Coke Oven Emissions Research Articles

Genetic damage induced by organic extract of coke oven emissions on human bronchial epithelial cells

Coke oven emissions are known as human carcinogen, which is a complex mixture of polycyclic aromatic hydrocarbon. In this study, we aimed to clarify the mechanism of action of coke oven emissions induced carcinogenesis and to identify biomarkers of early biological effects in a human bronchial epithelial cell line with CYP1A1 activity (HBE-CYP1A1). Particulate matter was collected in the oven area on glass filter, extracted and analyzed by GC/MS. DNA breaks and oxidative damage were evaluated by alkaline and endonucleases (FPG, hOGG1 and ENDO III)-modified comet assays. Cytotoxicity and chromosomal damage were assessed by the cytokinesis-block micronucleus cytome (CBMN-Cyt) assay. The cells were treated with organic extract of coke oven emissions (OE-COE) representing 5, 10, 20, 40μg/mL extract for 24h. We found that there was a dose–effect relationship between the OE-COE and the direct DNA damage presented by tail length, tail intensity and Olive tail moment in the comet assay. The presence of lesion-specific endonucleases in the assays increased DNA migration after OE-COE treatment when compared to those without enzymes, which indicated that OE-COE produced oxidative damage at the level of pyrimidine and purine bases. The dose-dependent increase of micronuclei, nucleoplasmic bridges and nuclear buds in exposed cells was significant, indicating chromosomal and genomic damage induced by OE-COE. Based on the cytotoxic biomarkers in CBMN-Cyt assay, OE-COE may inhibit nuclear division, interfere with apoptosis, or induce cell necrosis. This study indicates that OE-COE exposure can induce DNA breaks/oxidative damage and genomic instability in HBE-CYP1A1 cells. The FPG-comet assay appears more specific for detecting oxidative DNA damage induced by complex mixtures of genotoxic substances.

Development of stable HSPA1A promoter-driven luciferase reporter HepG2 cells for assessing the toxicity of organic pollutants present in air

HSPA1A (HSP70-1) is a highly inducible heat shock gene up-regulated in response to environmental stresses and pollutants. The aim of our study was to evaluate the sensitivity of the stable metabolically competent HepG2 cells containing a human HSPA1A promoter-driven luciferase reporter (HepG2-luciferase cells) for assessing the toxicity of organic pollutants present in air. The HepG2-luciferase cells were validated by heat shock treatment and testing three organic compounds (pyrene, benzo[a]pyrene, and formaldehyde) that are ubiquitous in the air. The maximal level of HSPA1A (HSP70-1) and relative luciferase activity induced by heat shock were over three and nine times the control level, respectively. Pyrene, benzo[a]pyrene, and formaldehyde all induced significantly elevated levels of relative luciferase activity in a dose-dependent manner. Extractable organic matter (EOM) from urban traffic and coke oven emissions in ambient air were tested on the HepG2-luciferase cells. The traffic EOM induced significant increase in relative luciferase activity at concentrations of picogram per liter. The coke oven EOM produced a strong dose-dependent induction of relative luciferase activity up to six times the control value. Significant increases in relative luciferase activity were observed at concentrations that were as low, or lower than the concentrations that the tested organic pollutants decreased cell viability, and increased malondialdehyde concentration, Olive tail moment, and micronuclei frequency. Therefore, we conclude that the HepG2-luciferase cells are a valuable tool for rapid screening of the overall toxicity of organic pollutants present in air.

Determination of urinary malondialdehyde by isotope dilution LC-MS/MS with automated solid-phase extraction: A cautionary note on derivatization optimization

