Objective: To analyze the level of PCDD/Fs exposure of occupational workers in the waste incineration industry and explore the risk of occupational exposure. Methods: In September 2021, literature on environmental PCDD/Fs exposure in waste incineration plants published from the establishment of the database to February 10, 2021 was retrieved from CNKI database. A total of 1365 literatures were retrieved, and 7 met the criteria for inclusion. The US Environmental Protection Agency (EPA) inhalation risk model was used to assess and analyze carcinogenic and non-carcinogenic risks of PCDD/Fs exposure among occupational workers in the waste incineration industry. Results: A total of 86 sampling sites were included in incineration plants in 7 regions. The study of Wuhan area showed that the concentration of working environment near the waste incinerator in the same factory was the highest, followed by the rest and office area in the factory. The concentration of PCDD/Fs in waste incinerators was the highest in Southwest China (4880.00-24880.00 pg TEQ/m(3)), and the lowest in Shenzhen (0.02-0.44 pg TEQ/m(3)). According to the cancer risk assessment, with the increase of exposure years, the risk of cancer increased. The highest risk of cancer was found in the waste incineration plants in Southwest China. When the exposure period was 1 year, the risk was moderate (22.40×10(-6)-114.20×10(-6)). When the exposure time was more than 5 years, the risk of cancer was high. In Jinan, workers working near the incinerator had a moderate risk of cancer after five years of exposure. In Zhejiang, workers were at medium risk of cancer after exposure for more than 20 years. Workers in Wuhan, Shanghai, Zhejiang Province, Shenzhen and the Pearl River Delta were still at low risk of cancer after 40 years of occupational exposure. HQ>1 of workers working near the waste incinerators in Jinan, Zhejiang Province and Southwest China, and the qualitative evaluation results showed that the non-carcinogenic risk was unacceptable. Conclusion: There are great differences in PCDD/Fs of occupational exposure in waste incineration industry, and the occupational exposure exceeding the occupational exposure limit has higher carcinogenic and non carcinogenic risks.
Humans ; Dibenzofurans ; Polychlorinated Dibenzodioxins/analysis* ; Air Pollutants/analysis* ; Incineration ; Dibenzofurans, Polychlorinated/analysis* ; China/epidemiology* ; Benzofurans ; Occupational Exposure/analysis* ; Carcinogens ; Risk Assessment ; Neoplasms ; Environmental Monitoring/methods*

In 2020, the mass concentration of PM_2.5 in Shijiazhuang urban area was(80.30±71.43)μg/m³. The Spearman correlation analysis between metals and metalloids showed that Sb with Cd, Pb, Ni, Se, Cd with Pb, Ni, Se, Pb with Ni, Se, Ni with Se, and Se with Tl were positively correlated, with a coefficient greater than 0.5. The main sources of metals and metalloids of PM_2.5 were traffic emissions, fuel combustion, metal smelting and dust. The HQ values of Pb, Hg and Mn for each population were less than 1, with lower non-carcinogenic risk. The R values of carcinogenic risk of Ni and Cd in each population were less than 1×10^-6, which could be acceptable risk level for the population. The R values of carcinogenic risk of As and Cr in different populations were between 1×10^-6 and 1×10^-4, with potential carcinogenic risk, particularly higher in adult males.
Adult ; Cadmium ; Carcinogens/analysis* ; Dust/analysis* ; Environmental Monitoring ; Humans ; Lead ; Male ; Metalloids/analysis* ; Risk Assessment

Carcinogens ; chemistry ; toxicity ; Chromium ; chemistry ; toxicity ; Chromium Compounds ; chemistry ; toxicity ; Humans ; Occupational Exposure ; analysis

OBJECTIVETo explore potential epigenetic biomarkers for toxic effects, tumor-related chemical prevention and biological monitor by a genome-wide screening for differential DNA methylation during human cell malignant transformation in vitro.

METHODSThe two in vitro cell transformation models included B(a)P-induced human bronchial epithelial cell introduced by H-Ras (HBER) cell transformation and simian vacuolating virus 40 small T antigen induced (SV40 ST-induced) HBER cell transformation. Methylated genes were collected by methylated DNA immunoprecipitation and whole genome amplification (MeDIP-WGA) at three time points during cell transformation which represented different transformation stage. Then, CpG island microarray was used to screen differentially methylated genes. The mRNA levels of hypermethylated genes were also observed by RT-PCR.

