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.

Although association between polycyclic aromatic hydrocarbons (PAHs) exposure and mitochondrial DNA copy number (mtDNAcn) was researched by traditional linear model extensively, most of these studies analyzed independent effect of each PAHs metabolite and adjust for the confounding other metabolites concomitantly, without considering others interactions. As a complex organic pollutant, a reasonable statistical method is needed to study toxic effects of PAHs.Therefore, we aimed to conduct a novel statistical approach, Bayesian Kernel Machine Regression (BKMR), to explore the effect of PAHs exposure on mtDNAcn among coke oven workers. In this cross-sectional study, the concentrations urinary of PAHs metabolites were measured using high performance liquid chromatography mass spectrometry (HPLC-MS). The mtDNAcn was measured using real-time quantitative polymerase chain reaction (RT-PCR) in peripheral blood of 696 Chinese coke oven workers. The relationship of urinary of PAHs metabolites and mtDNAcn were evaluated by BKMR model. And the results showed a significant negative effect of PAHs metabolites on mtDNAcn when PAHs metabolites concentrations were all above 35th percentile compared to the median and the statistically significant negative single-exposure effect of 2-OHNAP and 2-OHPHE on mtDNAcn when all of the other PAHs are fixed at a particular threshold (25th, 50th, 75th percentile). The changes in log 2-OHNAP and 2-OHPHE from the 25th to the 75th percentile when other PAHs metabolites were at the 50th percentile were associated with change in mtDNAcn of −0.082 (−0.021, −0.124) and −0.048 (−0.021, −0.090) respectively. And evidence of a linear effect of urinary 2-OHNAP and 2-OHPHE were found. Finally, our findings suggested that PAHs cumulative exposures and particularly single-exposure of 2-OHNAP and 2-OHPHE might compromise mitochondrial function by decreasing mtDNAcn in Chinese coke oven workers.

Telomeres are located at the end of eukaryotic chromosomes and vulnerable to exogenous chemical compounds. Exposure to coke oven emissions (COEs) leads to a dose-related telomere damage, and such chromosomal damage might trigger the cGAS/STING signaling pathway which plays an important role in immune surveillance. However, the relationship between the genetic variations in the cGAS/STING signaling pathway and telomere damage in the COEs-exposure workers has not been investigated. Therefore, we recruited 544 coke oven workers and 238 healthy control participants, and determined the level of COEs exposure, concentration of urinary 1-hydroxypyrene (1-OHPYR), genetic polymorphisms and telomere length. The results showed that the telomere length significantly decreased from the control-to high-exposure groups as defined by the external exposure level (P < 0.05). The results also indicated that STING rs7447927 CC, cGAS rs34413328 AA, and cGAS rs610913 AA could inhibit telomere shortening in the exposure group (P < 0.05), and cGAS rs34413328, urine 1-OHPYR and cumulative exposure dose (CED) had a significant association with telomere length by generalized linear model. In conclusion, telomere shortening was a combined consequence of short-term exposure, long-term exposure, and genetic variations among the COEs-exposure workers.

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.