A highly sensitive quantitative LC-MS/MS method was developed for measuring urinary malondialdehyde (MDA). With the use of an isotope internal standard and online solid-phase extraction, urine samples can be directly analyzed within 10min after 2,4-dinitrophenylhydrazine (DNPH) derivatization. The detection limit was estimated as 0.08pmol. This method was further applied to assess the optimal addition of DNPH for derivatization and to measure urinary MDA in 80 coke oven emission (COE)-exposed and 67 nonexposed workers. Derivatization optimization revealed that to achieve complete derivatization reaction, an excess of DNPH is required (DNPH/MDA molar ratio: 893–8929) for urine samples that is about 100 times higher than that of MDA standard solutions (molar ratio: 10–80). Meanwhile, the mean urinary concentrations of MDA in COE-exposed workers were significantly higher than those in nonexposed workers (0.23±0.17 vs 0.14±0.05μmol/mmol creatinine, P<0.005). Urinary MDA concentrations were also significantly associated with the COE (P<0.005) and smoking exposure (P<0.05). Taken together, this method is capable of routine high-throughput analysis and accurate quantification of MDA and would be useful for assessing the whole-body burden of oxidative stress. Our findings, however, raise the issue that derivatization optimization should be performed before it is put into routine biological analysis.

Repeated measurements for assessment of urinary 2-naphthol levels in individuals exposed to polycyclic aromatic hydrocarbons

A repeated measurement cohort study was conducted to determine whether 2-napthol can be a suitable biomarker for evaluating the magnitude of exposure to PAHs from coke oven emissions. Time-course patterns of urinary 2-naphthol levels in coke-oven workers were examined. Also, the correlation between urinary 2-naphthol levels and PAHs from personal breathing zone samples was analyzed while examining and adjusting possible confounding factors, such as smoking alcohol consumption, and age of human subjects. A total of 8 spot urine samples were collected from each high-exposure group (topside-oven workers, n = 17) and low-exposure group (side-oven workers, n = 25) during the whole working cycle, which consists of six consecutive working days followed by 2 days off. Personal breathing zone samples were collected to quantify PAH intake. A questionnaire was distributed and collected from each worker for assessment of demographic parameters. Our results confirmed that the topside-oven area contained significantly higher PAH levels than the side-oven area. Urinary 2-naphthol levels correlated with the levels of PAH species, including pyrene, benzo[k]fluoranthene, benezo[g,h,i]pyrene, naphthalene, phenanthrene, anthracene, indeno[1,2,3-cd]pyrene, benzo[k]fluoranthene, and total PAHs. During the working cycle, urinary 2-naphthol levels remained stable at around 46–97 ng/mg creatinine during the working days and dramatically increased during the off days. After stratification of data based on smoking status, smokers had significantly higher urinary 2-naphthol levels than non-smokers, and 2-naphthol levels positively correlated with smoking status. Coke-oven emissions are a source of exposure to naphthalene. Also, smoking is a significant source of exposure to naphthalene and served as a confounder factor. Due to its abundance, positive association with total PAHs and certain carcinogenic PAH compounds, and slower elimination kinetics, urinary 2-naphthol may have the potential to serve as a biomarker for PAH exposure, when smoking status is carefully adjusted.

Pollution Portrait: The Fourth National-Scale Air Toxics Assessment

Taken at face value, the results of the fourth edition of the U.S. Environmental Protection Agency’s (EPA) National-Scale Air Toxics Assessment (NATA), released 11 March 2011 are sobering.1 Every person in the country is at 10 times or greater risk for getting cancer from outdoor air pollutants than the agency’s general goal of 1 in 1 million,2 the average risk is 50 times greater than the goal, and about 5% of the population is at more than 100 times the risk. Almost one-quarter of the population is at increased risk for certain noncancer health effects, primarily respiratory effects. A closer look reveals the risks might be substantially lower, however. These estimates are based on 2005 emissions, and the EPA says numerous regulations approved and implemented since then have significantly reduced some emissions. The agency also notes that the total cancer toll exacted by the toxics tracked in NATA is very small compared with the risk posed by other known factors. Those combine to create a total risk of 336,000 in 1 million (based on the number of actual cancer cases), with the bulk of the risk widely attributed to lifestyle factors such as tobacco use, diet, lack of exercise, certain types of infections, and radiation.3 For additional context, the EPA says radon, which isn’t among the Clean Air Act toxics assessed for NATA, poses a cancer risk of about 2,000 in 1 million. But Mary Sullivan Douglas, a senior staff associate with the National Association of Clean Air Agencies, cautions that NATA remains incomplete. “There’s a lot that’s not known about the emissions and effects of toxic air pollutants,” she says. “Things could look much worse if we had all the data. We think hazardous air pollutants are very dangerous and need to be addressed, especially for some of the small sources that together form a large part of the NATA inventory.”

