Coke Oven Emissions Research Articles

Source-specific probabilistic health risk assessment of dust PAHs in urban parks based on positive matrix factorization and Monte Carlo simulation.

Understanding the health risks of polycyclic aromatic hydrocarbons (PAHs) in dust from city parks and prioritizing sources for control are essential for public health and pollution management. The combination of Source-specific and Monte Carlo not only reduces management costs, but also improves the accuracy of assessments. To evaluate the sources of PAHs in urban park dust and the possible health risks caused by different sources, dust samples from 13 popular parks in Kaifeng City were analyzed for PAHs using gas chromatograph-mass spectrometer (GC-MS). The results showed that the surface dust PAH content in the study area ranged from 332.34µg·kg-1 to 7823.03µg·kg-1, with a mean value of 1756.59µg·kg-1. Nemerow Composite Pollution Index in the study area ranged from 0.32 to 14.41, with a mean of 2.24, indicating that the overall pollution warrants attention. Four pollution sources were identified using the positive matrix factorization (PMF) model: transportation source, transportation-coal and biomass combustion source, coke oven emission source, and petroleum source, with contributions of 33.74%, 25.59%, 22.14%, and 18.54%, respectively. The Monte Carlo cancer risk simulation results indicated that park dust PAHs pose a potential cancer risk to all three populations (children, adult male and adult female). Additionally, the cancer risk for children was generally higher than that for adult males and females, with transportation sources being the main contributor to the carcinogenic risk. Lastly, sensitivity analyses results showed that the toxic equivalent concentration (CS) is the parameter contributing the most to carcinogenic risk, followed by Exposure duration (ED).

Effect and interaction of PINK1 genetic polymorphisms and environmental factors on blood pressure in COEs-exposed workers

ABSTRACT Coke oven emissions (COEs) contain a variety of polycyclic aromatic hydrocarbons (PAHs), which can cause damage to the human cardiovascular system. In addition, myocardial mitochondria are susceptible to damage in hypertensive patients. However, it is not clear whether genetic variation, in single nucleotide polymorphisms (SNPs) in PINK1 affects COEs exposure-induced abnormal blood pressure. We surveyed and tested 518 workers exposed to COEs and statistically analyzed them with SPSS 21.0 software. SBP was greater in the high-exposure group than in the low-exposure group. Generalized linear model analysis showed that the interaction of PINK1 rs3738136 (GA+AA) and COEs had an effect on SBP [β(95%CI) = -6.537(−12.072, −1.002), p = 0.021] and DBP [β(95%CI) = -4.811(−8.567, −1.056), p = 0.012]. This study is the first to identify the role of PINK1 rs3738136 in COE- induced abnormal blood pressure, and to prove that the abnormal blood pressure of workers is the result of environmental and genetic factors.

Simultaneous capture of trace benzene and SO2 in a robust Ni(II)-pyrazolate framework

Benzene and SO2, coexisting as hazardous air pollutants in some cases, such as in coke oven emissions, have led to detrimental health and environmental effects. Physisorbents offer promise in capturing benzene and SO2, while their performance compromises at low concentration. Particularly, the simultaneous capture of trace benzene and SO2 under humid conditions is attractive but challenging. Here, we address this issue by constructing a robust pyrazolate metal-organic framework (MOF) sorbent featuring rich accessible Ni(II) sites with low affinity to water and good stability. This material achieves a high benzene uptake of 5.08 mmol g–1 at 10 Pa, surpassing previous benchmarks. More importantly, it exhibits an adsorption capacity of ~0.51 mmol g–1 for 10 ppm benzene and ~1.21 mmol g–1 for 250 ppm SO2 under 30% relative humidity. This work demonstrates that a pioneering MOF enables simultaneous capture of trace benzene and SO2, highlighting the potential of physisorbents for industrial effluent remediation, even in the presence of moisture.

