Objective To investigate the effect of occupational noise on heart rate turbulence (HRT) in workers.Methods A total of 96 workers occupationally exposed to noise enrolled as exposed group and 95 workers without noise exposure enrolled as control group were chosen for examination of 24 h dynamic electrocardiograph (Holter).A total of 51 workers of exposed group showed ventricular premature complexes,while in workers of control group,49 workers showed ventricular premature complexes in records of Holter.According to two basic indices:turbulence onset(TO)and turbulence slope(TS) were obtained,the cut-off values for positive results in TO and TS were≥0 and ≤2.5 ms/RRI.Thereby,HRT might be classified into three categories:HRT 0 (TO＜0 and TS＞2.5 ms/RRI),HRT 1 (TO≥0 or TS≤2.5 ms/RRI) and HRT 2 (TO≥0 and TS≤2.5 ms/RRI).Results The results showed that compared with the control group,the levels of TO in exposed group were significantly higher [(-0.01±3.18)％ VS (-1.72±2.09)％],while the level of TS was significantly lower than that in control group [(7.23± 4.33) ms/RRI vs (9.72±5.03) ms/RRI,P＜0.05)];additionally,the proportion of HRT 0 in exposed group was significantly lower than that in control group (41.2％ vs 79.6％,P＜0.05),the proportions of HRT 1 and HRT 2 in exposed group were significantly higher than that in control group (39.2％ vs 16.3％ and 19.6％ vs 4.1％,P＜0.05).Conclusion The results indicated that HRT in noise exposed workers was significantly attenuated,which suggested that occupational noise exposure may result in impairment of cardiac autonomic nerve's activity.

通过对一起职业性急性加氢裂化催化剂中毒事故中的5位患者的临床表现、实验室检查结果和职业卫生学调查资料进行综合分析,探讨中毒途径、可能毒物和中毒原因.结果显示,该次事故是由加氢裂化催化剂暴露引起的以肝脏损害为主的中毒,中毒途径可能是皮肤,毒物可能是美国Criterion公司最新生产的加氢裂化催化剂DN-3552,致毒成分可能是五氧化二磷(P2 O5),事发的直接原因是更换催化剂过程中产生的大量粉尘透过汗湿的皮肤侵入人体导致中毒,但粉尘产生过多的原因尚不明确.提示,加氢裂化催化剂可致中毒性肝损伤,在启用新型催化剂时应严格按规范操作,作业过程中出现明显异常时应及时查找原因防止发生事故.

《环境与职业医学》杂志2017年第4期发表的《1例职业性急性中度中毒性脑病的诊断讨论》 [1] 一文作者（以下简称作者）结合职业病诊断中的实际案例,对1例印染企业涂层车间打卷岗位患者,诊断为职业性急性中度中毒性脑病的诊断过程进行了详尽的分析和讨论。病例资料和用人单位资料可以参见原文,笔者在此不再赘述。具体看一下作者对这一案例的诊断依据:"根据GBZ 71—2013《职业性急性化学物中毒的诊断总则》

Background: The Acute Physiology and Chronic Health Evaluation II (APACHE II) score is used to determine disease severity and predict outcomes in critically ill patients. However, the prognostic significance of APACHE after acute paraquat (PQ) poisoning remains unclear. The meta-analysis was aimed to study the value of APACHE II in predicting mortality in PQ-exposed Chinese and Korean patients. Methods: Databases that included PubMed, Embase, Cochrane Library, and the Chinese National Knowledge Infrastructure were searched through August 2016. Studies using APACHE II to predict mortality in PQ-poisoned patients were selected. The odds ratio and weighted mean difference (WMD) were used to pool binary and continuous data. Additionally, we aggregated sensitivity, specificity, and other measures of accuracy. Statistical analyses were made using the Stata V.13.0 software. Results: This study included 29 studies, and 25 studies evaluated APACHE II scores on admission. Pooled data showed that survivors had significantly lower total scores than nonsurvivors (WMD = –7.29, and I2 = 98.2%, both P <.05). The pooled sensitivity of an APACHE II score ≥5 for predicting mortality was 75% and the pooled specificity was 86%. The positive likelihood ratio (PLR) was 5.3 and the negative likelihood ratio (NLR) was 0.29. The pooled sensitivity of an APACHE II score ≥10 for predicting mortality was 88% and the pooled specificity was 84%. The pooled PLR and NLR was 5.5 and 0.15, respectively. Conclusion: This study showed PQ-poisoned nonsurvivors had significantly higher APACHE II score than did survivors. APACHE II scores satisfactorily predicted mortality.