Hypermethylation of O(6)-methylguanine-DNA methyltransferase in human bronchial epithelial cell induced by organic extracts of coke oven emissions

To elucidate the mechanism of carcinogenesis induced by coke oven emissions by investigating the cell genetic damage index and the methylation of O⁶-methylguanine-DNA methyltransferase (MGMT). The human bronchial epithelial cell 16HBE was treated by 1 µmol/L B(a)P for 48 h, and then was exposed continuously to either 1‰ dimethyl sulfoxide (DMSO) or organic extracts of coke oven emission (OE-COE) for five days at the concentrations of 0, 2.5, 5.0, 10.0 and 20.0 µg/ml. The methylation-specific PCR (MSP-PCR), RT-PCR and immunoblotting were applied to detect the methylation status, changes of mRNA and protein of MGMT, respectively. Single cell gel electrophoresis was used to detect DNA damage induced by OE-COE. Compared with the control group (DMSO), there was a significant hypermethylation in all study groups, along with the suppression of mRNA and protein in a dose-dependent manner, and the gradation ratio of them was 1.0, 0.96, 0.96, 0.85, 0.32 and 1.0, 1.0, 1.1, 0.41, 0.52, separately. There was a significant DNA damage with a dose-effect relationship in all study groups (F = 41.22, P < 0.05), and the comet Olive tail moment was (2.98 ± 1.43), (4.76 ± 1.79), (10.09 ± 1.75), (11.38 ± 1.77), (11.67 ± 1.88). The further study found that the index of DNA damage was negatively correlated to the expression of MGMT mRNA and its protein. The DNA damage induced by COE might be associated with the suppression of MGMT caused by its hypermethylation.

Atmospheric concentrations, sources and gas-particle partitioning of PAHs in Beijing after the 29th Olympic Games

A comprehensive sampling campaign was carried out to study atmospheric concentration of polycyclic aromatic hydrocarbons (PAHs) in Beijing and to evaluate the effectiveness of source control strategies in reducing PAHs pollution after the 29th Olympic Games. The sub-cooled liquid vapor pressure ( log P L o ) -based model and octanol-air partition coefficient ( K oa)-based model were applied based on each seasonal dateset. Regression analysis among log K P, log P L o and log K oa exhibited high significant correlations for four seasons. Source factors were identified by principle component analysis and contributions were further estimated by multiple linear regression. Pyrogenic sources and coke oven emission were identified as major sources for both the non-heating and heating seasons. As compared with literatures, the mean PAH concentrations before and after the 29th Olympic Games were reduced by more than 60%, indicating that the source control measures were effective for reducing PAHs pollution in Beijing.

Concentrations and sources of polycyclic aromatic hydrocarbons in topsoil of Benxi City, Northeast China

Polycyclic aromatic hydrocarbons (PAHs) contamination of topsoil in Benxi City, Northeast China was investigated in this study, and sampling sites were located in industrial area and residential area. Results demonstrate that there is high variability in the total PAHs concentrations, ranging from 783.00 ng/g to 729 076.29 ng/g dry weight in the topsoil of Benxi City and the pollution in industrial area is the most serious. The results also present that higher molecular weight PAHs (4–6 rings) contribute substantially (79.03%) to the overall content of PAHs. The PAHs sources were determined with factor analysis by nonnegative constraints, and the results show that PAHs originating from traffic tunnel, power plant, coke oven and residential emission sources, account for 27.10%, 40.81%, 20.11% and 11.98%, respectively, of the total. The PAHs pollution is the most serious around Benxi Iron and Steel Group Corporation, and the PAHs mainly originate from coke oven and traffic tunnel, with the average contribution rate of 57.40% and 42.60%, respectively. The source apportionment results are basically consistent with the industry distribution, and the geographical and climatic characteristics of the study area.

