MicroRNA expression in the serum of dust exposure population / 中国职业医学

OBJECTIVE: To analyze the microRNA levels in the serum of dust exposure population. METHODS: By cluster random sampling method,479 dust exposure workers were selected as dust exposure group. Four hundred and thirty-four normal healthy people without occupational dust exposure history were selected as control group. Forty-three pneumoconiosis patients were selected as pneumoconiosis group. The peripheral venous blood of the objects of 3 groups were collected,and the plasma serum were separated for detecting the relative expression of miR-16,miR-21,miR-29 a,miR-155,miR-200 c,miR-204 and miR-206 in serum by real time quantitative polymerase chain reaction. The difference of microRNA expression in the above 3 groups was observed. RESULTS: From high to low,the relative expression levels of miR-16,miR-29 a and miR-200 c were pneumoconiosis group > dust exposure group > control group( P < 0. 05),while the relative expression levels of miR-204 were control group > dust exposure group > pneumoconiosis group( P < 0. 05).The relative expression levels of miR-21 in dust exposure and pneumoconiosis groups were higher than that of control group,respectively( P < 0. 05). The relative expression level of miR-155 in dust exposure group was lower than that of control group( P < 0. 05). The relative expression level of miR-206 in pneumoconiosis group was higher than those of dust exposure group and control group respectively( P < 0. 05). CONCLUSION: The miR-16,miR-29 a,miR-200 c and miR-204 could be used as biomarkers in early diagnosis of pneumoconiosis disease.

Influence of ethylbenzene on oxidative damage and apoptosis in rat renal epithelial cells NRK-52e / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the oxidative damage and apoptosis of renal tubular epithelial cells (NRK-52e cell line) induced by ethylbenzene.</p><p><b>METHODS</b>NRK-52e cells were exposed to 30, 60, 90, 120 μmol/L ethylbenzene for 24 hours. Cell viability were measured using MTT, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), the contents of malondialdehyde (MDA) and glutathione (GSH) were detected respectively. PI fluorescent staining assay was applied to detect percentage of apoptosis in ethylbenzene-treated groups.</p><p><b>RESULTS</b>Compared with control group, cell outline became clear, cell diopter increased, cell became smaller and shrinkage, some cells broke in 60 μmol/L ethylbenzene-treated group. Plenty of cells died, suspension cells increased significantly in 90 μmol/L ethylbenzene-treated group. Compared with control group, cell viability the activities of SOD and CAT and the content of GSH were significantly decreased in 60 and 90 μmol/L ethylbenzene-treated groups (P<0.05). The MDA content were remarkably elevated in 90 μmol/L ethylbenzene-treated groups (P<0.05).</p><p><b>CONCLUSION</b>Ethylbenzene can induce oxidative stress and apoptosis in NRK-52e cells (P<0.05).</p>

The inhibitory effect of latent transforming growth factor β1 activation and silicosis by CD36 targeted RNA interference in silicosis model of rat / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the inhibitory effects of CD36-targeting RNA interference on the latent transforming growth factor β1 (L-TGF-β1) activation and silicotic fibrosis in rat silicosis model.</p><p><b>METHODS</b>Wistar rats were divided into four groups: saline control group (n=24), SiO2 model group (10 mg SiO2 per rat) (n=24), SiO2+Lv-shCD36 group (lentiviral vector expressing specific shRNA against CD36) (n=24), and SiO2+Lv-shCD36-NC group (non-silence control lentivirus) (n=24). At 7, 21, and 28 d after instillation, the rats were sacrificed. The activity of TGF-β1 in bronchoalveolar lavage fluid (BALF) was measured by evaluating its inhibitory effect on the proliferation of mink lung epithelial cells. The pathological changes of lung tissue were observed by HE staining and van Gieson staining. The hydroxyproline content in the lungs was determined by alkaline lysis method.</p><p><b>RESULTS</b>At 7 d after instillation, the expression of CD36 mRNA in alveolar macrophages was significantly lower in the SiO2+Lv-shCD36 group than in the saline control group, SiO2 model group, and SiO2+Lv-shCD36-NC group (P < 0.05); the quantity and percentage of active TGF-β1 in BALF were significantly lower in the SiO2+Lv-shCD36 group than in the SiO2 model group and SiO2+Lv-shCD36-NC group (P < 0.05). At 28 d after instillation, there were cellular silicotic nodules in the lungs of rats in SiO2+Lv-shCD36 group and fibrotic cellular silicotic nodules in the lungs of rats in SiO2 model group and SiO2+Lv-shCD36-NC group. At 21 and 28 d after instillation, the hydroxyproline content was significantly lower in the SiO2+Lv-shCD36 group than in the SiO2 model group and SiO2+Lv-sh CD36-NC group (P < 0.05).</p><p><b>CONCLUSION</b>CD36-targeting RNA interference has inhibitory effects on the L-TGF-β1 activation and silicotic fibrosis in rat silicosis model.</p>