Background:The Acute Physiology and Chronic Health Evaluation II (APACHE II) score is used to determine disease severity and predict outcomes in critically ill patients. However, the prognostic significance of APACHE after acute paraquat (PQ) poisoning remains unclear. The meta-analysis was aimed to study the value of APACHE II in predicting mortality in PQ-exposed Chinese and Korean patients. Methods:Databases that included PubMed, Embase, Cochrane Library, and the Chinese National Knowledge Infrastructure were searched through August 2016. Studies using APACHE II to predict mortality in PQ-poisoned patients were selected. The odds ratio and weighted mean difference (WMD) were used to pool binary and continuous data. Additionally, we aggregated sensitivity, specificity, and other measures of accuracy. Statistical analyses were made using the Stata V.13.0 software. Results:This study included 29 studies, and 25 studies evaluated APACHE II scores on admission. Pooled data showed that survivors had significantly lower total scores than nonsurvivors (WMD=-7.29, and I-2=98.2%, both P<.05). The pooled sensitivity of an APACHE II score >= 5 for predicting mortality was 75% and the pooled specificity was 86%. The positive likelihood ratio (PLR) was 5.3 and the negative likelihood ratio (NLR) was 0.29. The pooled sensitivity of an APACHE II score >= 10 for predicting mortality was 88% and the pooled specificity was 84%. The pooled PLR and NLR was 5.5 and 0.15, respectively. Conclusion:This study showed PQ-poisoned nonsurvivors had significantly higher APACHE II score than did survivors. APACHE II scores satisfactorily predicted mortality.

[目的]研究噪声对作业工人心率变异性(heart rate variability,HRV)的影响.[方法]选取某公司动力车间单纯接触噪声的作业人员96人为噪声接触组,同时选取同一单位不接触噪声的工作人员95人为对照组,两组均进行24 h动态心电图检查,测量或计算24 h平均心率(HR)和HRV时域指标24 h全部窦性RR间期的标准差(SDNN)、24 h内全部窦性RR间期差值的均方根(RMSSD)、24 h内相邻两个正常窦性RR间期差值大于50 ms的个数所占的百分数(PNN50),及频谱指标高频功率(HF)、低频功率(LF)、极低频功率(VLF),比较接触组与对照组各指标的差异,并分析接触组HRV各指标与工龄、年龄、性别、HR的相关性.[结果]接触组SDNN、PNN50、LF、VLF低于对照组,HR高于对照组(P<0.05);接触组中SDNN、PNN50、LF、VLF与工龄及HR呈负相关(r=-0.582~-0.283,P<0.05),与性别无相关性(P>0.05),SDNN、PNN50、LF与年龄呈负相关(r=-0.233~-0.211,P<0.05).[结论]噪声作业工人心率变异性降低,提示长期的噪声接触可引起作业工人自主神经功能紊乱.