Coke oven emissions exacerbate allergic asthma by promoting ferroptosis in airway epithelial cells

Epidemiological studies have shown that coke oven emissions (COEs) affect the deterioration of asthma, but has not been proven by experimental results. In this study, we found for the first time that COEs exacerbate allergen house dust mite (HDM)-induced allergic asthma in the mouse model. The findings reveal that airway inflammation, airway remodeling and allergic reaction were aggravated in the COE + HDM combined exposure group compared with the individual exposure group. Mechanism studies indicated higher levels of iron and MDA in the COE + HDM combined exposure group, along with increased expression of Ptgs2 and reduced GPX4 expression. Iron chelator deferoxamine (DFO) effectively inhibited ferroptosis induced by COE synergistically with HDM in vitro. Further studies highlighted the role of ferritinophagy in the COE + HDM-induced ferroptosis. 3-methyladenine (3-MA) could inhibit ferroptosis in the COE + HDM exposure group. Interestingly, we injected DFO intraperitoneally into mice in the combined exposure group and found DFO could significantly inhibit the COE-exacerbated ferroptosis and allergic asthma. Our findings link ferroptosis with COE-exacerbated allergic asthma, implying that ferroptosis may have important therapeutic potential for asthma in patients with occupational exposure of COE.

MiR-145a-5p/SIK1/cAMP-dependent alteration of synaptic structural plasticity drives cognitive impairment induced by coke oven emissions

Exposure to fine particulate matter (PM) is associated with the neurodegenerative diseases. Coke oven emissions (COEs) in occupational environment are important sources of PM. However, its neurotoxicity is still unclear. Therefore, evaluating the toxicological effects of COE on the nervous system is necessary. In the present study, we constructed mouse models of COE exposure by tracheal instillation. Mice exposed to COE showed signs of cognitive impairment. This was accompanied by a decrease in miR-145a-5p and an increase in SIK1 expression in the hippocampus, along with synaptic structural damage. Our results demonstrated that COE-induced miR-145a-5p downregulation could increase the expression of SIK1 and phosphorylated SIK1, inhibiting the cAMP/PKA/CREB pathway by activating PDE4D, which was associated with reduced synaptic structural plasticity. Furthermore, restoring of miR-145a-5p expression based on COE exposure in HT22 cells could partially reversed the negative effects of COE exposure through the SIK1/PDE4D/cAMP axis. Collectively, our findings link epigenetic regulation with COE-induced neurotoxicity and imply that miR-145a-5p could be an early diagnostic marker for neurological diseases in patients with COE occupational exposure.

Source apportionment and source specific health risk assessment of HMs and PAHs in soils with an integrated framework in a typical cold agricultural region in China

A new innovative methodology system framework for source apportionment and source-specific risk assessment has been proposed and actively applied to identify the contamination characteristics, oriented sources and health risks associated with contamination levels of Heavy metals (HMs) and Polycyclic Aromatic Hydrocarbons (PAHs) in soils, a typical cold agricultural region in Northeastern China. To achieve this meaningful goal, a large-scale dataset including 1780 top soil samples, 10 HMs and 16 priority PAHs has been organized and collected from a typical study area in China. The total concentrations of the 10 selected HMs in study area range from 0.05 to 2147.40 mg/kg, with an average of 549.25 ± 541.37 mg/kg. The average concentrations of PAHs for (3–6)-rings are 16.60 ± 18.90, 26.40 ± 28.20, 9.51 ± 13.00 and 1.99 ± 5.30 ng/g, respectively. On the base of optimized literature source fingerprints for HM and PAH, a widely used receptor model, positive matrix factorization (PMF) has been applied to apportion the contamination sources HMs and PAHs in soils. Then source-specific health risk of soil HMs and PAHs have been assessed using the probabilistic incremental lifetime cancer risk model incorporated with source apportionment results data. Fertilizer residues/coke oven comprise the primary contamination source contributors of HMs and PAHs with corresponding contributions of 32.23 % and 27.93 % for HMs and 37.94 % for PAHs. Fertilizer/pesticide residues contributes most to the risks of soil HMs (28.8 %), followed by fossil fuel combustion (24.6 %), mining activities (20.2 %), traffic and vehicle emission (16.3 %) and electroplating/dyeing (14.1 %). Meanwhile, the ranking of health risks from the five identified contamination sources of soil PAHs are resident discharge, coal-fired boilers, coke oven emission, gasoline combustion and power plant, with the contribution of 27.1 %, 25.3 %, 17.3 %, 15.5 % and 14.8 %.And relatively, source-specific risk assessment demonstrates fossil fuel and coal combustion contribute the greatest impact to the total risk of HMs and PAHs (61.7 % and 56.1 %), respectively. This study provides a good example of how the source specific health risk assessment can be utilized to reduce the contamination in soils.