Effect of subchronic inhalation of ethylbenzene on expression of heme oxygenase-1 in rat renal tissues / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of ethylbenzene on the expression of heme oxygenase-1 (HO-1) intrarenal tissues.</p><p><b>METHODS</b>Forty male Sprague-Dawley rats were randomly and equally allocated to control group, low-dose exposure group, moderate-dose exposure group, and high-dose exposure group to inhale different doses of ethylbenzene (0, 433.5 mg/m(3) (100 ppm), 4335.0 mg/m(3) (1000 ppm), and 6500.0 mg/m(3) (1500 ppm)) for 6 h per day, 5 days per week, for 13 weeks. After the rat model of subchronic ethylbenzene exposure was established, the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) in renal tissues were measured, and the mRNA and protein expression levels of HO-1 in renal tissues were measured by real-time PCR and Western blot.</p><p><b>RESULTS</b>Compared with the control group, all exposure groups showed significantly decreased activities of GSH-Px and CAT in renal tissues and the moderate- and high-dose exposure groups showed significantly decreased activity of SOD in renal tissues (P < 0.05). All exposure groups showed significantly higher expression of HO-1 than the control group (P < 0.05). The high-dose exposure group showed significantly higher expression of HO-1 than the low- and moderate-dose exposure group (P < 0.05), and the moderate- and high-dose exposure group had significantly higher expression of HO-1 than the control group and low-dose exposure group (P < 0.05).</p><p><b>CONCLUSION</b>A certain dose of ethylbenzene can induce elevated expression of HO-1 and decreased antioxidant levels in rat renal tissues, thus leading to oxidative stress damage.</p>

Effect of toluene diisocyanate on lung function of workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of long-term exposure to toluene diisocyanate (TDI) on the lung function of TDI-exposed workers.</p><p><b>METHODS</b>A factory was selected for this occupational epidemiological investigation. The workers who were exposed to TDI and had complete physical examination records in recent 3 years were the exposed group (n = 45), while the company's administrative staff, logistics staff, and other non-TDI-exposed workers who had complete physical examination records in recent 3 years were the control group (n = 47). The two groups were compared in terms of lung function indices.</p><p><b>RESULTS</b>Compared with the control group, the 2009 exposure group had significantly lower forced expiratory volume in one second (FEV1.0), FEV1.0/forced vital capacity (FVC), and maximal expiratory flow at 25% of FVC (MEF25) (P < 0.05), the 2010 exposure group had significantly lower FEV1.0, FEV1.0/FVC,maximum voluntary ventilation (MVV), and maximal expiratory flow at 50% of FVC (MEF50) (P < 0.05), and the 2011 exposure group had significantly lower FEV1.0, FEV1.0/FVC, peak expiratory flow (PEF), MEF25, and MEF50 (P < 0.05).</p><p><b>CONCLUSION</b>Long-term exposure to TDI can lead to certain impairment of lung function in workers, which may be reflected by decreased lung function indices such as vital capacity, FVC, FEV1.0, FEV1.0/FVC, PEF, and MVV.</p>

Time-series analysis on effect of air pollution on stroke mortality in Tianjin, China / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of air pollution on stroke mortality in Tianjin, China, and to provide basis for stroke control and prevention.</p><p><b>METHODS</b>Total data of mortality surveillance were collected by Tianjin Centers for Disease Control and Prevention. Meteorological data and atmospheric pollution data were from Tianjin Meteorological Bureau and Tianjin Environmental Monitoring Center, respectively. Generalized additive Poisson regression model was used in time-series analysis on the relationship between air pollution and stroke mortality in Tianjin. Single-pollutant analysis and multi-pollutant analysis were performed after adjustment for confounding factors such as meteorological factors, long-term trend of death, "days of the week" effect and population.</p><p><b>RESULTS</b>The crude death rates of stroke in Tianjin were from 136.67 in 2001 to 160.01/100000 in 2009, with an escalating trend (P = 0.000), while the standardized mortality ratios of stroke in Tianjin were from 138.36 to 99.14/100000, with a declining trend (P = 0.000). An increase of 10 µg/m³ in daily average concentrations of atmospheric SO₂, NO₂ and PM₁₀ led to 1.0105 (95%CI: 1.0060 ∼ 1.0153), 1.0197 (95%CI: 1.0149 ∼ 1.0246) and 1.0064 (95%CI: 1.0052 ∼ 1.0077), respectively, in relative risks of stroke mortality. SO₂ effect peaked after 1-day exposure, while NO₂ and PM₁₀ effects did within 1 day.</p><p><b>CONCLUSION</b>Air pollution in Tianjin may increase the risk of stroke mortality in the population and induce acute onset of stroke. It is necessary to carry out air pollution control and allocate health resources rationally to reduce the hazard of stroke mortality.</p>