Objective: To investigate the exposure to benzene, methylbenzene, and dimethylbenzene in workers in a petrochemical enterprise in Shanghai, China, and to conduct occupational hazard risk assessment. Methods: The environmental monitoring data on benzene series in the workplace of this petrochemical enterprise from 2010 to 2014 were collected, as well as workers' general status. The inhalation risk assessment model developed by United States Environmental Protection Agency (EPA) was used for risk assessment to determine the occupational hazard risk level of benzene, methylbenzene, and dimethylbenzene. Results: The pass rate of the monitoring concentration of benzene, methylbenzene, and dimethylbenzene in the workplace of this petrochemical enterprise was 100%. The results of the EPA model showed that benzene had a high carcinogenic risk, benzene and dimethylbenzene had a high non-carcinogenic risk, and methylbenzene had a low non-carcinogenic risk. Conclusion: The workers exposed to benzene in this petrochemical enterprise have a high health risk, and the EPA model can be used for occupational hazard risk assessment in chemical industry.

Many studies aimed at investigating bone repair have been conducted through animal models in recent years. However, limitations do exist in these models due to varying regeneration potential among different animal species. Even using the same animal, big differences exist in the size of critical size defects (CSD) involving the same region. This study aimed to investigate the standardization of radial bone defect models in rabbits and further establish more reliable CSD data. A total of 40 6-month-old New Zealand white rabbits of clean grade totaling 80 radial bones were prepared for bone defect models, according to the principle of randomization. Five different sizes (1.0, 1.2, 1.4, 1.7 and 2.0 cm) of complete periosteal defects were introduced under anesthesia. At 12 weeks postoperatively, with the gradual increase in defect size, the grades of bone growth were significantly decreased in all 5 groups. X-ray, CT scans and H&E staining of the 1.4, 1.7, and 2.0-cm groups showed lower grades of bone growth than that of the 1.0 and 1.2-cm groups respectively (P < 0.05). Using rabbit radial defect model involving 6-month-old healthy New Zealand white rabbits, this study indicates that in order to be critical sized, defects must be greater than 1.4 cm.

本文概述了急性钡中毒的流行病学、发病机制、临床表现、诊断及治疗,以期为研制标准提供科学依据.

Background/Aims: Benzene is a toxic chemical whose leukemogenic effects have been studied for decades. The mechanisms of benzene-induced toxicity and leukemogenicity are not fully understood, although the involvement of several pathways has been suggested, including oxidative stress, DNA damage, cell cycle regulation and programmed cell death. In the present study, we investigated the effect of hydroquinone (HQ), a major benzene metabolite, on the viability of bone marrow derived mesenchymal stem cells (BMSCs) and explored the underlying mechanisms. Methods: First, we study the the effect of HQ on BMSCs cell viability, apoptosis and the expressions of MDR1 and NF-κB. Then we investigate the MDR1 on cell viability and cell apoptosis for BMSCs under HQ treatment. Finally, we studied the impact of nuclear factor κB (NF-κB) on the expression of MDR1. Results: Our results showed that HQ decreased cell viability and promoted cell apoptosis of BMSCs, as determined by the MTT assay and flow cytometry. Western blotting and quantitative PCR showed that HQ downregulated the expression of the MDR1 gene by inhibiting the activation and nuclear translocation of the transcription factor NF-κB. Overexpression of MDR1 attenuated the inhibitory effect of HQ on cell viability in BMSC. Conclusion: The results of the present study suggest the involvement of the multidrug resistance membrane transporter MDR1 and the NF-κB pathway in the cytotoxicity of benzene and its metabolites. Further studies are necessary to clarify the role of the pathways involved and the crosstalk between them in mediating the effects of HQ in bone marrow progenitor cells.

Alterations in the expression of microRNAs (miRNAs or miRS) have been implicated in the pathogenesis of the majority of human malignancies, and the dysregulation of microRNA-144 (miR-144) has been associated with several diseases. However, the potential involvement of miR-144 in osteosarcoma, a common malignant bone tumor in children and adolescents with a high risk of relapse and metastasis, has not yet been fully investigated. In the present study, we examined the expression and roles of miRNAs in osteosarcoma as potential diagnostic markers and therapeutic targets, and we focused on miR-144 due to its known involvement in osteogenesis. We demonstrate that miR-144 is downregulated in osteosarcoma cell lines and primary human osteosarcoma tissue samples and that its ectopic expression inhibits osteosarcoma cell proliferation and invasion. We identified TAGLN as a downstream target of miR-144 and demonstrated that its expression is upregulated in osteosarcoma cell lines and tumor tissue and is inversely correlated with miR-144 expression. Our results indicate that miR-144 may regulate osteosarcoma cell proliferation and invasion by downregulating its target gene, TAGLN, suggesting that miR-144 may be a potential therapeutic target for the treatment of osteosarcoma.

