PIG-A gene mutation as a mutagenicity biomarker among coke oven workers.

PIG-A gene mutations can be detected in humans, and PIG-A assays can potentially predict the risk of exposure to carcinogens. However, extensive, population-based studies to validate this are lacking. We studied a cohort of occupational coke oven workers with chronic high exposure to carcinogenic polycyclic aromatic hydrocarbons, which are well-studied genotoxins classified by the IARC as carcinogenic to humans. Peripheral blood erythrocytes of workers were assessed for gene mutations using a PIG-A assay, and chromosome damage using the cytokinesis-block micronucleus test with lymphocytes. Two sample populations from a non-industrialized city and new employees in industrial plants were selected as controls. We observed a significantly elevated PIG-A mutation frequency (MF) and increased frequencies of micronuclei (MN) and nuclear buds (NBUDs) in coke oven workers, compared with levels in the control groups. We found that the coke oven workers with different lengths of service had a relatively high mutation frequency. Overall, the study findings showed that occupational exposure of coke oven workers increases the genetic damage and the PIG-A MF could be a potential biomarker for risk assessment of carcinogen exposure.

Benchmark dose estimation for coke oven emissions based on oxidative damage in Chinese exposed workers.

Coke oven emissions (COEs) can cause oxidative stress of the body, which in turn induces the occupational lung disease and also increases the risk of other diseases. COEs are the major occupational hazard factors for coke oven workers. The aim of the study is to explore the influences of COEs exposure on oxidative damage and estimate the benchmark dose (BMD) of COEs. A group of 542 workers exposed to COEs and 237 healthy controls from the same city were recruited in this study. The corresponding measuring kits were used to determine the plasma biomarkers of oxidative damage level. Generalized linear models and trend tests were used to analyze the relationship between COEs exposure and biomarkers. EPA Benchmark Dose Software was performed to calculate BMD and the lower confidence limit of the benchmark dose (BMDL) of COEs exposure. A significant association was observed between COEs exposure and oxidative damage with T-AOC as a biomarker. The BMD of COEs exposure were 2.83 mg/m3 and 1.39 mg/m3 for males and females, respectively, and the corresponding BMDL were 1.47 mg/m3 and 0.75 mg/m3, respectively. Our results suggested that the exposure level of COEs below the current national occupational exposure limits (OELs) would induce oxidative damage, and the OEL of COEs based on the T-AOC damage was suggested at 0.03 mg/m3 in this study.

Urinary Mercapturic Acids to Assess Exposure to Benzene and Other Volatile Organic Compounds in Coke Oven Workers.

Coke production was classified as carcinogenic to humans by the International Agency for Research on Cancer. Besides polycyclic aromatic hydrocarbons, coke oven workers may be exposed to benzene and other volatile organic compounds (VOCs). The aim of this study was to assess the exposure to several VOCs in 49 coke oven workers and 49 individuals living in the same area by determining urinary mercapturic acids. Active tobacco smoking was an exclusion criterion for both groups. Mercapturic acids were investigated by a validated isotopic dilution LC-MS/MS method. Linear models were built to correct for different confounding variables. Urinary levels of N-acetyl-S-phenyl-L-cysteine (SPMA) (metabolite of benzene), N-acetyl-S-(2-hydroxy-1/2-phenylethyl)-L-cysteine (PHEMA) (metabolite of styrene), N-acetyl-S-(2-cyanoethyl)-L-cysteine (CEMA) (metabolite of acrylonitrile), N-acetyl-S-[1-(hydroxymethyl)-2-propen-1-yl)-L-cysteine and N-acetyl-S-(2-hydroxy-3-buten-1-yl)-L-cysteine (MHBMA) (metabolites of 1,3-butadiene) were 2-10 fold higher in workers than in controls (p < 0.05). For SPMA, in particular, median levels were 0.02 and 0.31 µg/g creatinine in workers and controls, respectively. Among workers, coke makers were more exposed to PHEMA and SPMA than foremen and engine operators. The comparison with biological limit values shows that the exposure of workers was within 20% of the limit values for all biomarkers, moreover three subjects exceeded the restrictive occupational limit value recently proposed by the European Chemicals Agency (ECHA) for SPMA.

Benchmark dose assessment for coke oven emissions-induced telomere length effects in occupationally exposed workers in China.