Benchmark Dose Assessment for Coke Oven Emissions-Induced Mitochondrial DNA Copy Number Damage Effects*

ObjectiveThe study aimed to estimate the benchmark dose (BMD) of coke oven emissions (COEs) exposure based on mitochondrial damage with the mitochondrial DNA copy number (mtDNAcn) as a biomarker. MethodsA total of 782 subjects were recruited, including 238 controls and 544 exposed workers. The mtDNAcn of peripheral leukocytes was detected through the real-time fluorescence-based quantitative polymerase chain reaction. Three BMD approaches were used to calculate the BMD of COEs exposure based on the mitochondrial damage and its 95% confidence lower limit (BMDL). ResultsThe mtDNAcn of the exposure group was lower than that of the control group (0.60 ± 0.29 vs. 1.03 ± 0.31; P < 0.001). A dose–response relationship was shown between the mtDNAcn damage and COEs. Using the Benchmark Dose Software, the occupational exposure limits (OELs) for COEs exposure in males was 0.00190 mg/m3. The OELs for COEs exposure using the BBMD were 0.00170 mg/m3 for the total population, 0.00158 mg/m3 for males, and 0.00174 mg/m3 for females. In possible risk obtained from animal studies (PROAST), the OELs of the total population, males, and females were 0.00184, 0.00178, and 0.00192 mg/m3 respectively. ConclusionBased on our conservative estimate, the BMDL of mitochondrial damage caused by COEs is 0.002 mg/m3. This value will provide a benchmark for determining possible OELs.

Chain-mediating effect of interaction between telomeres and mitochondria under oxidative stress in coke oven workers

Coke oven emissions (COEs) exposure leads to oxidative stress, an imbalance between oxidant production and antioxidant defence in the body, which then leads to shortened relative telomere length (RTL) and reduced mitochondrial DNA copy number (mtDNAcn), ultimately leading to ageing and disease. By analysing the relationship among COEs, oxidative stress, RTL and mtDNAcn, we investigated the chain-mediating effects of oxidative stress and telomeres on mitochondrial damage and mitochondria on telomere damage in coke oven workers. A total of 779 subjects were included in the study. Cumulative COEs exposure concentrations were estimated, and the RTL and mtDNAcn of peripheral blood leukocytes were measured using real-time fluorescence quantitative PCR. Total antioxidant capacity (T-AOC) was measured to reflect the level of oxidative stress. The data were statistically analysed using SPSS 21.0 software and discussed using mediation effect analysis. After adjusting for age, sex, smoking, drinking and BMI, generalised linear model revealed dose–response associations between COEs and T-AOC, RTL and mtDNAcn, respectively. (Ptrend < 0.05). The results of chain-mediating effect showed that the proportion of the chain-mediating effect of “CED-COEs→T-AOC→ RTL→mtDNAcn” was 0.82% (β = −0.0005, 95% CI = [-0.0012, −0.0001]), and the proportion of the chain-mediating effect of “CED-COEs→T-AOC→ mtDNAcn → RTL ″ was 2.64% (β = −0.0013, 95% CI = [-0.0025, −0.0004]). After oxidative stress is induced by COEs, mitochondria and telomeres may interact with each other while leading further to potential bodily damage. This study provides clues to explore the association between mitochondria and telomeres.