OBJECTIVE:To explore the effects of acrylonitrile on T lymphocyte subsets, expression of toll-like receptor 4 and related cytokines in rats.METHODS:Sixty-four Sprague-Dawley rats were randomly divided into 4 female groups and 4 male groups, and there were 8 rats in each group. Rats in each group were respectively given a single dose of 0, 5, 10 and 20 mg/kg acrylonitrile by gavage, once a day, 5 days a week, for 13 weeks. Blood and spleen T lymphocyte subsets was detected by flow cytometry, the mRNA expression of TLR4, IL-1β and TNF-α was analyzed by real-time quantitative PCR, the protein expression of TLR4 was evaluated by Western blot.RESULTS:Compared with control group, the percentages of blood CD3, CD4 T cells in 20 mg/kg female group and CD4/CD8 ratio in 5, 10 and 20 mg/kg female groups was significantly decreased, CD8 T cells in 20 mg/kg group was significantly increased (P < 0.05 or P < 0.01), blood CD3 T cells in 5 mg/kg male group, CD4 T cells and CD4/CD8 ratio in 20 mg/kg male groups were lower than that of control group, CD8 T cells in 20 mg/kg make group was significantly in oreased (P < 0.05 or P < 0.01). Spleen CD4, CD8 T lymphocyte percentages and CD4/CD8 ratio in 20 mg/kg female group decreased significantly, CD8 T cells in 20 mg/kg male group was significantly increased (P < 0.05 or P < 0.01), spleen CD3, CD4, CD8 T cells in 20 mg/kg male group and CD4/CD8 ratio in 10, 20 mg/kg male groups was also significantly decreased, CD3 T cells in 20 mg/kg and CD8 T cells in 10, 20 mg/kg male groups were significantly increased (P < 0.05 or P < 0.01) (TLR4 mRNA was lower expressed in 5, 10 and 20 mg/kg male groups and 10 mg/kg female group (P < 0.05 or P < 0.01), and TLR4 protein in 5 mg/kg female group and 20 mg/kg male group was significantly lower than control group (P < 0.05). The expression level of IL-1β mRNA was significantly decreased in 5, 10 and 20 mg/kg female group and 5, 10 mg/kg male group (P < 0.05 or P < 0.01), TNF-α mRNA was lower expressed in 10, 20 mg/kg female groups and 5, 10 mg/kg male groups (P < 0.01).CONCLUSION:Acrylonitrile may lead to the changes of CD3, CD4, CD8 T lymphocyte percentages and CD4/CD8 ratio in rat blood and spleen, and also significantly effected the expression level of TLR4 mRNA and protein together with the secretion of IL-1β, TNF-α. This may cause effects on the cellular immune function.

OBJECTIVE:To evaluate the impact of exposure to low concentrations of benzene on the platelet-associated antibodies and platelet parameters.METHODS:We carried out an analysis on 121 benzene-exposed workers and 110 healthy workers whose blood samples were collected and the levels of platelet-associated antibodies and platelet parameters were assessed. Benzene emissions were monitored over 5 years.RESULTS:Large-platelet cell ratios (P-LCR), platelet distribution width (PDW), and mean platelet volume (MPV) were significantly higher in benzene-exposed participants than in control participants. In participants who smoke cigarettes or drank alcohol, P-LCR, PDW, and MPV were more significantly elevated in the benzene-exposed group than in nonsmokers and nondrinkers. Platelet-associated immunoglobulin (PAIg) levels in benzene-exposed participants were higher than those in the control group, and PAIgA and PAIgM levels correlated with cumulative benzene exposure.CONCLUSIONS:Exposure to low concentrations of benzene can induce changes in PAIg levels and platelet parameters.