Estimation of emissions of SO2, PM2.5, and metals released from coke ovens using high sulfur coals

AbstractCoal combustion processes have inherent characteristics that lead to the release of both gaseous and particulate matter in the atmosphere that have primary and secondary impact on air quality, human health, and climate. Coals from Northeastern region of India have high sulfur, low ash, and high volatile matter. In the present investigation, sulfur, metals and ash contents of feed coals were considered for making an emission inventory for these coals. For the calculation of emission factors of SO2 and metals, mass balance method was used, while for PM2.5, measured values near the coke ovens were taken. The emission factors and emission rates of SO2 for coke ovens ranged between 0.80 to 4.8 Kg/t and 204 to 1226 t/yr respectively. The emission factors for PM2.5, total carbon (TC), black carbon (BC) and organic carbon (OC) varied between 0.7 to 3 Kg/t, 0.48 to 2.1 Kg/t, 0.007 to 0.03 Kg/t and 0.47 to 2.1 Kg/t, respectively. Total emissions for PM2.5, TC, BC and OC ranged between 72–306 t/yr, 49–217 t/yr, 0.71–2.9 t/yr and 48–214 t/yr, respectively. Emission rates of metals (V, Cr, Mn, Co, Ni, Cu, Zn, As, Se, Mo, Cd, Sn, Te, Hg, Pb, and Bi) showed dependency on the volatility of the metals, condition of coke ovens (reductive) and rank of coal. Present investigation provides preliminary information on source profile of coke oven emissions (SO2, PM2.5 and trace metals) which is useful for assessing the impact of coke oven on ambient air quality, source apportionment study in the area and for designing the coke ovens to regulate the emissions. © 2010 American Institute of Chemical Engineers Environ Prog, 2011

Evaluating the national air toxics assessment (NATA): Comparison of predicted and measured air toxics concentrations, risks, and sources in Pittsburgh, Pennsylvania

Abstract The National Air Toxics Assessment (NATA) is an ongoing modeling effort by the Environmental Protection Agency to predict air toxics concentrations, sources, and risks at the census tract level throughout the continental United States. To evaluate NATA, archived data collected at seven sites in and around Pittsburgh, Pennsylvania were compared to 2002 NATA predictions. The sites represent 3 different source regimes (mobile dominated, industrial point source dominated, and background). The evaluation considered 49 air toxics (37 gas-phase organics, 10 metals, coke oven emissions and diesel particulate matter); NATA’s performance was judged based on model-measurement comparisons of concentrations, health risks, and source contributions. On a concentration basis, NATA performance varied widely ranging from excellent for carbon tetrachloride to differences of more than a factor of 100 for low concentration chlorinated compounds. However, predicted concentrations were generally within a factor of 2 of measured values for air toxics that were estimated to be the primary cancer risk drivers; therefore NATA provided reasonable estimates of the additive cancer risks and risk ranking of air toxics. NATA performs better on average in Pittsburgh than nationwide. Comparison of source apportionment results indicates that NATA consistently underestimated concentrations of compounds emitted by large point sources as well as concentrations of chlorinated compounds, but overestimated the risks from mobile sources in Pittsburgh. Therefore, in Pittsburgh, NATA sufficiently prioritizes air toxics that drive potential cancer risks, but does not identify the sources of these priority air toxics.

Spatial Variation in Ambient Air Toxics Concentrations and Health Risks between Industrial-Influenced, Urban, and Rural Sites

Concentrations of 38 gas-phase organic air toxics were measured over a 2-yr period at four different sites in and around Pittsburgh, PA, to investigate spatial variations in health risks from chronic exposure. The sites were chosen to represent different exposure regimes: a downtown site with substantial mobile source emissions; two residential sites adjacent to one of the most heavily industrialized zones in Pittsburgh; and a regional background site. Lifetime cancer risks and non-cancer hazard quotients were estimated using a traditional and interactive risk models. Although study average concentrations of specific air toxics varied by as a much as a factor of 26 between the sites, the additive cancer risks of the gas-phase organic air toxics varied by less than a factor of 2, ranging from 6.1 × 10-5 to 9.5 × 10-5. The modest variation in risks reflects the fact that two regionally distributed toxics, formalde-hyde and carbon tetrachloride (CCl4), contributed more than half of the cancer risk at all four sites. Benzene contributed substantial cancer risks at all sites, whereas trichloroethene and 1,4-dichlorobenzene only contributed substantial cancer risks at the downtown site. Only acrolein posed a non-cancer risk. Diesel particulate matter is estimated to pose a much greater cancer risk in Pittsburgh than other classes of air toxics including gas-phase organic, metals, polycyclic aromatic hydrocarbons, and coke oven emissions. Health risks of air toxics in Pittsburgh are comparable with those in other urban areas in the United States.

