Analysis on incidence of occupational diseases in Guangzhou from 2010 to 2020 / 中华劳动卫生职业病杂志

Objective: To analyze the incidence characteristics of occupational diseases in Guangzhou from 2010 to 2020, provide scientific basis for formulating occupational disease prevention and control policies. Methods: In January 2021, based on the data of occupational diseases in Guangzhou reported in the Information Monitoring System of Occupational Diseases and Occupational Health, descriptive epidemiological method was used to analyze the types and characteristics of occupational diseases in Guangzhou from 2010 to 2020. Results: A total of 1341 cases of 38 kinds of occupational diseases in 9 categories were reported in the past 11 years. The incidence of occupational pneumoconiosis, occupational otolaryngology and oral diseases and occupational chemical poisoning ranked the top three, accounting for 38.1% (511/1341) , 30.5% (409/1341) and 16.2% (217/1341) of the total cases respectively. The cases of pneumoconiosis in welders and silicosis accounted for 47.7% (244/511) and 34.4% (176/511) of the cases of occupational pneumoconiosis respectively. The cases of noise deafness accounted for 99.8% (408/409) of occupational otorhinolaryngology oral diseases. Acute occupational chemical poisoning cases accounted for 26.7% (58/217) of the occupational chemical poisoning cases, in which dichloroethane poisoning cases ranked the first, accounting for 79.3% (46/58) . Chronic occupational chemical poisoning cases accounted for 73.3% (159/217) of the occupational poisoning cases, in which benzene and lead poisoning cases ranked the top two, accounting for 79.2% (126/159) and 17.6% (28/159) respectively. Conclusion: Pneumoconiosis, silicosis, noise deafness, benzene poisoning, lead poisoning, dichloroethane poisoning should be supervised and managed as key occupational diseases in Guangzhou.

Study on biological monitoring indicators of exposure to 1,2-dichloroethane and its determination method in blood / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate the feasibility of using the concentration of 1,2-DCE in blood as a biological monitoring indicators and build the determination method of 1,2-DCE in blood.</p><p><b>METHODS</b>Dose-response relationship of the exposure of 1,2-DCE and the level of 1,2-DCE in rat blood were investigated using the Pearson's correlation analysis. The concentration of 1,2-DCE in blood was determined using Headspace Sampler-Gas Chromatography-Mass Spectrometer (HS-GC-MS). 3.0 ml blood sample diluting with 2.0 ml 1,2-DCE standard serial solution was placed in 15 headspace bottles respectively and heated at 80 ℃ for 20 min.The vapor upon the headspace bottle was separated by capillary column and the concentration of 1,2-DCE was determined by massspectrum in SIM mode to draw a standard work curve. The within-run precision and the between-run precision were calculated by the relative standard deviation (RSD) of the concentration of 1,2-DCE in blood which was determined 6 times in a day and 6 times within 3 days respectively. The recovery rate was calculated by P=(C2 -C0)/C1 × 100%.</p><p><b>RESULTS</b>When the treatment groups were exposed at dosage of 1,472, 2,550, 3,093, 3,976, and 4 418 mg/m(3), the average concentration of 1,2-DCE in rat blood was 24.1,231.6,344.3,395.1,538.5 μg/L. There was a positive correlation between the concentration of 1,2-DCE in rat blood and the exposed level of 1,2-DCE.The equation of dose-response relationship was y=0.162x -195.8,r=0.982 2,P=0.003 and the precision of exposure experiments was 7.04% -13.15%. 1,2-DCE contents within 0.259 -2 587 μg/L showed a good linear relationship and the regression equation was y=47 901x -357 446, r= 0.999 8. When the blood containing 0.259 μg/L 1,2-DCE was determined for six times, the average peak/peak signal-to-noise ratio was 56.55. The limit of detection (LOD) was 0.014 μg/L and the limit of quantification (LOQ) was 0.046 μg/L. The within-run precision was 1.23% -2.76% and the between-run precision was 2.21% -4.64%. The average recovery rate was 93.3% - 98.6%.</p><p><b>CONCLUSION</b>The concentration of 1,2-DCE in blood could be used as a biological monitoring indicator. The method of the concentration of 1,2-DCE in blood determining by HS-GC-MS was characterized by high sensitivity, wide linear range, small interference, high precision and easy operation.</p>