The changes of blood neurotransmitter levels in workers occupationally exposed to ethylbenzene / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of occupational ethylbenzene exposure on blood neurotransmitter levels in population.</p><p><b>METHODS</b>The exposure group consisted of 246 workers occupationally exposed to ethylbenzene and the control group was composed of 122 staffs from the offices. The basic information on ethylbenzene exposure was collected by the questionnaire. The mandelic acid (MA) and phenylglyoxylic acid (PGA) in the post-working urine were measured using the high performance liquid chromatography. The levels of gamma-aminobutyric acid (GABA), dopamine (DA) and acetylcholinesterase (AchE) activity were detected by reversed phase high performance liquid chromatography, spectrofluorometry and DTNB method, respectively. The blood biochemical indexes: alanine transaminase (ALT), aspartate aminotransferase (AST), total protein (TP), albumin (ALB), alkaline phosphatase (ALP), total bilirubin (TBIL) were examined. Also the hematologic indexes: red blood cell (RBC), white blood cell (WBC), hemoglobin (HGB) and platelet (PLT) were determined.</p><p><b>RESULTS</b>The levels of MA, PGA and MA+PGA of urine in the exposed group were significantly higher than those in the control group (P < 0.05). There were no significant differences of the biochemical indexes (AST, ALT, TP, ALB, BUN, Cr, ALP and TBIL), hematologic indexes (WBC, RBC, Hb and PLT) and serum GABA between the exposure group and the control group (P > 0.05). But the serum DA [(0.21 ± 0.011) mg/L] and AChE levels [(0.321 ± 0.066) U/L] in the exposure group were significantly lower than those in the control group [(0.25 ± 0.015) mg/L, (0.583 ± 0.125) U/L], respectively (P < 0.05).</p><p><b>CONCLUSION</b>MA and PGA in urine can serve as the biomarkers of internal exposure dose. Before the obvious changes of biochemical indexes and hematologic indexes appear, the exposure to ethylbenzene can influence the blood neurotransmitter levels in workers exposed to ethylbenzene.</p>

The neurobehavioral effects of population occupationally exposed to ethylbenzene / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To evaluate the influence of ethylbenzene on the neurobehavior of occupationally exposed workers.</p><p><b>METHODS</b>The exposure group consisted of 246 workers occupationally exposed to ethylbenzene and 172 staffs from the offices served as controls. The basic information on ethylbenzene exposure was collected by the questionnaire. The nervous behavior and function of workers were evaluated by Neurobehavioral Core Test Battery (NCTB).</p><p><b>RESULTS</b>There were no differences of the scores for four emotional states (tension, depression, angry and bewilderment) between exposure group and control group (P > 0.05). The score of emotion (vigor) in exposure group was significantly lower than that in control group (P < 0.05), but the fatigue score in exposure group was significantly higher than that in control group (P < 0.05). The score of mean reaction time in exposure group was significantly higher than that in control group (P < 0.05), the scores of digital span, manual dexterity, visual retention and target tracking in exposure group were significantly lower than those in control group (P < 0.05). The exposure group was divided into 5 sub-groups, according to working duration. There were no differences for the scores of visual retention and target tracking among 5 sub-groups (P > 0.05). The scores of five emotional states (tension, depression, angry, fatigue and bewilderment) in 3 sub-groups exposed to ethylbenzene for 3 ∼, 4 ∼ and 5 ∼ years were significantly higher than those in 2 sub-groups exposed to ethylbenzene for 0 ∼ and 2 ∼ years (P < 0.05). The scores of digital span in 2 sub-groups exposed to ethylbenzene for 3 ∼ or 4 ∼ years and the scores of manual dexterity and digital symbol in 3 sub-groups exposed to ethylbenzene for 3 ∼, 4 ∼ and 5 ∼ years were significantly lower than those in 2 sub-groups exposed to ethylbenzene for 0 ∼ and 2 ∼ years (P < 0.05).</p><p><b>CONCLUSION</b>Ethylbenzene can depress the neurobehavioral functions of exposed workers. The neurobehavioral functions of workers exposed to ethylbenzene for 3 years changed significantly. The workers exposed to ethylbenzene for 3 years may be the susceptible population of neurobehavioral function impairment.</p>