A comparative study of two factor analytic models applied to PAH data from inhalable air particulate collected in an urban-industrial environment

Two factor analysis (FA)-based receptor modeling methods were applied to a polycyclic aromatic hydrocarbon (PAH) dataset from extracts of 75 PM(10) air particulate samples collected concurrently at 4 sampling sites proximate to the urban-industrial area in Hamilton, Ontario, Canada. The total PAH concentrations of 48 target compounds ranged from 0.23 to 172 ng m(-3). Principal component analysis (PCA) and positive matrix factorization (PMF) analysis were followed by multilinear regression analyses to identify and quantify PAH source contributions, together with spatial and temporal trends. The correlations between predicted and observed total PAH levels were excellent in both models (R(2) > 0.98). The PCA afforded large negative contributions in a number of samples, so further analysis was abandoned. The PMF analysis showed 3 factors which were identified as gasoline emissions, diesel emissions and coke oven emissions. Contributions of gasoline emissions and diesel emissions factors were surprisingly similar at all 4 sites indicative of a background of vehicle emissions across the city. The PMF coke oven emission factor showed the greatest variability in total loadings, consistent with the large PAH emissions from the steel industries and the large influence of wind direction on PAH concentrations. The highest coke oven contributions were observed at sites closest to the industrial area on days when these sites were downwind of the industries. The PMF coke oven impact factor showed good correlations with two commonly used PAH diagnostic ratios when the ratios were combined into a single ratio. This integrated approach allowed us to categorize >90% of the samples based on the wind direction of the impacting source.

Occupational coke oven emissions exposure and risk of abnormal liver function: modifications of body mass index and hepatitis virus infection

ObjectivesOccupational coke oven emissions (COEs) have been considered an important health issue. However, there are no conclusive data on human hepatic injury due to COE exposure. The association of COE...

Probabilistic Ecological Risk Assessment and Source Apportionment of Polycyclic Aromatic Hydrocarbons in Surface Sediments from Yellow Sea

Based on the concentrations of polycyclic aromatic hydrocarbons (PAHs) in 12 surface sediment samples from Yellow sea, the relative risk of 9 PAHs was investigated using joint risk probability distribution curves and overlapping area, which were generated based on the distributions of exposure and acute toxicity data (LC(50)), and the sources of PAHs were apportioned using principal component analysis. It was found that joint probability curve and overlapping area indicated the acceptable ecological risk of individual PAHs, only a small fraction of the benthic organisms was affected. Among the nine PAHs studied, the overall risk of pyrene was the highest, with that of naphthalene the lowest. For lower exposure levels at which the percentage of species affected was less than 10%, the risk associated with phenanthrene and fluorene were clearly higher than that of the other seven PAHs. It was indicated that PAHs in surface sediments mainly originated from vehicular emissions, coal combustion sources, coke oven emission and wood combustion, petroleum origin made little influence on sources of PAHs by PCA.

Correlations and co-localizations of Hsp70 with XPA, XPG in human bronchial epithelia cells exposed to benzo[a]pyrene

Benzo[a]pyrene (BaP) is a ubiquitously distributed environmental pollutant known to cause DNA damage, which may be repaired through nucleotide excision repair (NER). The significantly negative correlation between Hsp70 levels and the level of DNA damage in workers exposed to coke oven emission had been found. However, little is known about how Hsp70 modulate the DNA repair process. In a series of experiments using the human bronchial epithelia cells (16HBE) exposed to different concentrations of BaP for 24 h, we measured expression of NER subunit xeroderma pigmentosum (XP) group A, C, F, G (XPA, XPC, XPF, XPG), excision repair cross-complementing 1 (ERCC1) and Hsp70, and analyzed their possible correlations. Co-localizations of Hsp70 with NER subunit were detected by confocal microscope. We found that in vitro exposure to BaP reduced cell viability in a dose-dependent manner ranging from 2 to 64 μM. Our results showed that levels of XPA, XPG and Hsp70 significantly increased at cells exposed to 1 or 2 μM BaP. In addition, curve estimation showed there was a significant correlation between relative ratios of Hsp70 and XPA, XPG in cells exposed to different concentrations of BaP. Moreover, confocal microscopy demonstrated increased co-localization of Hsp70 with XPA, XPG in nuclei of cells exposed to BaP. These results suggested that Hsp70 might play a role in nucleotide excision repair. However, the mechanisms underlying this observation need further investigation.