Dynamic observation of clinical course in patients with subacute 1, 2-dichloroethane poisoning / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the clinical characteristics and regular patterns of subacute 1, 2-dichloroethane poisoning patients for providing evidences to it's diagnosis, treatment and prognosis.</p><p><b>METHODS</b>51 cases of subacute 1, 2-dichloroethane poisoning analyzed. They were divided into 3 groups according to their main clinical manifestation: group A mainly with intracranial hypertension (n = 25), group B with limbs tremor (n = 18), group C with mental and behavior disorder (n = 8). All cases' clinical symptoms, cranial computer tomography, cerebrospinal pressure (Group A) were observed, the durations of the onset, deterioration, improvement, recovery and whole course of the disease were compared between groups and in each group.</p><p><b>RESULTS</b>In all of 51 cases, only the differences between the deterioration duration of cranial CT and symptom was significantly (t = 2.555, P<0.05), which indicate the deterioration of symptom was earlier than radiological change. The symptom deterioration of group C was the fastest than group A and group B (P<0.00). As to the change of symptom duration, group B's improvement, recovery and whole course was the longest comparing with group A and group C (P<0.05). As to the change of cranial CT duration, group B's recovery duration was the shortest and group A's recovery duration was the longest (P<0.01); group B's whole course was also the shortest and group A's whole course was the longest (P<0.05). The clinical course of symptoms, cranial computer tomography, cerebrospinal pressure (Group A) was compared in each group, in group A, the duration of improvement and whole course of the cranial CT and cerebrospinal pressure change was longer than that of the symptom change (P<0.01), this indicated that group A has longer asymptomatic intracranial hypertension and their cranial radiography recover slowly. In group B, their symptoms (3.94 ± 4.31 days) deteriorated is earlier than cranial CT changes (P<0.05), the recovery (92.39 ± 55.04 days) and whole course of symptom was longer than cranial CT change (all P<0.01). In group C, symptom deterioration was earlier than CT deterioration (P< 0.05).</p><p><b>CONCLUSION</b>The clinical characteristic of subacute 1, 2- dichloroethane poisoning is central nervous system damage, it differs according to the different stage of course, the regions and severity of pathology lesions.</p>

Establishment of a rat model of subacute toxic encephalopathy induced by 1, 2-dichloroethane / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To establish a rat model of 1,2-dichloroethane (DCE)-induced subacute toxic encephalopathy.</p><p><b>METHODS</b>Sixty Sprague-Dawley rats were randomly divided into five groups: negative control, positive control, low-dose DCE (1 472 mg/m(3)), middle-dose DCE (2 550 mg/m(3)), and high-dose DCE (4 418 mg/m(3)). The three DCE groups received static inhalation of DCE 6 hours a day for 6 consecutive days. The positive control group received intraperitoneal injection of lipopolysaccharide (5 mg/kg) and were sacrificed 8 hours after injection. Blood and brain tissue were collected, followed by determination of brain water content and HE staining for pathological examination of brain tissue.</p><p><b>RESULTS</b>The rats in DCE groups suffered decreased body weight with increasing DCE dose (P < 0.01), and brain water content rose with increasing DCEdose. The brain water content of middle-dose DCE group (80.09 ± 0.14%) and high-dose DCE group (80.28±0.10%) increased significantly as compared with that of the negative control group (79.46±0.23%) (P < 0.001). Optical microscopy discovered loose structure and vasodilation in the brain tissue of middle-dose DCE group, indicating obvious brain edema; the high-dose DCE group and positive control group had spongiform and vacuolated brain tissues with severe vascular dilation, indicating severe brain edema.</p><p><b>CONCLUSION</b>A rat model of subacute toxic encephalopathy induced by 1, 2-dichloroethane has been successfully established.</p>