Telomeres are DNA-protein structures that protect chromosome ends from degradation and fusion, which are shortened by oxidative stress, for example air pollution including benzene, toluene, Coke Oven Emissions (COEs), and so on. As a biomarker of health and disease, telomere length is associated with cardiovascular, diabetes and cancers. The aim of this study was to estimate the effects of COEs exposure on telomere length and the benchmark dose (BMD) of COEs. A total of 542 coke oven workers and 235 healthy controls without exposure to toxicants were recruited. Quantitative PCR was used to determine the telomere length in human peripheral blood leukocytes DNA. Propensity scoring was used to match coke oven workers to healthy controls. Linear regression models and trend tests were used to the relationship between COEs exposure and telomere length. Telomere length in COEs exposed group 0.764 (0.536, 1.092) was significantly shorter than that in the control group 1.064(0.762, 1.438), (P < 0.001). There were significantly dose-response relationships between COEs exposure and telomere damage with telomere length as a biomarker. A BMDL value lower than the present occupational exposure limits (OELs) of COEs exposure was evaluated using the BMD approach in coke oven workers. Our results suggested that shorter telomere length is related to occupational exposure to COEs and the level of COEs exposure lower than the current national OELs in China and many other countries could induce telomere damage.

Interaction of heat shock protein 70 (HSP70) polymorphisms and occupational hazards increases the risk of hypertension in coke oven workers.

OBJECTIVES: The interaction between genetic, epigenetic inheritance and environmental factors determines susceptibility to hypertension. Previous epidemiology studies have shown that coke oven workers who are frequently exposed to various occupational hazards have remarkable increase in the risk for hypertension. Among many genetic variants identified in hypertension, heat shock protein 70 (HSP70) was found to play important roles in the pathogenesis of hypertension and associated diseases. We therefore explore the possible role of HSP70 polymorphisms and their interaction with occupational environment in hypertension risk. METHODS: We carried out a case-control study among 367 coke oven workers in northwest China, focused on three common HSP70 polymorphisms (HSP70-1 G190C, HSP70-2 A1267G and HSP70-hom T2437C), and evaluated the association of HSP70 gene polymorphisms with work sites for high risk of hypertension. RESULTS: The results indicated that HSP70-1 GC and CC genotype had 2.73-fold and 4.26-fold increased relative risk (95% CI 1.33 to 5.55 and 1.17 to 15.53), respectively, comparing with HSP70-1 GG genotype. HSP70-2 AG and GG conferred a 47% and 36% reduced risk (95% CI 0.23 to 0.99 and 0.14 to 0.92) comparing with HSP70-2 AA genotype. Further analysis of the interaction of HSP70 polymorphisms with occupational environment indicated a strong positive interaction between HSP70 genotype (HSP70-1 GC+CC, HSP70-2 AA and HSP70-hom TC+CC) and oven top workplace. CONCLUSIONS: Collectively, these data indicate that HSP70 polymorphisms interact with occupational hazards might increase the risk of hypertension in coke oven workers.

Petroleum coke exposure leads to altered secretome profiles in human lung models.

Petroleum coke (PC) is a coal-like product that is produced during the refinement of crude oil and bituminous sand. Fugitive dust from open storage of PC in urban areas is a potential human health concern. Animal inhalation studies suggest that PC leads to an adverse pulmonary histopathology, including areas of fibrosis and chronic inflammation; however, little is known about its impact on human health. In order to identify biomarkers and cellular pathways that are associated with exposure, we performed two-dimensional liquid chromatography-mass spectrometric analyses on secreted proteins from two human lung culture models. A total of 2795 proteins were identified and relatively quantified from an immortalized cell line and 2406 proteins from primary cultures that were either mock treated or exposed to particulate matter with a diameter of 2.5-10 µm PC or filtered urban air particulates for 16 h. Pathway analysis on secretomes from primary lung cultures indicated that PC exposure suppressed the secretion of proteins involved in the organization of the extracellular matrix and epithelial differentiation. Because these cellular processes could facilitate fibrosis, we performed chronic 12-day exposure studies on three-dimensional human lung cultures consisting of epithelia and stromal fibroblasts. Relative to mock-treated cells, matrix metallopeptidase 9 levels in the conditioned media were lower by 4 days postexposure and remained suppressed for the duration of the experiment. Immunocytochemical staining of collagen III, a marker associated with fibrosis, showed increased accumulation in the epithelial layer and at the air-liquid interface.

