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    4 Disease Caused by Chemical and Physical Agents

    2015-03-22 06:06:40
    關(guān)鍵詞:張琳王峰新華

    4 Disease Caused by Chemical and Physical Agents

    2015146 The effect of nickel-smelting fumes on the expression of bcl-2and bax in NIH/3T3cells. ZHANG Lin(張琳),et al.Sch Public Heath,Harbin Med Univ,Harbin 150086.Chin J Ind Hyg Occup Dis 2015;33(3):175-179.

    Objective To investigate the effect of nickel-smelting fumes on the expression of bcl-2 and bax in mammalian cells.Methods Logarithmic growth NIH/3T3 cells were exposed to venom for 24 h,of which sample fumes concentration was respectively 0,6.25,12.50,25.00,50.00,100.00 μg/ml.Cell viability was assessed by MTT assay and the level of extracellular LDH activity was detected with Lactate Dehydrogenase(LDH)kit.Morphological changes of apoptotic were observed with Hoechst33342,while Western blot was used to measure the expression of bcl-2 and bax.Results In addition to 7 days of 6.25 μg/ml nickel-smelting fumes group,each time point and dose group's cell viability reduced with significant differences compared with the control group (P<0.05).The extracellular LDH activity increased with increasing dose of nickel-smelting fumes, and theextracellular LDH activity of 6.25,12.50,25.00,50.00,100.00 μg/ml nickel-smelting fumes group increased as compared with the control group(P<0.05).Simultaneously,the cells,treated with 100.00 μg/ml nickelsmelting fumes for 24 h,appeared obvious morphological changes of apoptosis,such as chromatin condensation and cell shrinkage.The expression of bcl-2 significantly increased in groups of 6.25,12.50,25.00 μg/ml nickelsmelting fumes(0.58±0.01,0.63±0.01 and 0.57±0.01)and decreased in groups of 50.00,100.00 μg/m nickelsmelting fume(0.35±0.01 and 0.27±0.01)as compared with that of the control group(P<0.05).And the expression of bax significantly decreased in the group of 6.25 μg/ml nickel-smelting fumes(0.58±0.00)and increased in groups of 50.00,100.00 μg/m nickel-smelting fumes(0.71±0.01 and 0.78±0.02)as compared with that of the control group(P<0.05).Conclusion Apoptosis was activated in NIH/3T3 cell after 24 h of exposure to Ni-smelting fumes,which may be induced by oxidative stress.

    (Authors)

    2015147 Analyses on relevant factors of the prognosis of patients with acute organophosphate poisoning. KE Xin(柯欣),et al.1st Affil Hosp,Wenzhou Med Univ,Wenzhou 325000.Chin J Ind Hyg Occup Dis 2015;33(3):186-189.

    Objective To find out a method which can assess the prognosis of patients with acute organophosphate poisoning objectively and increase the successful ratio of treatment by investigating relevant factors on the prognosis of the patients with acute organophosphate poisoning. Methods We retrospected 116 patients with acute organophosphate poisoning who were treated in our hospital emergency room from April 2006 to March 2014.According to the outcome of patients,we distributed the patients to death group and survival group,compared the clinic data and using multivariate analysis with Logistic regression to prognosis factors.Results 116 cases of acute organophosphate poisoning patients died in 23 cases,improvedin 93cases.Deathgrouppatients' APACHE-Ⅱscores were higher than those in the survival group(P<0.05).Compared with the survival group,patients'body temperature,blood pressure,pH,GCS index were lower in the death group(P<0.05)and Cr,WBC,ALT,AST,CK-MB,blood glucose,blood lactic acid,heart rate were higher in the death group(P<0.05).There were significant differences between the two groups.Low blood pressure,lower GCS score,hyperglycemia and high white blood cell count,were independent risk factors of poor prognosis,and hypotension was maximum value of all the factors(OR=54.22). Conclusion APACHEⅡ prognostic scoring system can response accurately,vital signs,white blood cell count,pH,serum creatinine,GCS score and serum sodium value which may be associated with prognosis.To evaluate the severity and prognosis of illness,blood glucose,ALT,AST,CK-MB's rising also have certain value.