Seasonal characterization, sources, and source-specific risks of PM2.5 bound PAHs at different types of urban sites in central China

Polycyclic aromatic hydrocarbons (PAHs) have been extensively investigated in China. However, most previous studies only focused on specific locations. Here, we conducted field studies simultaneously to explore the seasonal characterization, sources, and source-specific risks of 16 PAHs in four polluted cities in China. Similar seasonal Σ16 PAHs variations are observed in all four sites with relatively high values in winter and low values in summer and the ratios of Σ16 PAHs between winter and summer range from 2.7 to 4.4. From summer to winter, the extent of PAH increase outpaces that of PM2.5 increase resulting in significant increase of ∑16 PAHs/PM2.5 in winter. Five potential sources were resolved by PMF: (1) coal combustion (32–52%); (2) vehicle emissions (19–29%); (3) evaporation (9–26%); (4) coke oven emission (11–15%); and (5) biomass burning (5–13%). The highest fraction of evaporation is found in the Luoyang site due to the presence of many petrochemical plants, the largest oil refinery in Henan and large oil storage tanks. The coking factor contributes the largest proportion in Anyang site because of many out of date inefficient coking facilities. The source-related risks in four sites are all higher than the USEPA guideline value (1.0 × 10−6) except for biomass burning. The largest total risks are observed at Luoyang site, slightly higher than those of other cities. Our results suggest that the PAHs still need to be concerned due to the complexity of sources and source emitted risks in different type of cities, and specific source control strategies should be target in different regions.

Effect and interaction of TNKS genetic polymorphisms and environmental factors on telomere damage in COEs-exposure workers

Coke oven emissions (COEs) contain many carcinogenic polycyclic aromatic hydrocarbons (PAHs). Telomere damage is an early biological marker reflecting long-term COEs-exposure. Whereas, whether the genetic variations of telomere-regulated gene TNKS have an effect on the COEs-induced telomere damage is unknown. So we detected the environmental exposure levels, relative telomere length (RTL), and TNKS genetic polymorphisms among 544 COEs-exposure workers and 238 healthy participants. We found that the RTL of the wild homozygous GG genotype in rs1055328 locus was statistically shorter compared with the CG+CC genotype for the healthy participants using covariance analysis(P = 0.008). In the Generalized linear model (GLM) analysis, TNKS rs1055328 GG could accelerate telomere shortening (P = 0.011); and the interaction between TNKS rs1055328 GG and COEs-exposure had an effect on RTL (P = 0.002). In conclusion, this study was the first to discover the role of TNKS rs1055328 locus in COEs-induced telomere damage, and proved that chromosomal damage was a combined consequence of environmental and genetic factors.

Study on the relationship between the pathological type of lung cancer caused by coke oven discharge and the contact type and exposure time

Objective: To study the pathological types of lung cancer caused by coke oven emissions and analyze the correlation between different exposure levels. Methods: In October 2020, the relevant data of 86 confirmed cases of lung cancer caused by coke oven emissions (including basic information of patients, relevant occupational exposure and clinical data) were collected, The workers were grouped according to the different COEs concentrations in their posts: workers in auxiliary posts were taken as the low exposure group (11 persons) , The workers at coke side and furnace bottom are the medium exposure group (14 persons) , and the workers at furnace top are the high exposure group (61 persons) , and the correlation between pathological types of lung cancer and different exposure levels was analyzed. Results: There was no significant difference in age and length of service among the groups (P>0.05) ; The number of lung cancer cases and pathological types among workers in each group were statistically significant (P=0.044) . After adjusting for interference factors, the number of undifferentiated cancers (mainly small cell lung cancer) increased with the increase of exposure level, with a statistically significant difference (P=0.001) . The incidence of lung cancer increased gradually with the length of service, and the incidence rate of lung cancer among workers of different working ages was statistically significant (P<0.05) . Conclusion: Undifferentiated small cell carcinoma is the most common pathological type of lung cancer caused by coke oven emissions, and the incidence of lung cancer tends to increase with the length of service.