Effects of ethylbenzene on oxidative damage, ultrastructure and expressions of apoptosis-related genes in rat brain tissues / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the influence of ethylbenzene on oxidative damage, ultrastructure and the expressions of apoptosis-related genes in the rat brain tissues.</p><p><b>METHODS</b>Four groups of 10 males of Sprague-Dawley rats were allocated randomly, and inhaled daily with different doses of ethylbenzene: 0, 433.5 mg/m³, 4335.0 mg/m³, and 6500.0 mg/m³ 6 h daily, 5 days per week for 13 weeks. The contents of glutathione (GSH) and malondialdehyde (MDA) and activity of acetylcholinesterase (AChE) were assayed, respectively. The ultrastructure of brain tissues was observed via electron microscope. The gene expression levels of Bax, Bcl-2, cytochrome C, caspase-9 and caspase-3 in brain tissues were measured by real-time polymerase chain reaction (PCR), respectively.</p><p><b>RESULTS</b>The contents of MDA [(2.03 ± 0.56), (4.17 ± 1.31) nmol/mg pro] in the brain tissues of 4335.0 mg/m³ and 6500.0 mg/m³ ethylbenzene-treated groups were significantly higher than that [(1.08 ± 0.26) nmol/mg pro] in the control group (P < 0.05), while AChE activities [(0.321 ± 0.066), (0.276 ± 0.031), (0.202 ± 0.041) U/mg] and GSH contents [(35.19 ± 15.08), (33.42 ± 15.32), (27.99 ± 7.53) mg/g pro] in all ethylbenzene-treated groups were remarkably depressed (P < 0.05, P < 0.05, respectively). After 6500.0 mg/m³ ethylbenzene inhalation, the nucleolus exhibit demilune with decreased mitochondria. Electrondense of myelin occurred in the injured nerve, ascribing to lipid peroxidationed membrane. The gene expression level of Bax in brain tissue of 4335.0 mg/m³ and 6500.0 mg/m³ ethylbenzene-treated group was significantly higher than that in the control group (P < 0.05). Compared with the control group, the gene expression levels of cytochrome C, caspase-9 and caspase-3 in all ethylbenzene-treated groups were enhanced (P < 0.05, P < 0.05, respectively), while bcl-2 gene expression levels in all ethylbenzene-treated groups were decreased (P < 0.05).</p><p><b>CONCLUSION</b>Ethylbenzene can induce oxidative damage and apoptosis in brain tissues. The apoptotic mechanism might be involved with up-regulation of Bax, cytochrome C, caspase-9 and caspase-3, as well as restraint of Bcl-2.</p>

Influence of ethylbenzene on the levels of mandelic acid and phenylglyoxylic acid in urine, ultrastructure and the expressions of Mitochondrial apoptotic-related proteins in the rat nephridial tissues / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the influence of ethylbenzene on the levels of mandelic acid (MA) and phenylglyoxylic acid (PGA) in urine, the ultrastructure and the expressions of mitochondrial apoptotic-related genes in the rat nephridial tissues.</p><p><b>METHODS</b>Four groups of 10 males of Sprague-Dawley rats were allocated randomly into four groups: control (C) group, low (L) group, moderate (M) group and high (H) group, and inhaled daily with different doses of ethylbenzene: 0, 433.5 mg/m(3), 4335 mg/m(3), and 6500 mg/m(3) 6 h per day, 5 days per week for 13 weeks. The mandelic acid and phenylglyoxylic acid in the urine was assayed by high performance liquid chromatography. The ultrastructure of nephridial tissue was observed via electron microscope. The protein expression levels of Bax, Bcl-2, cytochrome C, Caspase-9 and Caspase-3 in nephridial tissues were measured by Western blot, respectively.</p><p><b>RESULTS</b>The levels of MA [(0.303 +/- 0.148) mg/L, (0.404 +/- 0.154) mg/L] and PGA [(0.168 +/- 0.104) mg/L, (0.174 +/- 0.092) mg/L] in the urine of M and H groups were significantly higher than that in the control and L group [(0.084 +/- 0.070) mg/L, (0.041 +/- 0.029) mg/L] (P < 0.05, respectively). It has been shown a dose-effect relationship between the contents of MA, PGA and MA + PGA and inhaled ethylbenzene, respectively. The mitochondria of rat nephridial tissue of H group became a compact and vacuolar structure with disorder and loss of cristae. The expression levels of Bax in mitochondria of nephridial tissues of M and H groups were significantly lower than that in the control group (P < 0.05). Caspase-3 expression level in H group was remarkably higher than that in the control group (P < 0.05). Compared with the control group, the expression levels of cytochrome C and Caspase-9 were enhanced, while the expression levels of Bcl-2 were restrained in all ethylbenzene-treated groups (P < 0.05, P < 0.05, respectively). The expression levels of Caspase-3 in M and H groups were significantly higher than that in the control group and L group (P < 0.05).</p><p><b>CONCLUSION</b>Ethylbenzene can induce apoptosis in the cells of nephridial tissues. The apoptotic mechanism might be involved with up-regulation of Bax, cytochrome C, Caspase-9 and Caspase-3, as well as restraint of Bcl-2. The level of MA and PGA in the rat urine could be a parameter of biological dose in vivo after ethylbenzene inhalation.</p>