Urinary 1-hydroxypyrene and smoking are determinants of LINE-1 and AhRR promoter methylation in coke oven workers.

Coke oven emissions (COE) containing polycyclic aromatic hydrocarbons (PAHs) are predominant toxic constituents of particulate air pollution that have been linked to increased risk of lung cancer. Aberrant DNA methylation is one of the best known epigenetic changes in human cancers and healthy subjects exposed to carcinogens. The purpose of this study is to explore the factors influencing the methylation of long interspersed nuclear element-1 (LINE-1) and aryl-hydrocarbon receptor repressor (AhRR) in coke oven workers. The study population is composed by coke oven workers (348) and water treatment workers (131). And their urinary PAH metabolites were analyzed by high performance liquid chromatography; DNA methylation were measured by pyrosequencing. The urinary PAHs metabolites were significantly elevated in coke oven workers (P < 0.01). The results from multivariate logistic regression analysis showed that a high level of urinary 1-hydroxypyrene was associated with a significantly increased risk of hypomethylation of LINE-1 (OR: 1.80; 95% CI: 1.25, 2.60), and heavy smoking was associated with a significantly increased risk of hypomethylation of AhRR (OR: 1.44; 95% CI: 1.04, 2.00). Our findings demonstrate that urinary 1-hydroxypyrene may be a useful biomarker for evaluating the role of PAHs exposure on hypomethylation of LINE-1 among coke oven workers and that smoking may be an important factor affecting hypomethylation of AhRR.

Health effects of banning beehive coke ovens and implementation of the ban in China.

Environmental legislation and proper implementation are critical in environmental protection. In the past, beehive coke ovens (BCOs) were popular in China, resulting in enormous emissions of benzo[a]pyrene (BaP), a common indicator of carcinogenic polycyclic aromatic hydrocarbons. BCOs were banned by the Coal Law in 1996. Although BCO numbers have declined since the ban, they were not eliminated until 2011 due to poor implementation. Here, we present the results of a quantitative evaluation of the health effects of historical BCO operation, the health benefits of the ban, and the adverse impacts of the poor implementation of the ban. With only limited official statistics available, historical and geospatial data about BCOs were reconstructed based on satellite images. Emission inventories of BaP from BCOs were compiled and used to model atmospheric transport, nonoccupational population exposure, and induced lung cancer risk. We demonstrated that more than 20% of the BaP in ambient air was from BCOs in the peak year. The cumulative nonoccupational excess lung cancer cases associated with BaP from BCOs was 3,500 (±1,500) from 1982 to 2015. If there was no ban, the cases would be as high as 9,290 (±4,300), indicating the significant health benefits of the Coal Law. On the other hand, if the ban had been fully implemented immediately after the law was enforced in 1996, the cumulative cases would be 1,500 (±620), showing the importance of implementing the law.

Athabasca Oil Sands Petcoke Extract Elicits Biochemical and Transcriptomic Effects in Avian Hepatocytes.

Petroleum coke or "petcoke" is a granular carbonaceous material produced during the upgrading of heavy crude oils, including bitumen. Petcoke dust was recently reported as an environmental contaminant in the Athabasca oil sands region, but the ecotoxicological hazards posed by this complex bitumen-derived material-including those to avian species-have not been characterized. In this study, solvent extracts (x) of delayed and fluid petcoke (xDP and xFP) were prepared and dissolved in dimethyl sulfoxide. A water-accommodated fraction of delayed petcoke (waDP) was also prepared. Graded concentrations of xDP, xFP, and waDP were administered to chicken and double-crested cormorant hepatocytes to determine effects on 7-ethoxyresorufin-O-deethylase (EROD) activity, porphyrin accumulation, and mRNA expression. Polycyclic aromatic compounds (PACs) were characterized, and xDP, xFP, and waDP had total PAC concentrations of 93 000, 270, and 5.3 ng/mL. The rank order of biochemical and transcriptomic responses was xDP > xFP > waDP (e.g., EROD EC50s were lower for xDP compared to xFP and waDP). A total of 22, 18, and 4 genes were altered following exposure to the highest concentrations of xDP, xFP, and waDP, respectively, using a chicken PCR array comprising 27 AhR-related genes. To provide more exhaustive coverage of potential toxicity pathways being impacted, two avian ToxChip PCR arrays-chicken and double-crested cormorant-were utilized, and xDP altered the expression of more genes than xFP. Traditional PAC-related toxicity pathways and novel mechanisms of action were identified in two avian species following petcoke extract exposure. Extrapolation to real-world exposure scenarios must consider the bioavailability of the extracted PACs compared to those in exposed organisms.