    (Authors)

    2015148 Effects on cell proliferation capacity and genome stability in periphery lymphocytes of occupational diesel exhaust exposed workers.XIAO Xinhua(肖新華),et al.Faculty Prev Med,Sch Public Health,Sun Yat-sen Univ,Guangzhou 510080.Chin J Prev Med 2015;49(3):228-232.

    Objective To investigate the cell proliferation and genome stability in workers with occupational exposure to diesel exhaust(DE).Methods In 2012,117 DE-exposed workers and 106 control workers were recruited by cluster sampling in this study.The demographic data were obtained by questionnaire survey.The airborne fine particle and enriched polycyclic aromatic hydrocarbons (PAHs)at different workplaces were collected and analyzed.The concentrations of main PAHs monohydroxy metabolites in the urine were determined by high performance liquid chromatography-mass spectrometry(LCMS),which could reflect the internal exposure levels of DE.The cell proliferation capacity and genome stability in the periphery lymphocytes of workers were evaluated by cytokinesis-block micronucleus(CBMN)cytome assay.Results The concentrations[median(P5-P95)]of total PAHs monohydroxy metabolites in the urine of exposed group and control group were 12.96(4.73-28.10),4.76(0.90-15.00)μg/L,respectively,and the exposed group was higher than that of controls(Z= -8.77,P<0.001).The nuclear division index(NDI)of exposed group and control group was 1.68±0.13,1.85±0.16,respectively,and the NDI of exposed group showed significantly decrease(t=8.86,P<0.001),while the genome instability index calculated by micronucleus,nuclear bridges and nuclear buds,of exposed group and control group was 13.27±6.26,4.83± 3.38,respectively,and the exposed group had statistically significant increase(Z=-10.08,P<0.001). The tertiles of total PAHs monohydroxy metabolites in the urine were categorized into low,medium and high groups(<5.96,5.96-12.46,>12.46 μg/L).With the NDI decreased,1.81±0.17,1.79±0.17,1.68± 0.14(F=13.14,P<0.001),genome instability index began to increase 5.80±4.15,9.97±7.14,11.99± 6.61(/1 000),respectively(χ2=36.74,P<0.001). Total PAHs monohydroxy metabolites level in corresponding groups was also increased.In addition,the NDI was negatively correlated with the frequencies of micronucleus,nuclear bridges,nuclear buds and genome instability index,respectively,and the difference was statistically significant(P<0.001).Conclusion DE exposure lead to inhibition of cell proliferation capacity and increase genome instability in the peripheral lymphocytes of occupational-exposed population,providing important clues and evidence for early biomarkers monitoring.

    (Authors)

    2015149 Expression of C3aR and C5aR in trichloroethylene-sensitized mouse liver.WANG Feng(王峰),et al.Dept Occup&Environ,Sch Public Health,Anhui Med Univ,Hefei 230032.Chin J Ind Hyg Occup Dis 2015;33(3):171-174.

    Objective To study the expression of C3aR and C5aR in trichloroethylene-sensitized mouse liver injury and discuss the pathogenesis of Dermatitis Medicamentosa-like of TCE(DMLT).Methods 6-8 w female BALB/c mouse were randomly divided into blank control group,solvent control group and TCE treatment group. TCE was given to the mouse for sensitization on 1st,4th, 7th,10th day and challenged on 17th day and 19th day. Before the killing of the mouse,liver weight and body weight were recorded.The livers were separated on 24 h,48 h,72 h and 7 d after challenge.And the liver sections were used for immunofluorescence stain and RTPCR to detect the expression levels of C3aR and C5aR. Results Microscopic examination showed no significant change in liver structure or organization in TCE non-sensitized group,while liver cell edema,cell necrosis and inflammatory cell infiltration were clearly observed in TCE-sensitized groups.The expression levels of C3aR and C5aR in 24 h,48 h,72 h and 7 d TCE-sensitized groups were significant higher than blank control group,solvent control group and related TCE non-sensitized groups(P<0.05).Conclusion Complement activation was involved in TCE-induced liver injury and C3aR and C5aR might play an essential role in the process.

