BACKGROUND:Prolonged occupational noise exposure poses potential health risks, but its impact on mitochondrial DNA (mtDNA) damage and methylation patterns remains unclear. METHOD:We recruited 306 factory workers, using average binaural high-frequency hearing thresholds from pure-tone audiometry to assess noise exposure. MtDNA damage was evaluated through mitochondrial DNA copy number (mtDNAcn) and lesion rate, and mtDNA methylation changes were identified via pyrophosphate sequencing. RESULTS:There was a reduction in MT-RNR1 methylation of 4.52% (95% CI: -7.43% to -1.62%) among workers with abnormal hearing, whereas changes in the D-loop region were not statistically significant (β = -2.06%, 95% CI: -4.44% to 0.31%). MtDNAcn showed a negative association with MT-RNR1 methylation (β = -0.95, 95% CI: -1.23 to -0.66), while no significant link was found with D-loop methylation (β = -0.05, 95% CI: -0.58 to 0.48). Mediation analysis indicated a significant increase in mtDNAcn by 10.75 units (95% CI: 3.00 to 21.26) in those with abnormal hearing, with MT-RNR1 methylation mediating 35.9% of this effect. CONCLUSIONS:These findings suggest that occupational noise exposure may influence compensatory increases in mtDNA content through altered MT-RNR1 methylation.

结合当前化学化工实验室现状和特点,阐述化学化工实验室职业危害通风防护技术进展,归纳变风量通风系统的组成及控制方法和原理,分析比较涉及实验室通风系统的现行标准规范及通风防护的关键技术参数,为化学化工实验室职业病危害防护的标准化研究和制定提供思路借鉴.

Although there are continuous progresses in economy and society, the accelerated aging process has brought widespread impacts on various aspects of society and economy in China, especially on the supply of the working-age population. Effectively addressing labor force aging has become an urgent challenge for China's economic and social development. North American countries, particularly the United States and Canada, are also facing severe aging population issues, and have entered an aging society earlier than China. These countries have alleviated labor supply shortages through proactive immigration policies, while implementing flexible retirement, reemployment of elderly individuals, and vocational training policies to effectively encourage elderly workers to remain in their jobs. Additionally, the occupational health programs of large enterprises in North America have yielded positive returns on their health investments. Building upon an overview of the current situation and corresponding measures in response to the aging working-age population in North America, this paper presented constructive recommendations to address the aging population issue in China.

Few studies have been conducted that use biomarkers as early warning signals for noise-associated health hazards. To explore potentially effective biomarkers for noise-exposed populations, we recruited 218 noise-exposed male workers in China. We calculated cumulative noise exposure (CNE) through noise intensity and noise-exposed duration. When the model was fully adjusted, ln-transformed relative mitochondrial DNA copy number (mtDNAcn) decreased by 0.014 (95% confidence interval (CI): -0.026, -0.003) units with each 1 dB(A)& BULL;year increase in CNE levels. CNE was further included in the model as a grouping variable, and the results showed a negative dose-effect relationship between relative mtDNAcn and CNE (P-trend = 0.045). However, we did not find a correlation between CNE and micronucleus (MN) frequencies. Our findings suggest that CNE in workers was associated with a decrease in relative mtDNAcn which may provide a potential biomarker for noise and for certain health risk but not with MN frequencies.

In the context of facing the dual challenges of aging population and declining birth rates, the absolute number of working-age population in China is decreasing, while the proportion of middle-aged and elderly workers is significantly increasing. However, China possesses a vast labor force, and the advantages of talent dividend are gradually emerging, both of which can offset the negative impact of the shrinking demographic dividend on social productivity. Labor is the most active factor among various production factors and is an important component for developing new quality productive forces. With the development of new quality productive forces, occupational health and occupational medicine are presented with new development opportunities. In the process of aging of the labor force, occupational health and occupational medicine can investigate how to utilize next-generation information technology, artificial intelligence, biotechnology, and other growth engines to safeguard the occupational health of workers, extend their working lives, actively unleash their creativity and initiative, and compensate for the labor shortage caused by an aging population and the potential decrease in labor productivity. This transformation in occupational health and occupational medicine is not only crucial for the health and career development of workers in an aging society, but will also have a positive impact on the creation of an age-friendly society and the sustainable development of productivity.