Coke oven emissions (COEs) are common particle pollutants in occupational environment and the major constituents of COEs are polycyclic aromatic hydrocarbons (PAHs). Previously, we identified aberrant methylation of the fms related tyrosine kinase 1 (FLT1) gene over the course of benzo(a)pyrene (BaP)-induced cell transformation via genome-wide methylation array. To quantify FLT1 methylation, we established a bisulfite pyrosequencing assay and examined the FLT1 hypermethylation in several human cancers. The results revealed that 70.0% (21/30 pairs) of lung cancers harbored hypermethylated FLT1 and concomitant suppression of gene expression compared to the adjacent tissues. This implies that FLT1 hypermethylation might play a role in malignant cell transformation. In addition, FLT1 hypermethylation and gene suppression appeared in primary human lymphocytes in a dose-response manner following COEs treatment. To explore whether FLT1 methylation is correlated with COEs exposure and DNA damage, we recruited 144 male subjects who had been exposed to high levels of COEs and 84 male control subjects. Notably, the FLT1 methylation in peripheral blood lymphocytes (PBLCs) of the COEs-exposed group (19.8 ± 3.2%) was enhanced by 17.9% compared to that of the control group (16.8 ± 2.8%) (P < 0.001). The FLT1 methylation status was positively correlated with urinary 1-hydroxypyrene (1-OHP) levels, an internal exposure marker of PAHs (β = 0.029, 95% CI = 0.010–0.048, P = 0.003) and positively correlated with DNA damage (βOTM = 0.024, 95% CI = 0.007–0.040, P = 0.005; βTₐᵢₗ DNA = 0.035, 95% CI = 0.0017–0.054, P < 0.001) indicated by comet assay. Taken together, these findings indicate that FLT1 might be a tumor suppressor, and its hypermethylation might contribute to PAHs-induced carcinogenicity.

In urbanized regions with expansive impervious surfaces and often low vegetation cover, air pollution due to motor vehicles and other combustion sources, is a problem. The poor air quality days in Montreal, Quebec are mainly due to fine particulate matter and ozone. Businesses using wood ovens are a source of particulates. Careful vegetation selection and increased green roof usage can improve air quality. This paper reviews different green roofs and the capability of plants in particulate matter (PM), ozone (O3) as well as nitrogen dioxide (NO2) level reductions. Both the recommended green roof category and plants to reduce these pollutants in Montreal's zone 5 hardiness region are provided. Green roofs with larger vegetation including shrubs and trees, or intensive green roofs, remove air pollutants to a greater extent and are advisable to implement on existing, retrofitted or new buildings. PM is most effectively captured by pines. The small Pinus strobus ‘Nana’, Pinus mugho var. pumilio, Pinus mugho ‘Slowmound’ and Pinus pumila ‘Dwarf Blue’ are good candidates for intensive green roofs. Drought tolerant, deciduous broadleaved trees with low biogenic volatile organic compound emissions including Japanese Maple or Acer palmatum ‘Shaina’ and ‘Mikawa-Yatsubusa’ are options to reduce O3 levels. Magnolias are tolerant to NO2 and it is important in their metabolic pathways. The small cold-tolerant Magnolia ‘Genie’ is a good option to remove NO2 in urban settings and to indirectly reduce O3 formation. Given the emissions by Montreal businesses' wood ovens, calculations performed based on their respective complex roof areas obtained via Google Earth Pro indicates 88% Pinus mugho var. pumilio roof coverage can annually remove 92.37 kg of PM10 of which 35.10 kg is PM2.5. The removal rates are 4.00 g/m2 and 1.52 g/m2 for PM10 and PM2.5, respectively. This paper provides insight to addressing air pollution through urban rooftop greening.

Polycyclic aromatic hydrocarbons (PAHs) are the main contaminants of coke oven emissions which can induce serious genetic damage in coke oven workers. Epigenetic alternations play essential roles in the regulation of DNA damage effect of PAHs. Previous studies indicate that H3K79 di-methylation (H3K79me2) is integral in DNA damage repair. However, the potential role of H3K79me2 in DNA damage response (DDR) following PAHs exposure is still unclear. In this study, we recruited 256 male coke oven workers and control workers, and examined H3K79me2 and DNA damage in their peripheral blood lymphocytes (PBLCs). The results showed that global H3K79me2 of coke oven workers was 29.3% less than that of the controls (P < 0.001). The H3K79me2 was negatively correlated with the concentration of urinary 1-hydroxypyrene (1-OHP) (β = -0.235, P < 0.001) and level of genetic damage evaluated by comet assay (βTₐᵢₗ DNA % = -0.313, P < 0.001; βOTM = -0.251, P = 0.008). Consistently, we found that benzo(a)pyrene (BaP) inhibited H3K79me2 in immortalized human bronchial epithelial (HBE) cells in a time-dependent manner. In order to explore the function of H3K79me2 in PAHs DDR, we established histone 3.1/3.3 K79A mutant cells (H3K79 A) to suppress H3K79me2. H3K79 A cells showed more serious DNA damage and decreased cell viability than control cells after BaP treatment. In addition, we also found that the expression of DOT1L, the only methyltransferase in H3K79, was repressed by BaP dose-dependently. DOT1L knockdown resulted in decreased H3K79me2 level and aggravated DNA damage after BaP exposure. This suggests that BaP induces H3K79me2 repression via inhibiting DOT1L expression. In conclusion, these findings indicate that PAH exposure decreases the level of global H3K79me2, which is integral for DNA damage response regulation of PAHs.