The effects of 1,2-dichloroethane on the cellular proliferation, cellular cycle and apoptosis of SW620 cells in vitro / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of 1,2-dichloroethane (1,2-DCE) on the cellular proliferation, cellular cycle and apoptosis of SW620 cells in vitro.</p><p><b>METHODS</b>SW620 cells were exposed to 1,2-DCE at different concentrations for 0.5 and 1 h. MTT assay was used to detect the relative number and relative viability, the low cytometry (FCM) assay was utilized to measure the cell cycle and apoptosis.</p><p><b>RESULTS</b>The results of MTT assay showed that the cellular relative viability decreased with the 1,2-DCE's dose and exposure time. Compared with the DMSO group, the relative cellular viability of cells exposed to 1,2-DCE at the doses of 75, 100, 125, 150, 175, 200 µmol/L for 1 h decreased (P<0.05 or P<0.01). Compared with the groups exposed to 1,2-DCE for 0.5 h, the relative cellular viability of cells exposed to 175 µmol/L 1,2-DCE for 1 h decreased significantly (P<0.01). IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 0.5 h was 89.41 µmol/L, and 95% confidence interval was 85.23 to 93.79 µmol/L. IC(50) of cellular proliferation in cells exposed to 1,2-DCE for 1 h was 87.68 µmol/L, and 95% confidence interval was 83.71 to 91.82 µmol/L. The results of FCM indicated that compared with the control group, the G(0)/G(1) phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h decreased significantly (P<0.05 or P<0.01), the S phase in groups exposed to 1,2-DCE at the doses of 25, 50 and 100 µmol/L for 1 h reduced significantly (P<0.05 or P < 0.01), the G(2)/M phase in groups exposed to 1,2-DCE at the doses of 25, 50, 100, 150 and 200 µmol/L for 1 h increased significantly (P<0.05 or P<0.01). However, 1,2-DCE could not induce apoptosis of SW620 cells.</p><p><b>CONCLUSION</b>1,2-DCE could inhibit the proliferation of SW620 cells, and arrest SW620 cells at G(2)/M phase, but could not induce the apoptosis of SW620 cells in vitro.</p>

Influence of 1, 2-dichloroethane on open field behavior and levels of neurotransmitters in brain of mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of 1,2-dichloroethane (1,2-DCE) on the behavior and the brain neurotransmitter levels in mice.</p><p><b>METHODS</b>Thirty mice were randomly divided into four groups, which were control group and groups of low, middle and high exposure (225, 450 and 900 mg/m3) to 1,2-DCE for 10 days (3.5 h a day) by inhalation. After the last exposure, the open field test was performed immediately. After exposure all mice were killed and the brain tissues were taken up rapidly. The levels of aspartate (Asp), glutamate (Glu) and gamma-aminobutyric acid (GABA) in the brain were detected by high performance liquid chromatography (HPLC).</p><p><b>RESULTS</b>Levels of Asp and Glu in all exposure groups increased with doses. As compared to the control group, levels of Glu in all exposure groups increased significantly (P < 0.05). Levels of GABA in the low exposure group were significantly lower than those in control group, but those in the high exposure group were significantly higher than those in control group. The results of the open field test showed that effect of low exposure to 1,2-DCE on the behavior was stimulant, but the high exposure to 1,2-DCE inhibited behavior of exploration, excitement and sport.</p><p><b>CONCLUSIONS</b>Subacute exposure to 1,2-DCE could result in the change of amino acid neurotransmitter content and ratio in the brain, thereby change the behavior of mice appeared, which might be the mechanism of neurotoxicity caused by 1,2-DCE in part.</p>