Based on previous exposure studies, benzene (BZ) has been classified as a human carcinogen and occupational exposure limit (OELs) for BZ has been set to be about 1 ppm around the world. However, health hazards have still been reported with exposure below the OEL. Thus, the OEL needs to be updated to reduce health risk. The overall aim of our study was therefore to generate new OEL for BZ via a benchmark dose (BMD) approach and based on quantitative and multi-endpoint genotoxicity assessments. Genotoxicities were determined using the novel human PIG-A gene mutation assay, the micronucleus (MN) test and the COMET assay in benzene-exposed workers. Among the 104 workers with below current OELs, they exhibited significantly higher PIG-A mutant frequencies (MFs) (15.96 +/- 14.41 x 10-6) and MN frequencies (11.55 +/- 6.83%o) than those among the controls (PIG-A MFs: 5.46 +/- 4.56 x 10-6, MN frequencies: 4.51 +/- 1.58 %o), but no difference in the COMET assay. A significant association was also observed between BZ exposure doses and PIG-A MFs and MN frequencies (P < 0.001). Our results indicate that health hazards were induced among workers with below OEL exposures. Based on results from the PIG-A and MN assays, the lower confidence limit of the BMD (BMDL) were calculated to be 8.71 mg/m3-year and 0.44 mg/m3-year, respectively. Based on these calculations, the OEL for BZ was deter-mined to be lower than 0.07 ppm. This value can be considered by regulatory agencies to set new exposure limits and to better protect workers.

目的 通过测定焊接工人佩戴的不同呼吸防护用品(respiratory protection equipment,RPE)对不同金属的工作场所防护因数(workplace protection factor,WPF),比较不同类型RPE对不同金属颗粒物的防护能力.方法 选择上海某船厂焊接岗位工人18人(17名男性和1名女性)为研究对象,根据工人日常工作实际佩戴的RPE类型,确定相应的RPE测试,其中5人佩戴过滤式半面罩(RPE1),13人佩戴三折折叠式防颗粒物口罩(RPE2),采用改良的美国WPF测试方法分别测试RPE内、外的金属颗粒物浓度,计算WPF值并进行对数转换,组间相关性采用Pearson相关分析,组间比较采用两因素非参数Scheirer-Ray-Hare检验.结果 锰颗粒和铁颗粒的WPF值符合对数正态分布,呼吸防护用品对锰颗粒和铁颗粒的WPF第5百分位数(WPF5％)分别为15.01和13.60,几何均数(GM)分别为114.76和82.37,RPE1和RPE2的WPF5％分别为11.25和22.28,GM分别为86.49和123.01.两种RPE对空气中金属粉尘颗粒物的WPF数值差异无统计学意义(P＞0.05),而铁和锰两种金属的WPF数值差异亦无统计学意义(P＞0.05),且RPE类型和不同金属颗粒物之间对防护效果不存在交互作用(P＞0.05).结论 改良的WPF测试方法能有效测试RPE的WPF值,本次测试的2种RPE对不同金属颗粒物均能起到防护作用,防护效果接近.