Toxicity of aqueous vanadium to zooplankton and phytoplankton species of relevance to the athabasca oil sands region.

Vanadium (V) is an abundant trace metal present in bitumen from the Athabasca Oil Sands (AOS) region in Alberta, Canada. The upgrading of bitumen can result in the production of large volumes of a carbonaceous material referred to as petroleum coke that contains V at elevated levels compared to the native bitumen. Previous studies have shown that coke has the capacity to leach ecotoxicologically relevant levels of V into water it contacts, yet limited data are available on the toxicity of aqueous V to planktonic organisms. Therefore, this study set out to evaluate the acute and chronic toxicity of V (as vanadate oxyanions) to freshwater zooplankton and phytoplankton species that are either commonly-used laboratory species, or species more regionally-representative of northern Alberta. Four cladoceran (2-d and 21-d tests) and two algal (3-d tests) species were exposed to V to obtain both acute and chronic toxicity estimates. Acute V toxicity (LC50s) ranged from 0.60mgV/L for Ceriodaphnia quadrangula to 2.17mgV/L for Daphnia pulex. Chronic toxicity estimates (EC50s) for cladoceran survival and reproduction were nearly identical within species and ranged from a low of 0.13 to a high of 0.46mgV/L for Daphnia dentifera and D. pulex, respectively. The lack of sublethal V toxicity in daphnia suggests a direct mechanism of toxicity through ion imbalance. Growth inhibition (EC50) of green algae occurred at concentrations of 3.24 and 4.12mgV/L for Pseudokirchneriella subcapitata and Scenedesmus quadricauda, respectively. Overall, cladocerans were more sensitive to V than green algae, with survival of the field-collected D. dentifera being approximately 2.5 to 3.5 times more sensitive to acute and chronic V exposure than the standard test species D. pulex. However, there were no significant differences in V toxicity between the field-collected cladocerans Simocephalus serrulatus and C. quadrangula, compared to the respective standard species D. pulex and Ceriodaphnia dubia. Similarly, there were no significant differences in sensitivity to V in the two algal species evaluated. Based on V concentrations reported in laboratory-generated coke leachates, zooplankton survival could be adversely impacted under conditions of chronic leachate exposure if V concentrations in the environment exceed 0.1mg/L. Furthermore, toxicity thresholds from commonly-used planktonic test species would likely have sufficed for derivation of a V water quality guideline (WQG) for protection of local aquatic communities near oil sands operations, but the new data presented here on V toxicity to more regionally-representative species will strengthen the database for WQG derivation.

Effects of coke oven emissions and benzo[a]pyrene on blood pressure and electrocardiogram in coke oven workers.

OBJECTIVE: To evaluate the effects of occupational exposures to coke oven emissions (COEs) and benzo[a]pyrene (B[a]P) on the prevalence of hypertension and abnormal electrocardiogram (ECG) in coke oven workers. METHODS: We included 880 coke oven workers and 710 oxygen employees in the exposed and control groups, respectively. Blood pressure (BP), ECG, blood lipid levels, and glucose levels of all subjects were measured. COE and B[a]P concentrations at the bottom, side, and top of the oven and control plants were estimated by weighing and high-performance liquid chromatography. RESULTS: The COE concentration at the top and side was higher than that at the bottom (P < 0.05). The levels of B[a]P at the top and side significantly exceeded the limit value. Abnormal BP, ECG, the detection ratio of hypertension and left ventricular high voltage were significantly greater in the exposed group than in the control group (P < 0.05). The logistic regression analysis results revealed that age and B[a]P exposure were risk factors for hypertension in coke oven workers (P < 0.05) and both were risk factors for abnormal ECG (P < 0.05). Moreover, B[a]P exposure, age, and gender were risk factors for impaired fasting glucose in coke oven workers (P < 0.05). CONCLUSIONS: B[a]P and COE exposures are risk factors for hypertension and abnormal ECG in coke oven workers.

