Ozone/toxicity* ; Air Pollution/analysis* ; Air Pollutants/analysis* ; China/epidemiology* ; Environmental Exposure/analysis* ; Mortality ; Particulate Matter/analysis*

Objective To quantitatively evaluate the associations of PM
Air Pollutants/toxicity* ; Air Pollution/adverse effects* ; Child, Preschool ; China ; Dermatitis, Atopic/epidemiology* ; Female ; Humans ; Male ; Outpatients ; Particulate Matter/analysis*

Objective: To screen the differential methylation sites, genes and pathways of air pollution fine particles (PM(2.5)) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PM(2.5) on HBE cells. Methods: In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM(2.5) aqueous solution for 24 h, namely PM(2.5) 10 μg/ml exposure group (low dose group) and PM(2.5) 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs). Results: Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; PIK3CA and ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; TNF genes related to tumor inhibition were found in the results of FEMs analysis. Conclusion: After PM(2.5) exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PM(2.5) may be related to DNA methylation.
Air Pollutants/toxicity* ; Basic Helix-Loop-Helix Transcription Factors/analysis* ; Carcinogenesis ; DNA Methylation ; Humans ; Particulate Matter/toxicity* ; Technology

OBJECTIVETo establish the method of detecting the concentrations of chlorpyrifos in air of workplace with high performance liquid chromatographic (HPLC).

METHODSAccording to standards of methods for determining the chemical substances in workplace air, chlorpyrifos in the air was collected by silicone tube, then dissolved by acetonitrile and determined by high performance liquid chromatography with UV-detector.

RESULTSThere was a linear relationship within the range of 0 ∼ 10.0 µg/ml, and regression equation was y = 5206.1x - 104.7, correlation coefficient was 0.9999, the detection limit was 0.006 µg/ml. The lowest detected concentration was 0.001 mg/m(3) (sampling volume 4.5 L). The average recoveries was 98.3% ∼ 102.5%. The within-run precision was 1.96% ∼ 4.39%, the between-run precision was 2.76% ∼ 5.87%. The desorption efficiencies were 99.0% ∼ 103.3% and the sampling efficiencies were 94%. The samples in silicone tube could be stored for 15 days at room temperature.

CONCLUSIONThe present method could meet with the requirements of Guide for establishing occupational health standards-Part 4 Determination methods of air chemicals in workplace and be feasible for determination of chlorpyrifos in workplace air.

Air Pollutants, Occupational ; analysis ; Chlorpyrifos ; analysis ; toxicity ; Chromatography, High Pressure Liquid ; methods ; Limit of Detection ; Reproducibility of Results ; Workplace

Air Pollutants ; analysis ; Animals ; Child ; Esters ; toxicity ; Humans ; Liver ; drug effects ; Phthalic Acids ; analysis ; metabolism ; toxicity ; Reproduction ; drug effects ; Soil Pollutants ; analysis ; Thyroid Gland ; drug effects ; Water Pollutants, Chemical ; analysis

OBJECTIVETo understand the exposed positions and levels of indium and its compounds in manufacture of liquid crystal displays, and to evaluate the degree of occupational hazard from indium and its compounds.

METHODSOn-site investigation of occupational health, occupational hazard monitoring, and occupational health examination were used to evaluate the degree of occupational hazard from indium and its compounds in three manufacturers of liquid crystal display panel in Shenzhen, Guangdong, China.

RESULTSThe time-weighted average (TWA) and short-term exposure limit (STEL) concentrations of indium and its compounds to which sputtering machine operating positions were exposed were less than 0.002~0.004 mg/m³ and 0.006~0.007 mg/m³, respectively, both of which complied with the National Hygienic Standard (PC-TWA = 0.1 mg/m³; PC-STEL = 0.3 mg/m³); the TWA and STEL concentrations of indium and its compounds to which grinding positions were exposed were 0.114~2.98 mg/m³ and 0.31~10.02 mg/m³, respectively, both of which exceeded the National Hygienic Standard with the highest concentration 33-fold higher than the standard. No significant health damages were found in exposed workers according to the results of occupational health examination.

CONCLUSIONThe grinding positions are the key to the control of occupational hazard from indium and its compounds in manufacture of liquid crystal display panel. The workers should be equipped with the anti-particulate full-face respirator, which is an effective way to prevent occupational hazard from indium and its compounds.

Air Pollutants, Occupational ; toxicity ; China ; Data Display ; Humans ; Indium ; toxicity ; Liquid Crystals ; Occupational Exposure ; analysis ; Occupational Health ; Risk Assessment ; Threshold Limit Values

OBJECTIVETo study the relationship between ambient air pollution and daily mortality of SARS in Beijing.

METHODSThe approach of time-series Poisson regression was used to assess the relationship between daily SARS mortality, ambient air pollution, and other factors from April 25 to May 31, 2003 in Beijing.

RESULTSAn increase of each 10 microg/m3 over a 5-day moving average of PM10, SO2 and NO2 corresponded to 1.06 (1.00-1.12), 0.74 (0.48-1.13) and 1.22 (1.01-1.48) relative risks (RRs) of daily SARS mortality, respectively. The relative risks (RRs) values depended largely on the selection of lag days.

CONCLUSIONThe daily mortality of SARS might be associated with certain air pollutants in Beijing.