RESULTSThe CpG island microarray showed that the number of hypermethylated genes in HBER, HBERNT, HBERT cells were 733, 661 and 738 respectively.83 genes were hypermethylated in pre-transformed cell and transformed cell. Moreover, 25 of 83 genes were also hypermethylated in SV40 ST-transformed cell (HBERST). We further confirmed that the mRNA expression of six of these 25 genes, namely family with sequence similarity 178, member A (FAM178A), retinoic acid receptor responder (tazarotene induced) (RARRES1), ubiquitin specific peptidase 28 (USP28), Scm-like with four mbt domains 2 (SFMBT2), family with sequence similarity 59, member A (FAM59A) and nuclear receptor subfamily 4, group A, member 3 (NR4A3) were suppressed during B(a)P-induced transformation.

CONCLUSIONThe abnormal hypermethylation of specific genes was a common event in the two kinds of human cell transformation models, which shed light on the study for chemical exposure monitor and tumor-related epigenetic biomarkers.

Biomarkers ; analysis ; Carcinogens, Environmental ; analysis ; Cell Line ; Cell Transformation, Neoplastic ; genetics ; CpG Islands ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Profiling ; Genome ; Humans

OBJECTIVETo establish a high performance liquid chromatographic method for the determination of kirenol in Herba Siegesbeckiae Praeparata.

METHODThe analysis was carried out on a Boston Crest ODS column (4.6 mm x 250 mm, 5 microm) with gradient elution using acetonitrile-water as mobile phases. The flow rate was 1.0 mL x min(-1) and the detection wavelength was at 215 nm.

RESULTThe calibration curve was linear over the range of 0.0202-20.02 microg for kirenol. The correlation coefficient of the calibration curve was 0.99975. The average recovery was 99.62% with relative standard derivation (RSD) of 2.0%.

CONCLUSIONThe results showed that the method is simple, accurate and repeatable and it is suitable for the determination of kirenol in Herba Siegesbeckiae Praeparata.

Acetonitriles ; chemistry ; Adenosine ; analysis ; Asteraceae ; chemistry ; Carcinogens ; analysis ; Chromatography, High Pressure Liquid ; methods ; Drugs, Chinese Herbal ; chemistry ; Quality Control ; Sweetening Agents ; analysis

OBJECTIVES: Determining the work-relatedness of lung cancer developed through occupational exposures is very difficult. Aims of the present study are to develop a decision tree of occupational lung cancer. METHODS: 153 cases of lung cancer surveyed by the Occupational Safety and Health Research Institute (OSHRI) from 1992-2007 were included. The target variable was whether the case was approved as work-related lung cancer, and independent variables were age, sex, pack-years of smoking, histological type, type of industry, latency, working period and exposure material in the workplace. The Classification and Regression Test (CART) model was used in searching for predictors of occupational lung cancer. RESULTS: In the CART model, the best predictor was exposure to known lung carcinogens. The second best predictor was 8.6 years or higher latency and the third best predictor was smoking history of less than 11.25 pack-years. The CART model must be used sparingly in deciding the work-relatedness of lung cancer because it is not absolute. CONCLUSION: We found that exposure to lung carcinogens, latency and smoking history were predictive factors of approval for occupational lung cancer. Further studies for work-relatedness of occupational disease are needed.
Academies and Institutes ; Carcinogens ; Decision Trees ; Lung ; Lung Neoplasms ; Occupational Diseases ; Occupational Exposure ; Occupational Health ; Regression Analysis* ; Smoke ; Smoking

OBJECTIVETo screen miRNA profiles of malignantly transformed human bronchial epithelial cells, 16HBE-T, induced by anti-benzo[a]pyrene-trans-7,8-diol-9,10-epoxide (anti-BPDE), and to analyze putative miR-10a targets in 16HBE-T.

METHODSA novel microarray platform was employed to screen miRNA profiles of 16HBE-T cells transformed by anti-BPDE. Microarray data for miR-10a and miR-320 were validated using quantitative real time polymerase chain reaction (QRT-PCR). The expression of a putative target for miR-10a, HOXA1, was analyzed by reverse transcription polymerase chain reaction (RT-PCR) and QRT-PCR.

RESULTSIn comparison with the vehicle-treated cells (16HBE-N), 16HBE-T exhibited differential expression of 54 miRNAs, in which, 45 were over-expressed and 9 were down-regulated. The five most highly expressed miRNAs were miR-494, miR-320, miR-498, miR-129, and miR-106a. The lowest expressed miRNAs were miR-10a, miR-493-5p, and miR-363*. Three members of miR-17-92 cluster, miR-17-5p, miR-20a, and miR-92, showed significantly higher abundance in 16BHE-T as miR-21, miR-141, miR-27a, miR-27b, miR-16 and miRNAs of the let-7 family. The putative target for miR-10a, HOXA1 mRNA was up-regulated 3-9-fold in 16HBE-T, as compared with 16HBE-N.