Detecting DNA damage of human lymphocytes exposed to 1,2-DCE with γH2AX identified antibody using flow cytometer assay / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study DNA damage of human peripheral blood lymphocytes exposed to 1,2-dichloroethane (1,2-DCE) with flow cytometry (FCM) assay.</p><p><b>METHODS</b>The lymphocytes were obtained from 21 workers who are occupationally exposed to 1,2-DCE (exposed group) and 27 workers who were not exposed to 1,2-DCE in the same factory (inner control) and 28 island residents who had never been occupationally exposed to adverse factors (external control). FCM assay was adopted to detect DNA damage of the lymphocytes of each group. Lymphocytes of the health people were incubated with 1,2-DCE at different doses, and FCM assay was used to detect DNA damage.</p><p><b>RESULTS</b>DNA damage rate (%) of the exposed group of exposed workers (4.05% ± 2.55%) was significantly higher than the inner control group of workers (1.97% ± 1.40%) and external control groups of island residents (0.23% ± 0.13%), and the DNA damage of inner control was higher than the external control, all the differences were statistically significant (P < 0.01 or P < 0.05). The geometric mean fluorescence intensity of the workers in the exposed group (3.33 ± 3.01) was significantly higher than the (2.07 ± 0.58) only (P < 0.05). There was no significant difference in the DNA damage rate as well as the geometric mean fluorescence intensity among the exposed group of workers with different years of working period (P > 0.05). In vitro, the fluorescence intensity at the dose of 20, 30 µmol/L for 0.5 h exposure showed statistical significance compared with the negative control group (P < 0.01). The DNA damage rate at the dose of 20, 30 µmol/L for 1.0 h exposure was statistically significant compared with the negative control group (P < 0.05, P < 0.01); The fluorescence intensity at the dose of 10, 20, 30 µmol/L for 1.0 h exposure was statistically significant compared with the negative control group (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>1,2-DEC can cause DNA damage. And γH2AX FCM assay can be a sensitive, objective and effective method of detecting DNA damage of peripheral blood lymphocytes.</p>

MRI image analysis of 1,2-dichloroethane chronic toxic encephalopath / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the MRI features of 1,2-dichloroethane Chronic Toxic Encephalopathy of 10 cases.</p><p><b>METHOD</b>10 cases were examined by MRI, slice thickness 8 mm, layer from 2 mm, axial and coronal line scan, T1WI, T2WI, FLAIR imaging.</p><p><b>RESULTS</b>10 cases show varying degrees of abnormal signal of white matters, low signal intensity on T1WI, high signal intensity on T2WI and FLAIR. MRI could also show extensive abnormal signal in cerebral white matter although the toxic manifestation is mild to moderate. Therefore the symptoms and the shows of MRI could be inconsistent.</p><p><b>CONCLUSION</b>Combined with a history of exposure, the show of varying degrees of abnormal signal of white matter in 1,2-dichloroethane Chronic Toxic Encephalopathy cases are characteristic.</p>

Clinical and cranial MRI analysis on five cases of toxic encephalopathy induced by dichloroethane / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the clinical features, cranial MRI and treatment of toxic encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE).</p><p><b>METHODS</b>The clinical, MRI features and treatment of 5 patients with toxic encephalopathy induced by 1,2-DCE were observed and analyzed.</p><p><b>RESULTS</b>Five patients all presented with subacute onset with a history of direct exposure to 1,2-DCE. Lumbar cerebrospinal fluid pressures were all increased in 5 patients. All 5 patients had obvious intracranial hypertension. Liver and kidney function had no obvious abnormalities; Cranial MRI showed T1WI low signal and T2WI high signal in bilateral hemispheric white matter, cerebellar dentate nucleus and globus pallidus. After the treatment of dehydrating agent, glucocorticoid and supportive treatment, four patients were clearly improved, and one patient had cerebral hernia formation.</p><p><b>CONCLUSION</b>The main neurological clinical features in patients with 1,2-DEC poisoning is obvious intracranial hypertension. The prognosis is usually good with early and long term use of glucocorticoids and dehydrating agent in poisoning patients.</p>

efficacy of turmeric to alleviate chlorinated solvents-induced oxidative status on rats