Repeated Measurements of Urinary Methylated/Oxidative DNA Lesions, Acute Toxicity, and Mutagenicity in Coke Oven Workers

We conducted a repeated-measures cohort study of coke oven workers to evaluate the relationships between the traditional exposure biomarker, urinary 1-hydroxypyrene (1-OHP), and a series of biomarkers, including urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), N7-methylguanine (N7-MeG), acute toxicity, and mutagenicity. A total of eight spot urine samples were collected from each high-exposed (at topside oven area) and low-exposed workers (at side oven area) during the whole working cycle, which consisted of 6 consecutive days of working followed by 2 days off. Our results showed that the high-exposed workers had significantly higher urinary levels of 1-OHP, 8-oxodG, and N7-MeG compared with the low-exposed workers. Acute toxicity and mutagenicity of urine were also found to be markedly increased in the high-exposed workers, as determined by Microtox assay and Ames test, respectively. Multivariate regressions analysis revealed that the urinary 8-oxodG, N7-MeG, or acute toxicity was significantly correlated with 1-OHP concentrations. Overall, the present study showed that exposure to coke oven emissions increased oxidatively damaged DNA products and mutagenicity of urine, and for the very first time, such exposure was also found to increase DNA methylation and urinary acute toxicity. The potential source of methylating agents in coke oven emissions warrants further investigation. Additionally, with repeated measurements, the pattern of time course for urinary 1-OHP was found to be different from those of 8-oxodG and N7-MeG, as well as acute toxicity and mutagenicity. This finding implies that the single measurement that was often conducted in occupational healthy investigations should be used with certain precautions, because single measurement may fail to provide the proper information of interest.

Characterisation of volatile organic compounds and polycyclic aromatic hydrocarbons in the ambient air of steelworks

Investigations have been undertaken at two integrated steelworks in the UK to characterise airborne organic micro-pollutants and to assess the contribution of iron ore sintering and coke making operations on the air quality. Concentrations of volatile organic compounds (VOCs), namely benzene, toluene and p-xylene, were measured continuously within the boundary of a coking plant using for the first time differential optical absorption spectrometry (DOAS) between 2004 and 2006. Concentrations were obtained along two monitoring paths surrounding the coke plant and the average benzene concentration measured along both paths over the campaign was 28 μg m −3. Highest benzene concentrations were associated with winds downwind of the coke oven batteries. Concentrations of polycyclic aromatic hydrocarbons (PAHs) in ambient air were measured during 27 consecutive days in 2005 at three different locations on an integrated steelworks. PAH profiles were determined for each sampling point and compared to coke oven and sinter plant emission profiles showing an impact from the steelworks. The mean benzo [ a] pyrene concentration determined in the immediate vicinity of the coke ovens downwind from the battery was 19 ng m −3, whereas for the two other sites average benzo [ a] pyrene concentrations were much lower (around 1 ng m −3). Data were analysed using principal components analysis (PCA) and results showed that coke making and iron ore sintering were responsible for most of the variation in the PAH concentrations in the vicinity of the investigated plant.