Roles of H19/miR-29a-3p/COL1A1 axis in COE-induced lung cancer

Occupational lung cancer caused by coke oven emissions (COE) has attracted increasing attention, but the mechanism is not clear. Many evidences show ceRNA (competing endogenous RNA) networks play important regulatory roles in cancers. In this study, we aimed to construct and verify the ceRNA regulatory network in the occurrence of COE-induced lung squamous cell carcinoma (LUSC). We performed RNA sequencing with lung bronchial epithelial cell (16HBE) and COE induced malignant transformed cell (Rf). Furthermore, we analyzed RNA sequencing data of LUSC and adjacent tissues in the cancer genome atlas (TCGA) database. Combined our data and TCGA data to determine the differentially expressed lncRNAs, miRNAs, mRNAs. lncBASE, miRDB and miRTarBase were used to predict the binding relationship between lncRNA and miRNA, miRNA and mRNA. Based on these, we construct the ceRNA network. FREMSA, dual-luciferase reporter assay, quantitative real-time PCR (qRT-PCR), western-blot were used to verify the regulatory axis. CCK8 assay, phalloidin staining, p53 detection were used to explore the roles of this axis in the COE induced malignant transformation. Results showed 7 lncRNAs, 7 miRNAs and 146 mRNAs were identified. Among these, we constructed a ceRNA network including 1 lncRNA, 2 miRNAs and 9 mRNAs. Further verification confirmed the trend of lncRNA H19, miR-29a-3p and COL1A1 were consistent with sequencing results. H19 and COL1A1 were significantly higher in Rf than in 16HBE and miR-29a-3p was reverse. Regulatory investigation revealed H19 increased COL1A1 expression by sponging miR-29a-3p. Knockdown of H19, COL1A1 or overexpression of miR-29a-3p in Rf cells could inhibit cell proliferation, increased cell adhesion and p53 level. However, knockdown of H19 while suppressing the miR-29a-3p partially rescue the malignant phenotype of Rf caused by H19. In conclusion, all these indicated H19 functioned as a ceRNA to increase COL1A1 by sponging miR-29a-3p and promoted COE-induced cell malignant transformation.

Pollution levels, sources and risk assessment of polycyclic aromatic hydrocarbons in farmland soil and crops near Urumqi Industrial Park, Xinjiang, China

This study investigated the concentration, source, and risk assessment of polycyclic aromatic hydrocarbons (PAHs) in farmland soil and crops around the Urumqi Industrial Park in Xinjiang, China. The total concentration of 16 different PAHs in the soil (Quantity: 51) and crop (Species: onion, cabbage, coriander, beans, spinach, celery, lettuce, and sunflower) samples ranged between 2.32 and 225.11 ng/g and between 132.44 and 504.03 ng/g respectively, with average values of 39.29 ± 2.39 ng/g for the soil samples and 295.81 ± 105.00 ng/g for the crop samples. The source analysis of PAHs was performed using the positive matrix factorization and ratio method and identified the high-temperature combustion of fossil fuels, the volatilization of petroleum, coke oven emissions, and traffic emissions as main sources of PAHs in soil. The ecological risk posed by the PAHs detected in the soil samples was within a safe range. The incremental lifetime cancer risk (ILCR) value quantifies resulting from human exposure to soil containing PAH is at a safe level except for the potential carcinogenic risk to children due to ingestion exposure (ILCRs > 1.0 × 10–6). The ILCR posed by crops exceed 1.0 × 10–6 and the risk from sunflower crop was the highest. The highest ILCR values for each crop high exposed for the adult female population. These results indicate that the farmland soil and crops near the Urumqi Industrial Park have been contaminated by PAHs and require urgent remediation to minimize adverse effects of exposure to carcinogens.