Purpose is to examine the possible influence of turmeric as natural antioxidant on 1,2-dichloroethane [1,2DCE] induced oxidative status in rats. Thirty five adult male albino rats Sprague-Dawley strain were divided into five groups [7rats each]. Group A served as negative control fed basal diet. Group B [positive control] fed standard diet and 1,2DCE added [313mg / 100 g diet] for 4 weeks. Group C fed standard diet + 1,2DCE + curcumin 0.5% for 4 weeks as a protective group. Group D fed standard diet + curcumin 0.5% for 4 weeks after that added 1,2 DCE to 4 weeks as a preventive group. Group E fed standard diet + 1,2DCE for 4 weeks after that added turmeric 0.5% for 4 weeks as a curative group. Levels of Glutathione [GSH], Superoxide dismutase [SOD] and Malondialdehyde [MDA] were determined in homogenate kidneys, brain, and lungs of rats. RNA and DNA were extracted from brain homogenate. Determination of serum: total protein, urea, uric acid and creatinine. The results showed that both of GSH, SOD, RNA and DNA increased in rats' tissue for treated groups with turmeric but MDA is decreased versus positive groups. The analysis of serum explains alleviating the adverse effect of chlorinated solvents on rats that fed turmeric. kidney, lung and brain, these organs representing important target organs of chlorinated solvents toxicity and the turmeric as a natural antioxidants alleviated effect of these pollutant

Expression of N-methyl-D-aspartate receptor 1 in acute intoxicated encephalopathy induced by 1,2-dichloroethane / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the role of N-methyl-D-aspartate receptor 1 in acute intoxicated encephalopathy induced by 1,2- dichloroethane(1,2-DCE).</p><p><b>METHODS</b>Forty-two Sprague-Dawley rats, which had been randomly divided into 1 control, 3 exposure and 3 after-exposure observation groups were exposed to 1,2-DCE for 12 hr by continual static inhalation except control group. Dosage of exposure groups was 5.0, 10.0, 20.0 g/m(3) on sequence. That of after-exposure observation groups was 10.0 g/m(3). Rats of after-exposure observation groups were observed continually for 2,4,6 hr after exposure. The expression of N-methyl-D-aspartate receptor-1 (NMDAR1) was detected by immunohistochemical method.</p><p><b>RESULTS</b>NMDAR1 stained neurons were mainly distributed at cerebral cortex and hippocampus. Compared with that of control group, the percentages of positive cells of NMDAR1 increased evidently at 10.0, 20.0 g/m(3) groups (P < 0.05). They were (18.33 +/- 1.86)%, (64.17 +/- 2.86)% at cerebral cortex, (15.5 +/- 1.87)%, (47.83 +/- 2.16)% at hippocampus. The percentages were also elevated obviously in 2, 4, 6 h after-exposure observation groups. They were (39.07 +/- 3.01)% (70.17 +/- 2.93)% (39.83 +/- 2.32)% at cerebral cortex, (16.30 +/- 1.03)% (19.80 +/- 1.17)% (16.50 +/- 1.05)% at hippocampus; Compared with that of 10.0 g/m(3) group, the percentages increased significantly only in 4 hr group at hippocampus.</p><p><b>CONCLUSION</b>The overactivation of NMDAR1 is the main route by which excitatory amino acids chose to join the development of acute intoxicated encephalopathy induced by 1,2-DCE.</p>

