions to adolescent metabolic syndrome to reveal the multiple exposure effects and relative weights of each PAH. ResultsAmong the 827 adolescents, 183 (22.13 %) had metabolic syndrome. The levels of 2-hydroxynaphthalene (2-NAP), 2-hydroxyphenanthrene (2-PHE), 2-hydroxyfluorene (2-FLU), 1-hydroxynaphthalene (1-NAP), 3-hydroxyfluorene (3-FLU) and 1-hydroxypyrene (1-PYR) were higher in the group of adolescents with metabolic syndrome. There were positive associations between higher concentrations of 2-NAP, 2-FLU and odds of metabolic syndrome after adjustment, which odds ratios (ORs) in the 3rd tertile were 2.22 (95%CI:1.45–3.44) and 2.09 (95%CI:1.36–3.10), respectively. In subgroups analysis, the ORs between the 3 tertile concentrations of 2-NAP, 2-PHE and high fasting blood glucose (FBG) were 2.20 (95%CI:1.37–3.57) and 1.99 (95%CI:1.16–3.48). ConclusionThe present study suggested that PAHs may be associated with odds of metabolic syndrome as well as individual metabolic syndrome components among adolescents. A cohort study should be designed to clarify the cause and effect between PAHs and metabolic syndrome in future research.

Benchmark dose analysis for PAHs hydroxyl metabolites in urine based on mitochondrial damage of peripheral blood leucocytes in coke oven workers in China

ObjectivesThe aim was to explore the dose-response relationship between occupational polycyclic aromatic hydrocarbons (PAHs) exposure and mitochondrial damage in coke oven plants workers. Methods544 workers and 238 healthy people were recruited. The ultra-high performance liquid chromatography was used to determine the level of 1-hydroxypyrene, 1-hydroxynaphthalene, 2-hydroxynaphthalene and 3-hydroxyphenanthrene. The real-time fluorescence quantitative polymerase chain reaction was used to determine the mitochondrial DNA copy number (mtDNAcn). The benchmark dose software was used to analyze the benchmark dose. ResultsThe mtDNAcn in the exposure group was lower than that in the control group. The concentrations of 1-hydroxypyrene, 1-hydroxynaphthalene, 2-hydroxynaphthalene and 3-hydroxyphenanthrene in the exposure group were higher than those in the control group. There is a dose-response relationship between 1-hydroxypyrene, 3-hydroxyphenanthrene and mitochondrial DNA damage. The benchmark dose lower confidence limit (BMDL) of 1-hydroxypyrene were 0.045, 0.004, and 0.058 pg/μg creatinine in the total, male, and female population, respectively. The BMDL of 3-hydroxyphenanthrene were 5.142, 6.099, and 2.807 pg/μg creatinine in the total, male, and female population, respectively. ConclusionsThe BMDL of 1-hydroxypyrene and 3-hydroxyphenanthrene initially explored can provide a reference to establish occupational exposure biological limits.

The preliminary investigation of potential response biomarkers to PAHs exposure on childhood asthma.

Exposure to polycyclic aromatic hydrocarbons (PAHs) is a potential risk factor for asthma prevalence. This study aims to explore whether PAHs exposure is associated with childhood asthma by altering microbial diversity and metabolic profiles. Thirty children with asthma and 30 children as control in Nanjing, China were recruited. Urinary 1-hydroxypyrene (1-OHPyr) level was determined by UPLC-Orbitrap-MS as a PAHs exposure biomarker. Logistic regression was conducted to investigate the association between 1-OHPyr and childhood asthma. Microbial diversity was analyzed by 16S rRNA gene sequencing. Metabolic profiles were obtained by UPLC-Orbitrap-MS methods. Differential microbiota and metabolites were screened and selected as response biomarkers or intermediates. Mediation analysis was conducted to assess the association between PAHs and asthma mediated by intermediates. Participating children with and without asthma aged 6.43 ± 2.23 years. The urinary 1-OHPyr level ranged from 0.10 to 1.51 μmol/mol (creatinine corrected) in the participants. The urinary 1-OHPyr level was associated with childhood asthma (OR = 7.21, 95% CI: 1.03-50.42 per 1 μmol/mol unit). Microbial diversity was decreased in the group with asthma and there was a significant shift in the abundance of Proteobacteria (at the phylum level), Veillonella and Prevotella (at the genus level). The enrichment pathway analysis showed that differentially expressed metabolites were involved in purine metabolism, amino acid metabolism, and lipid and fatty acid metabolism. The urinary 1-OHPyr level was associated with the abundance of Actinomyces sp. oral clone IO076 and 7-methylguanine that showed a mediation effect on the association between urinary 1-OHPyr levels and childhood asthma by mediation analysis. Urinary 1-OHPyr exposure was associated with childhood asthma, microbial diversity, and metabolic profiles. Microbial diversity and metabolic profiles may be intermediates as response biomarkers to PAHs exposure in childhood asthma. Further research is needed to confirm these study results and determine the underlying mechanism.