Evaluation of Source Emissions Dispersion Potential Near a Coastal Village of Maharashtra, India

Industrial emissions are a serious environmental problem worldwide due to particulates and toxic gases. This study aims to generate an activity-specific emission inventory and estimate emissions dispersion extent in the vicinity of the coastal industrial village by simulating the existing coke oven and pellet plant emissions using the steady-state plume model. Continuous air quality monitoring results were compared with the predicted consequential emissions for the year 2018-19. The maximum ground-level concentrations of particulate and gases within the modeling simulation domain were observed at 9005 m away from the center. They were predicted to be 116.39 μg.m-3, 79.14 μg.m-3, 52.97 μg.m-3, and 211.86 μg.m-3. Data analysis showed that air mass transport from the project to the receptor sites resulted in ambient air concentrations higher than those observed in the other sites. Overall predicted results obtained from AERMOD Cloud simulations were shown to have less bias than the measured results. They recommended considering it as appropriate for the prediction of annual average concentration.

Relationship between miRNAs polymorphisms and peripheral blood leukocyte DNA telomere length in coke oven workers: A cross-sectional study

ObjectiveThe purpose of this study was to investigate the factors affecting telomere length (TL) in coke oven workers by analyzing the interaction between miRNAs polymorphisms and coke oven emissions (COEs) exposure. MethodsA total of 544 coke oven workers and 238 healthy controls were recruited. Peripheral blood was collected from the subjects, genomic DNA was extracted, leukocyte TL was detected by real-time quantitative polymerase chain reaction, and fifteen polymorphisms of eight miRNAs were genotyped by flight mass spectrometry. ResultsStatistical analysis showed that the peripheral blood DNA TL in the exposure group was shorter than that in the control group (P < 0.001). Generalized linear model found that COEs-exposure [β (95%CI) = -0.427 (−0.556, −0.299), P < 0.001], genotype CC+CT for miR-612 rs1144925 [β (95%CI) = −0.367 (−0.630, −0.104), P = 0.006], and the interaction of miR-181B1 rs12039395 TT genotype and COEs-exposure [β (95% CI) = 0.564 (0.108, 1.020), P = 0.015] were associated with the shortened TL. ConclusionCOEs-exposure and miR-612 rs1144925 TT could promote telomere shortening in coke oven workers. The interaction of miR-181B1 rs12039395 TT genotype and COEs-exposure could protect telomere. This provides clues for further mechanistic studies between miRNA and telomere damage.

The Association Between Polymorphisms in Cell-Cycle Genes and Mitochondrial DNA Copy Number in Coke Oven Workers.

The mitochondrial DNA (mtDNA) copy number is a vital component in maintaining normal mitochondrial function. It is affected by environmental and occupational exposures, as well as polymorphisms in nuclear genes. Nonetheless, the specific roles of polymorphisms in cell-cycle genes and mtDNA copy number are still unknown. This study enrolled a sample of 544 coke oven workers and 238 non-exposed controls so as to assess the effect of exposure of coke oven emissions (COEs) and polymorphisms in cell-cycle genes on the mtDNA copy number. We found that the mtDNA copy number in the exposed group (0.60 ± 0.29) was significantly lower than that in the control group (1.03 ± 0.31) (t =18.931, P < 0.001). The analysis of covariance showed that both the rs1801270 (CA+CC) and the rs1059234 (CT+CC) in p21 gene were associated with lower mtDNA copy number in the exposed group (P = 0.001). Generalized linear models indicated COEs-exposure (β = −0.432, P < 0.001) and rs1059234 (CT+CC) in p21 gene (β = −0.060, P = 0.024) were the factors in mtDNA copy number reduction. In conclusion, this study suggests that the decrease of the mtDNA copy number is associated with COEs-exposure and the rs1059234 (CT+CC) in the p21 gene.

Trend Analysis of Occupational Lung Cancer from Coke Oven Emission Exposure - China, 2008-2019.

What is already known about this topic?Coke oven emissions are a complex mixture of particulate matter and gases, some with carcinogenicity, released during coke production. Lung cancer caused by coke oven emissions has been listed as a statutory occupational cancer in China and many countries.What is added by this report?In this study, coke oven emissions-induced lung cancer was mainly found in the manufacturing industries. Coke oven workers exposed to higher levels of polycyclic aromatic hydrocarbons in different workplaces had a high risk of occupational lung cancer.What are the implications for public health practice?It is necessary to take efforts to greatly reduce emissions from coke production and effectively monitor the health of workers.