Health status among urban residents living in proximity to petroleum coke storage: a first examination.

We conducted an in-person survey in neighborhoods in south Chicago to examine whether residence near outdoor petroleum coke storage piles was associated with poorer health status and illness symptoms. A total of 223 adults (≥18) completed the surveys in English or Spanish, including 136 from a neighborhood exposed to the petroleum coke and 87 from a nearby comparison neighborhood. Exposure was defined based on prevailing winds and distance. We conducted a propensity score regression analysis, and found that residents in the exposed neighborhood were significantly more likely to report poor self-rated health, more unhealthy physical and mental health days, more illness symptoms including in particular respiratory and neurological symptoms, and worse perceived environmental conditions. The survey is limited by the small sample and the self-report nature of the data, but provides initial quantitative evidence that residence near outdoor petroleum coke storage piles may pose a public health risk.

A case study of potential human health impacts from petroleum coke transfer facilities.

Petroleum coke or "petcoke" is a solid material created during petroleum refinement and is distributed via transfer facilities that may be located in densely populated areas. The health impacts from petcoke exposure to residents living in proximity to such facilities were evaluated for a petcoke transfer facilities located in Chicago, Illinois. Site-specific, margin of safety (MOS) and margin of exposure (MOE) analyses were conducted using estimated airborne and dermal exposures. The exposure assessment was based on a combined measurement and modeling program that included multiyear on-site air monitoring, air dispersion modeling, and analyses of soil and surfaces in residential areas adjacent to two petcoke transfer facilities located in industrial areas. Airborne particulate matter less than 10 microns (PM10) were used as a marker for petcoke. Based on daily fence line monitoring, the average daily PM10 concentration at the KCBX Terminals measured on-site was 32 µg/m3, with 89% of 24-hr average PM10 concentrations below 50 µg/m3 and 99% below 100 µg/m3. A dispersion model estimated that the emission sources at the KCBX Terminals produced peak PM10 levels attributed to the petcoke facility at the most highly impacted residence of 11 µg/m3 on an annual average basis and 54 µg/m3 on 24-hr average basis. Chemical indicators of petcoke in soil and surface samples collected from residential neighborhoods adjacent to the facilities were equivalent to levels in corresponding samples collected at reference locations elsewhere in Chicago, a finding that is consistent with limited potential for off-site exposure indicated by the fence line monitoring and air dispersion modeling. The MOE based upon dispersion model estimates ranged from 800 to 900 for potential inhalation, the primary route of concern for particulate matter. This indicates a low likelihood of adverse health effects in the surrounding community. Implications: Handling of petroleum coke at bulk material transfer facilities has been identified as a concern for the public health of surrounding populations. The current assessment, based on measurements and modeling of two facilities located in a densely populated urban area, indicates that petcoke transport and accumulation in off-site locations is minimal. In addition, estimated human exposures, if any, are well below levels that could be anticipated to produce adverse health effects in the general population.

Petroleum coke in the urban environment: a review of potential health effects.

Petroleum coke, or petcoke, is a granular coal-like industrial by-product that is separated during the refinement of heavy crude oil. Recently, the processing of material from Canadian oil sands in U.S. refineries has led to the appearance of large petcoke piles adjacent to urban communities in Detroit and Chicago. The purpose of this literature review is to assess what is known about the effects of petcoke exposure on human health. Toxicological studies in animals indicate that dermal or inhalation petcoke exposure does not lead to a significant risk for cancer development or reproductive and developmental effects. However, pulmonary inflammation was observed in long-term inhalation exposure studies. Epidemiological studies in coke oven workers have shown increased risk for cancer and chronic obstructive pulmonary diseases, but these studies are confounded by multiple industrial exposures, most notably to polycyclic aromatic hydrocarbons that are generated during petcoke production. The main threat to urban populations in the vicinity of petcoke piles is most likely fugitive dust emissions in the form of fine particulate matter. More research is required to determine whether petcoke fine particulate matter causes or exacerbates disease, either alone or in conjunction with other environmental contaminants.

Women are more susceptible than men to oxidative stress and chromosome damage caused by polycyclic aromatic hydrocarbons exposure.