Change of neurocytes in acute intoxicated encephalopathy induced by 1, 2-dichloroethane after intervention with antagonists / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the role of N-methyl-D-aspartate receptor and Ca(2+) in acute intoxicated encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE) in vitro.</p><p><b>METHODS</b>Neurocytes of new born rats were cultured in vitro, which were administered with different doses of 1, 2-DCE, and NMDAR and Ca(2+) antagonists including Ketamine and Nimodiping respectively. The cell morphologic structures were observed under light microscope, and its proliferation was detected by Cell Counting Kit-VIII.</p><p><b>RESULTS</b>1, 2-DCE could damage the normal morphological structure of neurocytes: the cell body swelled and broke down, the karyon slurred or disappeared, the axone became shorten and thick, connection of neurocytes was reduced, the cell membrane was half-baked, injury of neurocytes became severer with the increase of the dose of 1, 2-DCE. There was no statistical difference in the proliferation of neurocytes between every 1, 2-DCE groups (P > 0.05), but there was significantly statistical difference between 1, 2-DCE groups, the control group, and the retarder groups (P < 0.01).</p><p><b>CONCLUSION</b>1, 2-DCE can damage the normal morphological structure of neurocytes, and the damage will become severer with the increase of the dose of 1, 2-DCE. However, the cell morphologic structures and proliferation of antagonist groups are much better than those in the 1, 2-DCE groups.</p>

Effect of 1, 2-dichloroethane on blood brain barrier / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of 1, 2-dichloroethane (1, 2-DCE) on blood brain barrier.</p><p><b>METHODS</b>Acute toxic encephalopathy model was copied with the consecutive static inhalation of 1, 2-DCE. The water content of brain tissue was measured, and the blood brain barrier permeability was detected with lanthanum nitrate. The brain microvascular endothelial cells and neuroglial cells were cultured in vitro, which were administrated with 1, 2-DCE. The cell morphologic structures were observed under light microscope and electron microscope.</p><p><b>RESULTS</b>(1) The extracellular edema was most found in the cerebral tissue and the leakage of lanthanum particles through the barrier were found with the lanthanum tracking method. (2) The water content in cerebral cortex in the moderate and high dose groups was significantly higher than that in the control group and became severer with the increases of the intoxicated time. The water content in cerebral medulla was significantly increased only at 6 hours after the intoxication. (3) The normal morphological structure of brain microvascular endothelial cells and neuroglial cells could be injured by 1, 2-DCE, and the injury to neuroglial cells caused by 1, 2-DCE occurred earlier and severer than that to brain microvascular endothelial cells.</p><p><b>CONCLUSION</b>1, 2-DCE can damage blood brain barrier and induce cerebral edema.</p>

The relationship between excitatory amino acids and acute intoxicated encephalopathy induced by 1,2-dichloroethane / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the relationship between excitatory amino acids (EAAs) and acute in toxicated encephalopathy induced by 1,2-dichloroethane (1,2-DCE).</p><p><b>METHODS</b>SD rats were randomly divided into 7 groups: 1 control group, 3 exposure (5.0, 10.0, 20.0 g/m(3)) groups and 3 duration (2, 4, 6 h after 10.0 g/m(3) exposure) groups. Rats were exposed to 1,2-DCE for 12 h by continual static inhalation. Water content of cerebral cortex and medulla was measured by wet-dry method; The contents of glutamate (Glu), aspartate (Asp), glycine (Gly) and gamma-aminobutyric acid (GABA) in brain tissues were determined by high performance liquid chromatography (HPLC).</p><p><b>RESULTS</b>Water content of cerebral cortex in 3 exposure groups (76.10% +/- 1.41%, 76.45% +/- 0.75%, 79.95% +/- 1.45% respectively) were higher than that of control group (74.22% +/- 1.77%, P < 0.05, P < 0.01). That of medulla was increased significantly merely at 20.0 g/m(3) (71.77% +/- 3.07%, P < 0.05). Water content of cortex in 3 duration groups (79.36% +/- 2.10%, 79.48% +/- 1.21%, 80.64% +/- 1.93% respectively) were higher than that of 10.0 g/m(3) instant exposure group (P < 0.05). The content of Asp [(4.83 +/- 0.35) micro mol/g, (7.17 +/- 0.40) micro mol/g, (10.52 +/- 0.39) micro mol/g], Glu [(23.86 +/- 0.62) micro mol/g, (31.21 +/- 2.50) micro mol/g, (28.23 +/- 1.58) micro mol/g] and Gly [(5.59 +/- 1.01) micro mol/g, (6.06 +/- 0.83) micro mol/g, (7.26 +/- 1.34) micro mol/g] in exposure groups were higher than those of corresponding control groups [(3.72 +/- 0.48) micro mol/g, (21.09 +/- 1.20) micro mol/g, (3.83 +/- 0.44) micro mol/g, P < 0.05, P < 0.01]. Compared to 10.0 g/m(3) instant group, Asp content was increased at 2, 4, 6 h (P < 0.01), Glu content at 2, 4 h (P < 0.05), and peak value of Glu appeared at 4 h [(35.40 +/- 2.40) micro mol/g] while Gly content was significantly decreased (P < 0.01). GABA did not show evident changes in both exposure or duration groups (P > 0.05).</p><p><b>CONCLUSION</b>EAAs appears to be related with the development of acute intoxicated encephalopathy induced by 1,2-DCE, and its damage to neuron might be one of the mechanisms of brain edema.</p>