To master the distribution patterns and environmental risk of 16 USEPA preferential polycyclic aromatic hydrocarbons (PAHs) in surface sediments from Laizhou Bay, 20 samples were collected and investigated in this survey. The average PAH concentration in these sediments ranged from 268.97 ng/g to 895.37 ng/g with an average of 612.52 ng/g, thereby suggesting a relatively low PAH pollution in Laizhou Bay compared with other bays in the world. Tricyclic PAHs account for 79% of the total PAH content and were eventually identified as the most crucial component of these sediments. The PCA–MLR results identify fossil fuel combustion, biomass burning, and coke oven as the main sources of PAHs that account for 26.69%, 67.16%, and 6.15% of the total PAH concentration in the collected sediments, respectively. The effect range low/effect range median (ERL/ERM) reveal the low toxicity of PAHs in these sediments. However, the concentration of Fle at each survey site exceeds the ERL level. Meanwhile, the mean effects range–median quotient (M-ERM-Q) indicates the low level of ecological risk of PAHs in the surface sediments from Laizhou Bay. However, the contingency risk of Fle and Phe cannot be ruled out.

Sixteen USEPA priority polycyclic aromatic hydrocarbons (PAHs) were analyzed by gas chromatography–mass spectrometry. Twenty-three samples were collected from the surface sediments of Qinhuangdao coastal wetlands in this survey. This research aimed to identify the PAHs contamination level, composition pattern, pollution sources, and assess the ecological risk of PAHs. The results showed that the sum of PAH concentrations ranged from 341.61ng/g to 4703.80ng/g (mean: 1367.80ng/g), which is higher than the reported values for different wetlands worldwide. Five- and four-ring PAHs (34.08% and 32.97% of Ʃ16PAHs, severally) were predominant in the wetland sediment. The PAH source distribution in the surface sediments was determined using diagnostic ratio and PCA/MLR. Consequently, multiple PAH sources were found. Of the total PAHs, 70.01% was derived from vehicular emission, 25.73% from coke oven, and 4.26% from petroleum-based product spills. The effect range low/effect range median (ERL/ERM) values indicated a low toxicity risk level. However, the DBahA concentrations exceeded the ERL level, and even the ERM level, in some stations. The mean effects range–median quotient (M-ERM-Q) suggests a low ecological risk for the PAHs, but a medium risk for some stations in the coastal wetland sediments.

The behaviours of PAHs (containing 2–6 aromatic rings) in the Pearl River estuary were examined each month in 2011. This study was designed to investigate the abundance of 16 priority PAHs and their response to the seasonal dynamics of anthropogenic activities and hydrological cycles. Monthly mean concentrations of ∑16PAHs in water and suspended particulate matter (SPM) were 88.31ng/L and 252.31ng/L respectively, with higher concentrations in the wet season (April to September). Heavy precipitation in the wet season resulted in relatively increased PAH input via riverine discharges and atmospheric deposition. Seasonal variations in suspended sediment concentration (SSC), temperature and salinity have considerably affected the PAH phase association. Higher SSC in the wet season contributed to higher concentration of the PAHs in SPM, and higher temperature and lower salinity facilitated desorption from SPM. The PAH sources were largely attributed to vehicular emissions, coal combustion and coke ovens.