目的 探讨接触低浓度苯乙烯对线粒体DNA含量和微核率的影响,以寻找潜在的生物标志.方法 招募上海某塑料生产企业接触苯乙烯的男性工人127名为研究对象,检测工作车间空气中苯乙烯浓度,应用高效液相色谱法对苯乙烯的尿中代谢物进行检测,应用分光光度法测定尿中肌酐进行校正;按照尿中苯乙醇酸水平,将≤0.000 9 mg/g(以肌酐校正)者纳入低接触组,＞0.000 9～0.001 4 mg/g(以肌酐校正)者纳入中接触组,＞0.001 4 mg/g(以肌酐校正)者则纳入高接触组.通过实时荧光定量PCR实验检测工人外周血的线粒体DNA含量,通过胞质分裂阻滞微核实验检测外周血淋巴细胞的微核率.结果 工作场所定点采样显示环境空气中苯乙烯浓度低于1.2 mg/m3,尿中苯乙醇酸水平的中位数和四分位数为0.001 1(0.000 8,0.001 8)mg/g(以肌酐校正).广义线性模型分析结果显示:与低接触组相比,中接触组工人的mtDNAcn(自然对数转换后)升高0.271(P=0.042);中性粒细胞计数与淋巴细胞计数比值每升高1个单位,mtDNAcn(自然对数转换后)降低0.227(P＜0.01).泊松回归模型分析结果显示:年龄每增加1岁,微核率升高至原来的1.043倍(P＜0.001);尿中苯乙醇酸水平并非微核率的影响因素(P＞0.05).结论 即使是低于职业接触限值的苯乙烯接触亦可引起线粒体DNA拷贝数水平的改变,但未引起微核率的遗传毒性指标的改变,提示低浓度的苯乙烯可能通过氧化应激引起早期效应.

电离辐射是一种广泛存在于环境中的危害因素,不仅存在于自然环境中,随着工业和医学上的应用,人们接触电离辐射的机会也越来越多.电离辐射不仅直接导致细胞损伤,也具有遗传毒性,可引起多种远后效应,包括基因不稳定性、辐射致癌等.表观遗传可以调节基因活性和表达,而DNA甲基化是研究较多的表观遗传修饰方式,DNA甲基化在电离辐射所致损伤中也发挥着作用.从电离辐射与基因组甲基化、与重复序列DNA甲基化、与特定基因甲基化,以及电离辐射致甲基化改变的可能机制等方面,综述了电离辐射对DNA甲基化的影响及可能的作用机制.

目的 探索低浓度苯接触工人线粒体DNA拷贝数的变化及其影响因素.方法 选择上海某化工厂150名低浓度苯接触工人作为2018、2019年连续两年的追踪研究对象,采用问卷调查收集研究对象一般情况,采用实时荧光定量PCR法检测外周血相对线粒体DNA拷贝数并作为氧化应激的检测指标,利用重复测量分析以及广义估计模型分析两年间苯接触工人线粒体DNA拷贝数情况的变化,并探讨其与作业环境中苯接触的关系.结果 研究对象在追踪期间的苯接触浓度中位数为0.46 mg/m3,第25百分位数为0.14 mg/m3,第75百分位数为0.49 mg/m3.2018年苯接触工人相对线粒体DNA拷贝数为5.79±0.84,2019年工人相对线粒体DNA拷贝数显著降低,为(4.66±0.58),差异有统计学意义(P＜0.01).重复测量方差分析结果显示:不同接触浓度工人相对线粒体DNA拷贝数差异有统计学意义(P＜0.05);不同时间观察的线粒体DNA拷贝数不全相同,差异有统计学意义(P＜ 0.05).广义估计模型分析结果显示:与高接触浓度组相比,中接触浓度组工人相对线粒体DNA拷贝数降低了0.25(P＜ 0.05).未发现工龄、年龄、吸烟和饮酒对相对线粒体DNA拷贝数的影响.结论 在低于我国现行职业卫生标准的情况下,接触低浓度苯的作业工人仍可出现相对线粒体DNA拷贝数的改变,提示职业性苯接触可能导致线粒体损伤以及氧化应激的产生.