Characterization and sources of PAHs in an urban river system in Beijing, China

Water samples from 20 locations on rivers in the Tongzhou District of Beijing were collected four times from July 2005 to March 2006. In addition, sediment samples were collected in July 2005. All samples were analyzed for 16 US Environmental Protection Agency (EPA) priority pollutants polycyclic aromatic hydrocarbons (PAHs). The concentration, distribution, seasonal variation, and sources of the 16 PAH compounds identified in the water samples, suspended particles, and surface sediments were then evaluated. The concentrations of PAHs in the water and suspended particle and surface sediment samples ranged from 87.3 to 1,890 ng l(-1), 1,330 to 27,700 ng g(-1), and 156 to 8,650 ng g(-1), respectively. These results demonstrated that rivers in the Tongzhou District of Beijing had a high level of PAH pollution, especially in the suspended particles. The highest and lowest concentrations of PAHs in the water samples were observed in summer and spring. However, the seasonal variations in the concentration of PAHs in the suspended particles were more complicated. The dominant compounds in the water, suspended particle, and surface sediment samples were two-, three- and four-ring PAH compounds, respectively. Ratio analysis illustrated that fuel-burning was the primary source of PAHs in the study area. Gasoline, diesel, coal, and coke oven sources were identified and the contributions of the different fuel-burning sources were then calculated using factor analysis and multiple linear regression. These analyses revealed that coal combustion, gasoline combustion plus coke oven emission, and diesel combustion accounted for 38.8%, 38.5%, and 22.7% of the PAHs in suspended particles, respectively.

Association of Aryl Hydrocarbon Receptor Gene Polymorphisms and Urinary 1-Hydroxypyrene in Polycyclic Aromatic Hydrocarbon–Exposed Workers

Polycyclic aromatic hydrocarbons (PAH) in coke oven emissions could cause lung cancer in human. Individual's genotype of the metabolic enzymes and early biological changes were known to be associated with the susceptibility of cancer development. Knowledge of metabolic gene polymorphisms, which affect on the urinary 1-hydroxypyrene (1-OHP), could benefit us in understanding the interindividual difference in the mechanism of PAH-induced carcinogenesis. In this study, we investigated the association of aryl hydrocarbon receptor (AhR) gene polymorphisms and urinary 1-OHP. One hundred forty-seven workers exposed to PAH and 69 nonexposure workers were recruited. Seven tagging single nucleotide polymorphisms in AhR gene were selected by pariwise r(2) method and minor allele frequency cutoff of 0.05 from Chinese genotype data in HapMap project. These seven tagging single nucleotide polymorphisms were genotyped by PCR-based methods. Multivariate analysis of covariance revealed that the levels of 1-OHP in PAH-exposed workers carrying genotype CT were lower than workers carrying wild genotype TT at loci rs10250822 and rs2282885 of AhR gene (P = 0.032 and 0.044, respectively). In PAH-exposed workers, the urinary 1-OHP levels showed a linear correlation (P(trend) = 0.041) with the genotypes at locus rs2282885, especially in low and moderate exposure groups. In contrast, no significant association was found between urinary 1-OHP level and AhR genotypes among nonexposed workers. Our findings indicated that polymorphisms of AhR gene were associated with the level of 1-OHP among PAH-exposed workers, suggesting that AhR-mediated signaling might contribute to individual susceptibility to PAH exposure.

Mutagen sensitivity in peripheral blood lymphocytes among coke-oven workers

To investigate the sensitivity to bleomycin (BLM) in peripheral blood lymphocytes (PBL) among coke-oven workers. Ninty-four coke-oven workers with exposure to a high level of polycyclic aromatic hydrocarbons and 64 non-coke-oven workers (control) were recruited into this study. PBL was challenged by 8 microg/ml BLM, a known carcinogen, to induce certain amount of DNA damage, the difference of olive tail moment (TM) measured by comet assay before and after BLM treatment reflected the sensitivity towards mutagens. The distribution of age, sex, and prevalence of smoking and drinking were not significantly different between these two groups. The geometric mean of urinary 1-hydroxypyrene (1-OHP) was significantly higher in coke-oven workers than in controls (9.0 versus 1.5 microg/L, t = -9.317, P < 0.01). The coke-oven workers showed significantly higher sensitivity to BLM than controls (17.7 versus 14.9, t = -2.583, P = 0.01). A large inter-group difference in sensitivity to BLM was observed in both controls and coke-oven workers. Stratification analysis revealed the significant association between high 1-OHP level (> 9.0 microg/L) and increased sensitivity to BLM (F = 4.001, P = 0.05) among coke-oven workers. Smoking subjects showed a significant higher value of sensitivity than nonsmokers in controls but not in coke-oven workers. No significant difference was observed between age, drinking status, coking history or external exposure class and BLM sensitivity. Exposure to coke oven emission could increase the sensitivity to mutagens, which might be a reason of high incidence of lung cancer among coke-oven workers.