Growth inhibitory and antifeedant activity of extracts from Melia dubia to Spodoptera litura and Helicoverpa armigera larvae.

The growth inhibitory activity and deterrency of Melia dubia (Meliaceae) extracts to Spodoptera litura and Helicoverpa armigera were investigated. Artificial diet bioassays using neonate larvae of both S. litura and H. armigera indicated that dichloroethane (DCE) and methanol (Me) extracts of M. dubia inhibited growth in a dose dependent manner. DCE and Me-5II fractions also resulted in 50% deterrency at concentrations of 22.5 and 16.8 micrograms/cm2 respectively against S. litura larvae in a leaf disc-choice test. The DCE-5 fraction was found to be more toxic to larvae (LC50 of 0.65%) than the Me-5II (LC50 of 0.8%), 72 hr after topical application. Both fractions lack contact toxicity, but the deterrent effect persisted for at least 60 hr under laboratory conditions. Although salannin was isolated from the DCE fraction to show antifeedant activity, the physico-chemical characteristics of the active fractions DCE-5 and Me-5II were not identical with either salannin or azadirachtin.

Development of a modified method for the simultaneous determination of vinyl chloride monomer and ethylene dichloride in the air

A commercial grade activated carbon has been used as an adsorbent medium. It has been loaded via a simple device with different mixtures of vinyl chloride and ethylene dichloride each administered separately. About 3 g of loaded active carbon is put in a vacutainer tube while 10 ml of technical grade CS2 as adsorbent is added. The tube is stoppered and stored at 4C. After 24 hours, 1 ml aliquot is injected through a closed loop to a precalibrated infrared gas analyzer to assess the percentage recovery of vinyl chloride and ethylene dichloride. The spent activated carbon is washed thoroughly with water and is dried in two stages [at 50C for 8 hours and at 120C for 16 hours] to be used again. The procedure is accurate, precise, simple and economic. It gave percentage recoveries of 85% for VCM and 100% for EDC. It depends on the available resources, making it a suitable methodology to be applied in a developing country

Performance of a modified method for the simultaneous determination of vinyl chloride monomer and ethylene dichloride in the atmosphere of a petrochemical plant in Alexandria

Ethylene dichloride [EDC] and vinyl chloride monomer [VCM] are considered the major air pollutants associated with any petrochemical industry. The two pollutants are categorized as carcinogenic substances for man and animal. Large number of samples were collected from the air of a Petrochemical Plant in Alexandria during a period of 12 months to study the efficiency, accuracy and applicability of a modified method for the simultaneous determination of VCM and EDC in the air. For this purpose, different sampling stations were selected inside the plant and at its walls. Samples of VCM and EDC were collected simultaneously by adsorption on the surface of activated charcoal and then analyzed by a chemical desorption process using carbon disulfide [CS2]. Levels of VCM and EDC were determined by an infrared spectrophotometer