Air Pollutants ; adverse effects ; analysis ; toxicity ; Air Pollution ; adverse effects ; analysis ; China ; epidemiology ; Cities ; Dust ; analysis ; Environmental Monitoring ; Epidemiological Monitoring ; Humans ; Nitrogen Dioxide ; analysis ; Particle Size ; Retrospective Studies ; Risk ; Severe Acute Respiratory Syndrome ; epidemiology ; mortality ; Sulfur Dioxide ; analysis

OBJECTIVETo compare PM2.5 pollation level between the city of coal-fuel pollution (Taiyuan) and the city of pollution mixed with coal fuels and vehicle exhausts (Beijing), to analyze the concentration of B[a]p and Pb in the pollutants, and to study the DNA damage by PM2.5.

METHODSAir fine particles (PM2.5) were collected in Beijing and Taiyuan by means of the filter membrane method, the concentration of B[a]p and Pb were analyzed by high performance liquid chromatography and atomic absorption spectroscopy respectveily, and the damage of DNA by PM2.5 was detected by single cell gel-electrophoresis (SCGE) using the human lung epithelial cells (A549) as target cells.

RESULTSThe concentration of PM2.5 in the winter of Beijing was 0.028-0.436 mg/m(3), and that in Taiyuan was 0.132-0.681 mg/m(3). The concentration of B[a]p was 0.104 and 0.156 microg/mg on PM2.5 of Beijing and Taiyuan, respectively, whereas the concentration of Pb was 1.094 and 1.137 microg/mg on PM2.5 of Beijing and Taiyuan, respectively. Exposure to PM2.5 at the concentrations of 5, 50, and 200 microg/mL for 12 h and 24 h caused DNA damage of the human alveolar epithelium, and the ratios of the tailing and length of the tail were all significantly different from those of the negative control group (P < 0.05), and indicated a dose-response relationship.

CONCLUSIONPM2.5 has certain genetic toxicity.

Air Pollutants ; analysis ; toxicity ; Animals ; Benzo(a)pyrene ; analysis ; toxicity ; China ; DNA Damage ; drug effects ; Dose-Response Relationship, Drug ; Drug-Related Side Effects and Adverse Reactions ; Environmental Monitoring ; methods ; Humans ; Lead ; analysis ; metabolism ; toxicity ; Particle Size ; Pulmonary Alveoli ; drug effects ; metabolism ; Seasons

OBJECTIVETo assess the effect of benzene on sperm DNA.

METHODSTwenty-seven workers exposed to benzene for over two years were included in the experiment group and 35 unexposed ones were chosen as controls. Damage by benzene on sperm DNA was detected by modified single cell gel electrophoresis (SCGE).

RESULTSThe benzene concentration in the air of the workplace of the exposed workers was (86.49 +/- 2.83) mg/m3, twice that of the national maximum allowance (40 mg/cm3). Urinary, trans-muconic acid in the exposed group was (1.40 +/- 0.62) mg/L (n = 27), significantly higher than that of the controls [(0.82) +/- 0.16) mg/L, n = 35]. After SCGE, the percentage of head DNA in the exposed group [(70.18% +/- 7.36%, n = 13 ] was significantly lower than that of the controls (90.62% +/- 2.94%, n = 16), P < 0.001.

CONCLUSIONHigher concentration of benzene could cause damage to the sperm DNA of the workers exposed to it.

Adult ; Air Pollutants, Occupational ; analysis ; Benzene ; analysis ; toxicity ; Comet Assay ; DNA Damage ; drug effects ; Humans ; Male ; Occupational Exposure ; Spermatozoa ; drug effects ; Surveys and Questionnaires

OBJECTIVES: The association between concentrations of sulfur dioxide (SO), nitrogen dioxide (NO), carbon monoxide (CO), ozone (O), and emergency ambulance dispatches (EADs) for asthma was explored in the central Sichuan Basin of southwestern China for the first time. METHODS: EADs for asthma were collected from the Chengdu First-Aid Command Center. Pollutant concentrations were collected from 24 municipal environmental monitoring centers and including SO, NO, CO, daily 8-h mean concentrations of O (O-8 h), and particulate matter less than 2.5 μm in aerodynamic diameter (PM). The climatic data were collected from the Chengdu Municipal Meteorological Bureau. All data were collected from years spanning 2013-2017. A time-stratified case-crossover design was used to analyze the data. RESULTS: After controlling for temperature, relative humidity, and atmospheric pressure, IQR increases in SO (13 μg/m), NO (17 μg/m), and CO (498 μg/m) were associated with 18.8%, 11.5%, and 3.1% increases in EADs for asthma, respectively. The associations were strongest for EADs and SO, NO, and CO levels with 3-, 5-, and 1-day lags, respectively. CONCLUSIONS This study provides additional data to the limited body of literature for potential health risks arising from ambient gaseous pollutants. The results of the study suggest that increased concentrations of SO, NO, and CO were positively associated with emergency ambulance dispatches for asthma in Chengdu, China. Further studies are needed to investigate the effects of individual air pollutants on asthma.
Air Pollutants ; analysis ; toxicity ; Asthma ; chemically induced ; epidemiology ; Carbon Monoxide ; analysis ; toxicity ; China ; epidemiology ; Cities ; Cross-Over Studies ; Emergency Medical Dispatch ; statistics & numerical data ; Environmental Monitoring ; statistics & numerical data ; Humans ; Nitrogen Dioxide ; analysis ; toxicity ; Ozone ; analysis ; toxicity ; Particle Size ; Particulate Matter ; analysis ; toxicity ; Risk ; Sulfur Dioxide ; analysis ; toxicity