目的 分析不同中毒途径急性甲苯及二甲苯中毒的临床特点,为修订GBZ 16-2002《职业性急性甲苯中毒诊断标准》提供依据.方法 利用生物医学全文期刊(OVID)、中国生物医学文献数据库(CMBDisc)、中国科技期刊数据库、中国知网、万方数据资源系统等数据库,检索1979年1月至2011年12月国内公开发表的急性甲苯或二甲苯中毒病例的中文文献,将病例分为呼吸道中毒和消化道中毒,并进行比较.结果 呼吸道中毒潜伏期31～60 min 24例(32.43％)、61～120 min 13例(17.57％)、＞120 min 1例(1.35％).消化道中毒潜伏期0～30 min 0例(0.00％)、31～60 min 5例(27.78％)、61～120 min11例(61.11％)、＞120 min 2例(11.11％).急性甲苯、二甲苯中毒的主要临床表现依次为头晕(87.26％)、恶心(66.02％)、呕吐(61.78％)、头痛(57.92％)、乏力(55.60％)、意识障碍(47.88％).呼吸道中毒的突出临床表现为头晕(91.58％)等神经系统症状,消化道中毒的突出临床表现为呕吐(75.36％)等消化系统症状,辅助检查可见肝肾异常功能异常.6例猝死仅见于呼吸道中毒.结论 呼吸道中毒和消化道中毒的起病特征有所不同,在诊治急性甲苯、二甲苯中毒时,应首先区分呼吸道或消化道中毒。

OBJECTIVE:To analyze the clinical features and diagnostic points of occupational acute dimethylformamide (DMF) poisoning and to explore the mechanism of occupational acute DMF poisoning.METHODS:A comprehensive analysis was performed on the clinical data of 16 cases of occupational acute DMF poisoning, including symptoms, signs, and laboratory testing results.RESULTS:The main clinical features of occupational acute DMF poisoning were digestive system impairments, especially abdominalgia. Hemorrhagic gastroenteritis was not found by gastroscopy. There was no significant correlation between the degree of abdominalgia and alanine aminotransferase level (r(s) = 0.109, P>0.05).CONCLUSION:Abdominalgia is recommended to be one of the reference indices for the diagnosis and degrading of occupational acute DMF poisoning, The mechanism of DMF poisoning remains unclear but it is considered to be related to methyl isocyanate, the intermediate product of DMF metabolism.

Objective To study the impact of acrylonitrile(AN)on Bcl10 protein and mitogen activated protein kinase in signal transmission and to explore the mechanism of its immune-toxicity in rat.Methods Jurkat cell lines were divided into control group and three AN exposed groups,i.e.low concentration group(20 umol/L),medium concentration group(100 umol/L)and high concentration group(500 umol/L),and cultivated in vitro.Lipid raft and Bc110 protein were separated and analyzed.Levels of MEK1 and p-MEK1 were detected by Western Blot.Results As AN concentration of exposure increased,the total amount of Bcl10 kept unchanged;however,the location concentrated mainly in lower area.Western Blot results showed that in a definite range of exposure the secretion of MEK1 protein increased.After the exposure exceeded the definite concentration,the secretion of MEK1 protein decreased,and the concentration of P-MEK1 increased as the exposure increased showing a tendency of gradual lowering.In comparison with the control,the difference showed statistical significant(P0.05).Conclusions AN may produce the immune toxicity through damaging the lipid raft structure and causing the separation of Bcl10 protein and lipid raft,finally inhibiting the mitogen activated tyrosine kinase signal transmission pathway.