    (Authors)

    2015150 Effects of excessive fluoride on glucose metabolism in mice.LI Tian(李甜),et al.Dept Histol& Embryol,Preclin Coll,Xinjiang Med Univ,Urumqi 830054.Chin J Endemiol 2015;34(3):178-180.

    Objective To observe glucose metabolism in C57 mice treated with different doses of fluoride.Methods Forty male C57 mice(body weight 20-24 g)were divided into four groups which were exposed to 0,50,100 and 150 mg/L sodium fluoride(NaF)by random number table according to body weight,10 mice in each group. 2,4,6,8,10 and 12 weeks after fluoride exposure,body weight was measured,blood glucose and glycosylated hemoglobin were detected by blood glucose meter and glycosylated hemoglobin meter,serum insulin and glucagon were detected by enzyme-linked immunosorbent assay(ELISA).Results 10 and 12 weeks after fluride exposure,the differences of fasting glucose between groups of C57 mice were statistically significant(F=35.12,21.92,all P<0.05),the fasting glucose of 100,150 mg/L fluoride groups[(7.7±0.2),(7.3±0.3),(8.6± 0.5),(9.1±0.7)mmol/L]were higher than those of the control group[(5.4±0.3),(5.0±0.3)mmol/L,all P<0.01] .The differences of glycosylated hemoglo-bin,glucagons between groups were statistically significant(F=3.85,8.74,all P<0.05).The glycosylated hemoglobin of 100,150 mg/L fluoride groups[(7.73± 0.76),(7.80±1.15)mmol/L]were higher than those of the control group[(5.43±1.27)mmol/L,all P<0.05];serum glucagon levels of 50,100,150 mg/L fluoride groups[(19.15±11.84),(26.55±15.97),(20.05±7.29)ng/L]were lower than that of the control group[(48.35±2.79)ng/L,all P<0.01].Conclusion Long term excess fluoride intake can reduce the function of sugar metabolism in C57 mice.

    (Authors)

    2015151 Investigation of iodine deficiency disorders among boarding students and commuting students aged 8-10 in Nangqian County,Qinghai Province. GAN Peichun(甘培春),et al.Dept Endemiol,Qinghai Dis Endemiol Instit,Xining 811602.Chin J Endemiol 2015;34(3):192-194.

    Objective To master epidemiological condition of iodine nutrition among 8-10 years old school children in Nangqian County,and to provide evidence for making prevention and control strategy.Methods In 2012,students aged 8-10 from schools in 10 towns of Nangqian County were selected,and instant urinary samples were collected and the urinary iodine was detected with As-Ce catalytic spectrophotometry method,the thyroid volume was measured with B ultrasonic method and IQ test with Combined Raven Test-C2(CRT-C2).Results Urinary iodine of 553 children were detected,the urinary iodine median of 203 boarding students was 133.2 μg/L,among these,under 100 μg/L was 32.0% (65/203);while the urinary iodine median of 350 commuting students was 70.4 μg/L,under 100 μg/L was 71.1%(249/350),and the difference of the urinary iodine median between boarding students and commuting students was statistically significant(Z=-6.947,P<0.05);among 499 school children,thyroid rate of the commuting students and the boarding students was 2.2% and 2.3%,respectively;220 school children were taken IQ test with Combined Raven Test-C2(CRT-C2),average points of IQ tests in boarding students was 82.29, and 15.5% (17/110)less than 69 points;average points of IQ tests in commuting students was 82.07,and 12.7%(14/110)less than 69 points.Conclusion The difference of the iodine nutrition level between boarding students and commuting students was statistically significant.Coverage rate of iodized salt,urinary iodine levels and thyroid rate are low in Nangqian County,which highlights the epidemiological features of iodine deficiency disorders in this region.Although iodine deficiency does not cause obvious goiter,intelligence harm should not be ignored.

    (Authors)

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