To provide a more comprehensive understanding of genotoxic effects from benzene exposure, its effects on induction of mitochondrial DNA copy number (MtDNAcn) and of micronucleus (MN) were investigated using peripheral blood from workers in China. Changes in mtDNAcn and MN were determined using quantitative real-time polymerase chain reaction (PCR) and cytokinesis-block micronucleus assays (CBMN), respectively, in 58 control and 174 benzene-exposed workers in Shanghai, China. Among the exposed workers, relative mtDNAcn increased and then decreased with increasing doses of benzene exposure. Significant and dose-dependent increase in MN frequencies were observed among the different exposure groups. In addition, the relative mtDNAcn were significantly associated with the MN frequencies in the low-level exposure group (P = 0.046), but not in the high dose groups. Therefore, the mechanisms for induction of MtDNAcn and MN by benzene may be similar from exposure to low doses but different from high doses. Similar increase of MN frequencies and MtDNAcn may be due to oxidative stress induced by benzene at low concentrations, while higher concentrations may start to initiate the cell death pathway. The pathway may be associated with excessive MtDNAcn which can initiate apoptosis while MN can continue to be induced. However, the differential mechanisms need to be investigated because they may represent different levels of risk for different health consequences. On the other hand, our data indicate that induction of MtDNAcn may be a sensitive genotoxic biomarker for workers with exposure to low dose of benzene. Environ. Mol. Mutagen. 2020. (c) 2020 Wiley Periodicals, Inc.

《建设项目职业病防护设施竣工验收规范》(DB31/T 1158-2019)于2019年7月1日正式实施.通过分析说明该标准的主要内容及其应用,综合概括其创新内容以及使用中的注意事项.DB 31/1158-2019标准明确了竣工验收程序和内容,细化了评分表,量化了评分证据,统一了判断标准,进一步规范了上海市职业病防护设施竣工验收工作,可操作性强,值得推广.

To provide a more comprehensive understanding of genotoxic effects from benzene exposure, its effects on induction of mitochondrial DNA copy number (MtDNAcn) and of micronucleus (MN) were investigated using peripheral blood from workers in China. Changes in mtDNAcn and MN were determined using quantitative real-time polymerase chain reaction (PCR) and cytokinesis-block micronucleus assays (CBMN), respectively, in 58 control and 174 benzene-exposed workers in Shanghai, China. Among the exposed workers, relative mtDNAcn increased and then decreased with increasing doses of benzene exposure. Significant and dose-dependent increase in MN frequencies were observed among the different exposure groups. In addition, the relative mtDNAcn were significantly associated with the MN frequencies in the low-level exposure group ( P = 0.046), but not in the high dose groups. Therefore, the mechanisms for induction of MtDNAcn and MN by benzene may be similar from exposure to low doses but different from high doses. Similar increase of MN frequencies and MtDNAcn may be due to oxidative stress induced by benzene at low concentrations, while higher concentrations may start to initiate the cell death pathway. The pathway may be associated with excessive MtDNAcn which can initiate apoptosis while MN can continue to be induced. However, the differential mechanisms need to be investigated because they may represent different levels of risk for different health consequences. On the other hand, our data indicate that induction of MtDNAcn may be a sensitive genotoxic biomarker for workers with exposure to low dose of benzene. Environ. Mol. Mutagen. 61:355–360, 2020. © 2020 Wiley Periodicals, Inc.

目的 通过调查上海市某区职业病防护设施“三同时”工作开展情况,找出政策执行存在问题,提出针对性的对策建议.方法 抽样调查上海市某区2015-2018年应开展职业病防护设施“三同时”的60个项目,分析项目所属经济类型、行业类别、风险类别构成情况以及不同风险类别、投资类型项目职业病防护设施“三同时”不同阶段工作开展情况,不同风险类别项目、不同级别技术服务机构完成项目的技术服务报告质量情况等.结果 调查的60个项目均开展了预评价,53个(88.3％)项目开展了防护设施设计,47个(81.0％)项目开展了控制效果评价,但仅有39个(67.2％)项目开展了竣工验收.从建设项目职业病危害风险分类上分析,防护设施设计、控制效果评价执行率上存在差异(P＜0.05),职业病危害风险越严重,执行情况越好;竣工验收执行率差异无统计学意义(P＞0.05),均执行较差.不同投资类型项目防护设施设计、控制效果评价和竣工验收执行率差异无统计学意义(P＞0.05).不同风险类别项目、不同级别机构间报告质量差异无统计学意义(P＞0.05),均存在一定的质量问题.结论 职业健康监管部门应加强职业病防护设施“三同时”相关法律法规宣贯,对建设单位以及职业卫生技术服务机构“三同时”工作的事中事后予以监管,提高“三同时”工作执行率和执行质量,从而更好地防治职业病.