CpG site-specific methylation as epi-biomarkers for the prediction of health risk in PAHs-exposed populations

Environmental insults can lead to alteration in DNA methylation of specific genes. To address the role of altered DNA methylation in prediction of polycyclic aromatic hydrocarbons (PAHs) exposure-induced genetic damage, we recruited two populations, including diesel engine exhausts (low-level) and coke oven emissions (high-level) exposed subjects. The positive correlation was observed between the internal exposure marker (1-hydroxypyrene) and the extents of DNA damage (P < 0.05). The methylation of representative genes, including TRIM36, RASSF1a, and MGMT in peripheral blood lymphocytes was quantitatively examined by bisulfite-pyrosequencing assay. The DNA methylation of these three genes in response to PAHs exposure were changed in a CpG-site-specific manner. The identified hot CpG site-specific methylation of three genes exhibited higher predictive power for DNA damage than the respective single genes in both populations. Furthermore, the dose-response relationship analysis revealed a nonlinear U-shape curve of TRIM36 or RASSF1a methylation in combined population, which led to determination of the threshold of health risk. Furthermore, we established a prediction model for genetic damage based on the unidirectional-alteration MGMT methylation levels. In conclusion, this study provides new insight into the application of multiple epi-biomarkers for health risk assessment upon PAHs exposure.

CC16 as a Marker of COE-Induced the Early Change of Blood Composition of Coke Oven Workers

Objective: This project aims to enhance the occupational health insurance for coke oven workers. Methods: A total of 136 coke oven emissions workers and 61 oxygen plant workers were recruited to receive physical examinations. The coke oven emissions concentration at the workplace was measured by weighing method. The CC16 concentration was detected by enzyme-linked immunosorbent assay. Results: Logistic regression analysis revealed that exposure to coke oven emissions was correlated with CC16. Correlation analysis revealed that CC16 was related to some physical examination indicators. Multivariate general linear models showed that CC16 was indeed positively correlated with albumin after adjusting for confounding factors. Conclusions: Coke oven emissions affected multiple tissues and multiple systems. The blood system might be the earliest system affected and could be detected by the CC16 protein concentration.

Estimations of benchmark dose for urinary metabolites of coke oven emissions among workers.

Coke oven emissions (COEs), usually composed of polycyclic aromatic hydrocarbons (PAHs) and so on, may alter the relative telomere length of exposed workers and have been linked with adverse health events. However, the relevant biological exposure limits of COEs exposure has not been evaluated from telomere damage. The purpose of this study is to estimate benchmark dose (BMD) of urinary PAHs metabolites from COEs exposure based on telomere damage with RTL as a biomarker. A total of 544 exposed workers and 238 controls were recruited for participation. High-performance liquid chromatography and qPCR were used to detect concentrations of urinary mono-hydroxylated PAHs and relative telomere length in peripheral blood leukocytes for all subjects. The benchmark dose approach was used to estimate benchmark dose (BMD) and its lower 95% confidence limit (BMDL) of urinary OH-PAHs of COEs exposure based on telomere damage. Our results showed that telomere length in the exposure group (0.75 (0.51, 1.08)) was shorter than that in the control group (1.05 (0.76,1.44))(P<0.05), and a dose-response relationship was shown between telomere damage and both 1-hydroxypyrene and 3-hydroxyphenanthrene in urine. The BMDL of urinary 1-hydroxypyrene from the optimal model for telomere damage was 1.96, 0.40, and 1.01 (μmol/mol creatinine) for the total, males, and females group, respectively. For 3-hydroxyphenanthrene, the BMDL was 0.94, 0.33, and 0.49 (μmol/mol creatinine) for the total, males, and females. These results contribute to our understanding of telomere damage induced by COEs exposure and provide a reference for setting potential biological exposure limits.