CONCLUSIONThe findings of the study provide information on differentially expressed miRNA in malignant 16HBE-T, and also suggest a potential role of these miRNAs in cell transformation induced by anti-BPDE. HOXA1 is similarly up-regulated, suggesting that miR-10a is associated with the process of HOXA 1-mediated transformation.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide ; toxicity ; Carcinogens ; toxicity ; Cell Transformation, Neoplastic ; chemically induced ; genetics ; metabolism ; Cells, Cultured ; Gene Expression Profiling ; Homeodomain Proteins ; genetics ; metabolism ; Humans ; MicroRNAs ; metabolism ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors ; genetics ; metabolism

Air Pollutants, Occupational ; analysis ; Carcinogens, Environmental ; analysis ; Chromium ; analysis ; Environmental Monitoring ; methods ; Workplace

OBJECTIVETo investigate the carcinogenic and mutagenic mechanism of bitumen fume.

METHODSThe experimental mice were forced to inhale the bitumen fume at different exposure level (55 mg/m(3), 165 mg/m(3)) and in different time (30 days, 60 days). The pathological changes of the lung tissue in mice were observed with H.E staining. The content of the DNA in the lung tissue of mice and the cell circles were determined with flow cytometry.

RESULTSThe lesion of the lung tissue in mice comprised the atypical hyperplasia of different levels and the carcinoma in situ with the increase of the containment time and dosage; the cycle index was changed: the number of the G 1 phase cells was decreased, the S phase was retarded, the cells entering the G 2/S phase were decreased, the cell proliferation index (P I) was increased and the heteroploid DNA index (DI) was increased (P < 0.05). The cell index in the 55 mg/m(3) group and the 165 mg/m(3) group was higher than that in the control group when the containment time was same. The heteroploid DNA index (DI) in the 55 mg/m(3) group was significantly higher than that in the 165 mg/m(3) group (P < 0.05 or P < 0.01). When the containment dosage was same, the DI in the 60 days treatment group (1.16 +/- 1.51 x 10(-2), 1.20 +/- 2.3 x 10(-2)) was all significantly higher than those in the 30 days treatment group (1.14 +/- 8.8 x 10(-2), 1.16 +/- 1.47 x 10(-2)) (P < 0.05).

CONCLUSIONThe precancerous lesion in the lung tissue of the mice induced by the bitumen fume may be related with the changes of the cell cycle.

Animals ; Carcinogens ; toxicity ; Cell Cycle ; drug effects ; DNA ; analysis ; Dose-Response Relationship, Drug ; Female ; Flow Cytometry ; Hydrocarbons ; toxicity ; Lung ; drug effects ; pathology ; Male ; Mice ; Mice, Inbred Strains ; Precancerous Conditions ; chemically induced ; pathology

OBJECTIVETo study the role of cyclinD1 and CDK4 in malignant transformation of human fetal lung diploid fibroblast cell line (2BS) induced by silica.

METHODSRecombination vectors with sense and antisense pXJ41-cyclinD1 and pXJ41-CDK4 were constructed, and then transfected into the malignant transformed cells induced by silica, respectively. At the same time, pXJ41-neo was used as the control.

RESULTSDuring the progress of the malignant transformation of 2BS cells induced by silica, cyclinD1 and CDK4 were overexpressed. Antisense RNA suppressed cyclinD1 and CDK4 gene expression in the antisense pXJ41-cyclinD1 and pXJ41-CDK4 transfected cells. Antisense RNA led to cell cycle arrest, resulting in lengthened G1 phase (the percentages of cells in the G1 phase changed from 45.1% to 52.7% and 58.0% for cyclinD1 and CDK4 transfected cells, respectively), and eventually attenuated the increase of the proliferation of malignant transformed cells induced by silica. Compared with malignant transformed cells induced by silica, cells transfected with antisense pXJ41-cyclinD1 and pXJ41-CDK4 showed obviously reduced growth rates. On the 8th day, the suppression rates were 58.69 and 77.43% (the growth rate of malignant transformed cells induced by silica was 100%), doubling time changed from 21.0 h to 31.4 h and 21.0 h to 42.7 h, respectively, the growth capacities on soft agar of cells transfected by antisense pXJ41-cyclinD1 and pXJ41-CDK4 decreased obviously.

CONCLUSIONCyclinD1 and CDK4 play an important role in maintaining transformed phenotype of the cancer cells.

Carcinogens, Environmental ; toxicity ; Cell Line ; Cell Proliferation ; Cell Transformation, Neoplastic ; chemically induced ; Cyclin D1 ; genetics ; metabolism ; physiology ; Cyclin-Dependent Kinase 4 ; genetics ; metabolism ; physiology ; Humans ; Plasmids ; RNA, Antisense ; metabolism ; RNA, Messenger ; analysis ; metabolism ; Silicon Dioxide ; toxicity