Exposure to environmental polycyclic aromatic hydrocarbons (PAHs) has been associated with increased risk of cancer, but evidence for gender differences in this association is limited. The aim of this study was to examine the gender differences in PAHs caused early genotoxic effects such as oxidative stress and chromosome damage, which are potential carcinogenic etiology of PAHs. A total of 478 nonsmoking workers (272 men and 206 women) from a coke oven plant were recruited. We determined 16 environmental PAHs in their workplaces, and measured concentrations of 12 urinary PAH metabolites (OH-PAHs), plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, urinary 8-hydroxydeoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F2α (8-iso-PGF2α), and micronucleus frequencies in lymphocytes in all subjects. It showed that, women working at the office, adjacent to the coke oven, and on the bottom or side of the coke oven displayed significantly higher levels of urinary 8-OHdG and 8-iso-PGF2α, and lymphocytic micronucleus frequencies compared with men working at above areas, respectively (all P < 0.05). These gender differences remain significant after adjusted for potential confounders and urinary ΣOH-PAHs or plasma BPDE-Alb adducts. A significant interaction existed between gender and BPDE-Alb adducts on increasing micronucleus frequencies (Pinteraction < 0.001). We further stratified all workers by the tertiles of urinary ΣOH-PAHs or plasma BPDE-Alb adducts, and the above gender differences were more evident in the median- and high-exposure groups (all P < 0.05). In conclusion, women were more susceptible than men to oxidative stress and chromosome damage induced by PAHs, which may add potential evidence underlying gender differences in PAH exposure-related lung cacinogenesis.

Toxicological assessment of green petroleum coke.

Green petroleum coke is primarily inorganic carbon with some entrained volatile hydrocarbon material. As part of the petroleum industry response to the high production volume challenge program, the potential for reproductive effects was assessed in a subchronic toxicity/reproductive toxicity screening test in rats (OECD 421). The repeated-dose portion of the study provided evidence for dust accumulation and inflammatory responses in rats exposed to 100 and 300 mg/m(3) but there were no effects at 30 mg/m(3). In the reproductive toxicity screen, the frequency of successful matings was reduced in the high exposure group (300 mg/m(3)) and was not significantly different from control values but was outside the historical experience of the laboratory. The postnatal observations (external macroscopic examination, body weight, and survival) did not indicate any treatment-related differences. Additional tests conducted to assess the potential hazards to aquatic (fish, invertebrates, and algae) and soil dwelling organisms (earthworms and vascular plants) showed few effects at the maximum loading rates of 1000 mg coke/L in aquatic studies and 1000 mg coke/kg soil in terrestrial studies. The only statistically significant finding was an inhibition of algal growth measured as either biomass or growth rate.

Estimation of cytogenetic risk among coke oven workers exposed to polycyclic aromatic hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) result from the incomplete combustion of natural or synthetic organic materials. The working environment at a coke plant can negatively affect the employed workers who were exposed to coke oven emissions containing PAHs, which formed and released into the environment by the process of pyrolysis of coke. This study aims to analyze the relationship between the exposure of PAHs and the risk of genetic damages such as chromosomal alteration (CA), micronucleus (MN), and DNA damage (PCR-RFLP) in peripheral blood lymphocytes of 27 coke oven workers and equal number of control subjects. The exposed subjects and controls were divided into two groups based on their age (group I<35 years and group II ≥35 years). The exposed subjects were further classified into two groups based on the exposure period (<12 years and ≥12 years). The frequencies of CA and MN in exposed subjects are relatively high with respect to controls. The XRCC1 399 Arg/gln polymorphism showed a substantial smaller difference in allele frequencies between exposed and control subjects. Based on present data, it was concluded that coke oven workers under risk should be monitored for adverse effects of the any long-term exposure.

The dose-response decrease in heart rate variability: any association with the metabolites of polycyclic aromatic hydrocarbons in coke oven workers?