Determination of polycyclic aromatic hydrocarbon metabolites in urine of coke oven workers in Turkey and exposure assessment

Coke-oven workers are occupationally exposed to high concentrations of polycyclic aromatic hydrocarbons. In this study, 1-hydroxypyrene, 9-hydroxyphenantrene, and 3-hydroxybenzo[a]pyrene levels were determined in the urine of occupationally exposed coke-oven worker as markers of exposure to polycyclic aromatic hydrocarbons. The validated high-pressure liquid chromatography method with fluorescence detection was performed for metabolite analysis. Average values of 1-hydroxypyrene were 1.26 µmol/mol creatinine and of 9-hydroxyphenantrene 3.68 µmol/mol creatinine in the workers group, and 0.04 and 0.06 µmol/mol creatinine in the control group. While the average value of 3-hydroxybenzo[a]pyrene was 0.007 µmol/mol creatinine in the workers group, it was below the limit of detection in the control group. All of the mean 1-hydroxypyrene values (coke-oven workers overall mean = 1.26 μmol/mol creatinine; high exposure group mean = 1.91 μmol/mol creatinine; low exposure group mean = 0.66 μmol/mol creatinine) obtained in the workers group were higher than the biological exposure index (0.5 μmol/mol creatinine) that warrants occupational exposure proposed by American Conference of Government Industrial Hygienists. Urinary 1-hydroxypyrene mean levels of all coke-oven workers and the high exposure group exceeded the no observed genotoxic effect level of 1 μmol/mol creatinine.

Grill Workers Exposure to Polycyclic Aromatic Hydrocarbons: Levels and Excretion Profiles of the Urinary Biomarkers.

Grilling activities release large amounts of hazardous pollutants, but information on restaurant grill workers’ exposure to polycyclic aromatic hydrocarbons (PAHs) is almost inexistent. This study assessed the impact of grilling emissions on total workers’ exposure to PAHs by evaluating the concentrations of six urinary biomarkers of exposure (OHPAHs): naphthalene, acenaphthene, fluorene, phenanthrene, pyrene, and benzo(a)pyrene. Individual levels and excretion profiles of urinary OHPAHs were determined during working and nonworking periods. Urinary OHPAHs were quantified by high-performance liquid-chromatography with fluorescence detection. Levels of total OHPAHs (∑OHPAHs) were significantly increased (about nine times; p ≤ 0.001) during working comparatively with nonworking days. Urinary 1-hydroxynaphthalene + 1-hydroxyacenapthene and 2-hydroxyfluorene presented the highest increments (ca. 23- and 6-fold increase, respectively), followed by 1-hydroxyphenanthrene (ca. 2.3 times) and 1-hydroxypyrene (ca. 1.8 times). Additionally, 1-hydroxypyrene levels were higher than the benchmark, 0.5 µmol/mol creatinine, in 5% of exposed workers. Moreover, 3-hydroxybenzo(a)pyrene, biomarker of exposure to carcinogenic PAHs, was detected in 13% of exposed workers. Individual excretion profiles showed a cumulative increase in ∑OHPAHs during consecutive working days. A principal component analysis model partially discriminated workers’ exposure during working and nonworking periods showing the impact of grilling activities. Urinary OHPAHs were increased in grill workers during working days.