目的 分析不同中毒途径急性甲苯及二甲苯中毒的临床特点,为修订GBZ 16-2002《职业性急性甲苯中毒诊断标准》提供依据.方法 利用生物医学全文期刊(OVID)、中国生物医学文献数据库(CMBDisc)、中国科技期刊数据库、中国知网、万方数据资源系统等数据库,检索1979年1月至2011年12月国内公开发表的急性甲苯或二甲苯中毒病例的中文文献,将病例分为呼吸道中毒和消化道中毒,并进行比较.结果 呼吸道中毒潜伏期31～60 min 24例(32.43％)、61～120 min 13例(17.57％)、＞120 min 1例(1.35％).消化道中毒潜伏期0～30 min 0例(0.00％)、31～60 min 5例(27.78％)、61～120 min11例(61.11％)、＞120 min 2例(11.11％).急性甲苯、二甲苯中毒的主要临床表现依次为头晕(87.26％)、恶心(66.02％)、呕吐(61.78％)、头痛(57.92％)、乏力(55.60％)、意识障碍(47.88％).呼吸道中毒的突出临床表现为头晕(91.58％)等神经系统症状,消化道中毒的突出临床表现为呕吐(75.36％)等消化系统症状,辅助检查可见肝肾异常功能异常.6例猝死仅见于呼吸道中毒.结论 呼吸道中毒和消化道中毒的起病特征有所不同,在诊治急性甲苯、二甲苯中毒时,应首先区分呼吸道或消化道中毒.

目的 分析8例急性环氧乙烷中毒的临床特征.方法 采用描述性方法对该组病例的临床表现、治疗和中毒机制等进行分析.结果 急性环氧乙烷中毒观察对象1例,轻度中毒4例(其中合并轻度化学性皮肤灼烧2例),中度中毒1例,重度中毒2例.中毒病例以中枢神经系统损害表现为主,呼吸系统症状表现不明显,部分病例有心肌、肝脏等损害；肌红蛋白升高,病程中胆碱能兴奋症状较明显.给予控制脑水肿、改善脑细胞代谢及高压氧治疗等综合治疗6例轻中度中毒患者痊愈,2例重度中毒患者死亡.结论 吸入高浓度环氧乙烷可致死亡,轻、中度中毒经早期积极治疗预后较好.肌红蛋白可作为早期心肌损伤的参考指标；抗胆碱治疗值得进一步探讨.

目的 分析8例急性环氧乙烷中毒的临床特征.方法 采用描述性方法对该组病例的临床表现、治疗和中毒机制等进行分析.结果 急性环氧乙烷中毒观察对象1例,轻度中毒4例(其中合并轻度化学性皮肤灼烧2例),中度中毒1例,重度中毒2例.中毒病例以中枢神经系统损害表现为主,呼吸系统症状表现不明显,部分病例有心肌、肝脏等损害；肌红蛋白升高,病程中胆碱能兴奋症状较明显.给予控制脑水肿、改善脑细胞代谢及高压氧治疗等综合治疗6例轻中度中毒患者痊愈,2例重度中毒患者死亡.结论 吸入高浓度环氧乙烷可致死亡,轻、中度中毒经早期积极治疗预后较好.肌红蛋白可作为早期心肌损伤的参考指标；抗胆碱治疗值得进一步探讨。

Objective To analyze lipid raft and MEK levels in Ras/Raf/MEK/ERK signal transduction and explore the mechanism of immunotoxicity of T lymphocyte induced by acrylonitrile.Methods Jurkat cells were divided into control group,low concentration group,medium concentration group and high concentration group(ACN 0,20,100 and 500 μmol / l) and analyze lipid raft,Caveolin-l protein and MEK protein level in vitro.Results Cholesterol content was less after 4 hour,which showed that the amount of lipid raft is statistically difference between exposed group and control group(F = 215.42,P 0.05),localization of caveolin-1 was changed for signal transduction.P-MEK strip in higher concentration becomes shallow.Conclusion Acrylonitrile may destroy lipid raft structure,lipid raft decreasing and Caveolin-1 being displaced,signal transduction may be suppressed and then play immunotoxicity.