GBZ 2.1—2019《工作场所有害因素职业接触限值第1部分:化学有害因素》的发布,引起了业内的广泛关注和讨论。从国外系统性职业接触评估方法的角度,以美国工业卫生协会（American Industrial Hygiene Association,AHIA）职业接触评估与管理策略和日本《化学物质个人接触监测指南》为例,探讨新的职业接触限值标准给我国职业卫生工作带来的新思路、新变化,认为需要有配套的指导规范文件尽快出台,以促进用人单位职业病危害防控工作。

为降低复工复产用人单位新型冠状病毒肺炎传人并发生风险,顺利复工复产,从用人单位外部环节(职工外地返回、上下班途中、下班回到社区以及出差环节)、内部环节(聚集性场所、共用设施物品、外来访客)进行分析,对复工复产单位新型冠状病毒感染关键风险点进行分析评估,并提出针对性的防控建议.分析表明:用人单位职工外地返回,上下班途中,单位内部电梯间、会议室、办公室、食堂以及下班回到社区以及出差环节为防控的关键风险点.为此提出了相应防控建议:明确风险环节,落实防控策略;强化疫情排查,落实疫情报告义务;加强各环节监测和风险管理;压实防疫主体责任,提升各环节防控水平.

在我国新型冠状病毒肺炎疫情发生后,防疫一线的医务人员承受极高的职业暴露风险.通过分析医务人员在疫情防控工作中的职业健康危害,探讨将医务人员在疫情应对中因职业暴露而感染的传染病纳入职业病目录的理论依据和法律基础,为今后职业病目录的修订提出理论和法律依据,以促进医务人员在应对疫情防控工作中职业健康保障的规范化、法制化.

目的 了解全国防毒技术支撑机构现状,调研防毒技术支撑机构布局、职能、经费投入、技术能力、工作业绩、存在问题及需求,为完善防毒技术支撑体系建设提供决策依据.方法 采用统一的调查表对全国防毒技术支撑机构进行调查,对不同类型的防毒技术支撑机构的人员、场地、经费投入、科研能力、设备状况等进行分析评估.结果 全国现有防毒技术支撑机构51家,分布在23个省(直辖市、自治区),其中属事业单位9家,国有企业21家,高等院校8家,民营企业及其他机构13家.42家(占82.4％)机构具备咨询、设计、施工、安装、检测类相关资质,各类机构咨询类、设计类资质具备率差异均有统计学意义(P＜0.05).共有防毒技术相关专业人员3 168人,建立了79个防毒工程相关专业实验室.各类防毒技术相关专业的分布、毒性研究室的分布在不同类型机构间差异有统计学意义(P＜0.05).共有毒物类科研、检测设备3 871台(套),设备资产共32 173万元,不同类型机构设备资产均值差异有统计学意义(P＜0.01).防毒工程重点实验设备共49台,仅占所有毒物类科研、检测设备的1.3％,各防毒技术支撑机构配置均较少.2015-2019年开展了345项危害工程治理项目,防毒设施防护效果检测23 867项.2017-2019年各机构获得国家财政投入经费共14 749万元,省级财政投入经费29 287万元,不同类型机构获财政经费投入率差异有统计学意义(P＜0.05).“十三五”期间各机构共获得各级防毒科研经费资助6 134万元,主持或参与防毒技术研究共183项.结论 防毒技术支撑机构发展不平衡,在人力、物力、科研能力、防毒技术支撑能力等方面均需要进一步提升,各机构在加强自身建设的同时,需要政府的扶持.

伴随着经济发展,“过劳死”现象已成为一个全球性的职业健康问题.“过劳死”直接导致劳动人口的减少,增加疾病负担,对劳动者本人及其家庭均造成极大的不良影响.然而,目前亚洲仅日本、韩国及中国台湾地区制定有专门的认定基准.因此,本文拟通过对过劳死概念及中国、日本和韩国“过劳死”认定基准的发展进行综述,为今后我国制定相应的认定基准(标准)提供工作基础.