BACKGROUND: Air pollution has been associated with an increased risk of cardiopulmonary mortality and decreased heart rate variability (HRV). However, it is unclear whether coke oven emissions (COEs) and polycyclic aromatic hydrocarbons (PAHs) are associated with HRV. OBJECTIVES: Our goal in the present study was to investigate the association of exposure to COEs and the urinary metabolite profiles of PAHs with HRV of coke oven workers. METHODS: We measured benzene soluble matter, carbon monoxide, sulfur dioxide, particulate matters, and PAHs at different workplaces of a coke oven plant. We determined 10 urinary PAH metabolites and HRV indices of 1333 workers using gas chromatography-mass spectrometry and a 3-channel digital Holter monitor, respectively. RESULTS: Our results showed that there was a significant COEs-related dose-dependent decrease in HRV, and an inverse relationship between the quartiles of urinary 2-hydroxynaphthalene and five HRV indices (p(trend)<0.01 for all). After adjustment for potential confounders, elevation per interquartile range (IQR) (1.81 µg/mmol creatinine) of urinary 2-hydroxynaphthalene was associated with a 5.46% (95% CI, 2.50-8.32) decrease in standard deviation of NN intervals (SDNN). As workers worked more years, SDNN gradually declined in the same quartiles of 2-hydroxynaphthalene levels (p(trend) = 1.40×10(-4)), especially in workers with the highest levels of 2-hydroxynaphthalene. CONCLUSIONS: Occupational exposure to COEs is associated with a dose-response decrease in HRV. In particular, increased exposure to 2-hydroxynaphthalene is associated with significantly decreased HRV. Increase of working years and exposure levels has resulted in a gradual decline of HRV.

[Using the stable HSPA1A promoter-driven luciferase reporter HepG2 cells to assess the overall toxicity of coke oven emissions].

OBJECTIVE: Using the stable HSPA1A (HSP70-1) promoter-driven luciferase reporter HepG2 cells (HepG2/HSPA1A cells) to assess the overall toxicity of coke oven emissions. METHODS: The stable HepG2/HSPA1A cells were treated with different concentrations of coke oven emissions (COEs) collected from the top, side, and bottom of a coke oven battery for 24 h. After the treatments, luciferase activity, cell viability, malondialdehyde (MDA) concentration, Olive tail moment, and micronuclei frequency were determined, respectively. RESULTS: The bottom COEs induced significant increases (P < 0.01) in relative luciferase activity up to 1.4 times the control level at 0.15 µg/L. The low dose of side COEs (0.02 µg/L) led to a significant increase (P < 0.01) in relative luciferase activity that progressively increased to 2.1 times the control level at 65.4 µg/L. The top COEs produced a strong dose-dependent induction of relative luciferase activity up to over 5 times the control level at the highest concentration tested (202 µg/L). In HepG2/HSPA1A cells treated with the bottom COEs, relative luciferase activity was positively correlated with MDA concentration (r = 0.404, P < 0.05). For the three COEs samples, positive correlations were observed between relative luciferase activity and Olive tail moment and micronuclei frequency. CONCLUSION: The relative luciferase activity in HepG2/HSPA1A cells can sensitively reflect the overall toxicity of COEs. The stable HepG2/HSPA1A cells can be used for rapid screening of the overall toxicity of complex air pollutants in the workplace.

Influence of inorganic anions on metals release from oil sands coke and on toxicity of nickel and vanadium to Ceriodaphnia dubia.

In a previous study it was shown that pH significantly influences the release of metals from oil sands coke, particularly Ni and V which were identified as the cause of coke leachate toxicity. Coke comes in contact with oil sands process water (OSPW) during its transport to and long term storage in reclamation landscapes. However, the influence of dominant inorganic anions present in OSPW (i.e. HCO(3)(-), Cl(-) and SO(4)(2-)) on metals release from coke and on speciation and toxicity of Ni and V, has not been characterized before. Coke was subjected to a 15-d batch leaching process at four levels of HCO(3)(-), Cl(-) and SO(4)(2-) to determine the influence on metals release and speciation. Further, the effects of each of the three anions on Ni and V toxicity, as well as the mixture toxicity of Ni and V, were assessed using the three-brood Ceriodaphnia dubia test. Inorganic anions had a significant influence on the type and amount of metals released from coke. Specifically, sulfate increased the mobilization of cationic metals (e.g. Ni, Fe, Mn and Zn), whereas bicarbonate enhanced the release of oxyanion forming metals (e.g. Al, As, Mo and V) from coke. Chloride had no particular effect on the type and amount of metals released. With respect to toxicity, elevated bicarbonate levels decreased the 7-d Ni IC50 from 6.3 to 2.3 µg L(-1), whereas sulfate showed an ameliorative effect against V toxicity to C. dubia. In combination, Ni and V acted additively at their highest sub-lethal concentrations. Aqueous chemistry and toxicity of Ni and V are discussed with the goal of informing reclamation efforts at the Athabasca oil sands.