TDW2—100穿甲弹爆震对豚鼠听力影响和耳蜗肌动蛋白免疫组…

豚鼠分别暴露于发射ＴＤＷ２－１００穿甲弹５９式坦克车内和穿甲弹击穿坦克靶车内时的强脉冲噪声中。发射穿甲弹的坦克车内脉冲声为１７０．０ｄＢ（ＳＰＬ），９发；击穿坦克靶车脉冲声大于１９４．０ｄＢ（ＳＰＬ），５发。用听生理脑干反应阈值来确定听力损失程度，并用ＡＢＣ免疫组织化学方法观察耳蜗内肌动蛋白免疫活性变化。结果是：震后８ｈ发射车内豚鼠听力下降平均为１１ｄＢ，４８ｈ全部恢复；而被击穿靶车内豚鼠听力下降     

次声刺激诱导大鼠听中枢FOS表达

用抗ＦＯＳ蛋白免疫组织化学的方法，在次声（８Ｈｚ，１２０ｄＢ）作用２ｈ后，大鼠耳蜗核、下丘、内侧膝状体、皮质听区等部位均发现ＦＯＳ阳性神经元（ＦＯＳｌｉｋｅｉｍｍｕｎｏｒｅａｃｔｉｖｅｎｅｕｒｏｎＦＬＮ）；上述各部位ＦＯＳ表达呈同步的时程变化，次声暴露停止后０５ｈ即有ＦＯＳ表达，２ｈ达高峰，４ｈ开始降低，２４ｈＦＯＳ表达基本消失。     

１８００ ＭＨｚ电磁辐射对小鼠皮肤细胞的氧化损伤作用研究

摘要：目的　研究１８００ ＭＨｚ电磁辐射对细胞的氧化损伤作用。方法　使用１８００ ＭＨｚ，比吸收率为２、３、４ Ｗ／ｋｇ电磁辐射辐照小鼠皮肤细胞（ＪＢ６），细胞分为辐照组与对照组。辐照结束后，采用流式细胞术，ＤＣＦＨ ＤＡ 荧光探讨针检测细胞内活性氧（ＲＯＳ）水平，再加入ＲＯＳ中和剂富氢水，以观察其对ＲＯＳ的中和作用。通过硫代巴比妥酸比色法检测丙二醛含量，来评价电磁辐射后细胞氧化损伤程度。结果　比吸收率为２、３ Ｗ／ｋｇ 时，暴露２ｈ内细胞内ＲＯＳ水平变化差异无统计学意义；４ Ｗ／ｋｇ暴露２０ ｍｉｎ、８０ ｍｉｎ、１２０ｍｉｎ后，暴露组细胞与假暴露组比较ＲＯＳ水平均显著升高（犘＜０．０５）；加入富氢水后，暴露组与普通培养基暴露组比较，降低了５０．７９％；４ Ｗ／ｋｇ暴露１２０ ｍｉｎ后丙二醛含量显著升高（P＜０．０５）。结论　４Ｗ／ｋｇ１８００ ＭＨｚ电磁辐射会引发细胞内ＲＯＳ升高并造成细胞氧化损伤。     

职业性铅接触者红细胞嘧啶5＇－核苷酸酶、超氧化物歧化酶活性测定

本文对１６名铅接触者、１４名铅中毒者和２０名非铅接触者进行了红细胞嘧啶５＇－核苷酸酶（Ｐ５Ｎ）和超氧化物歧化酶（ＳＯＤ）活性测定，并进行统计分析。结果表明铅可抑制红细胞Ｐ５Ｎ的活性，其抑制程度与铅毒效应密切相关：对照组（非接铅组）活性范围５．６～１４．２，平均１０．２μｍｏｌ尿嘧啶／ｈ／Ｈｂｇ／ｄｌ；接铅组活性范围为２．３～７．２，平均为４．４μｍｏｌ尿嘧啶／ｈ／Ｈｂｇ／ｄｌ，与非接铅组比较Ｐ＜０．００１；铅中毒组活性范围１．５～３．７，平均２．５μｍｏｌ尿嘧啶／ｈ／Ｈｂｇ／ｄｌ，与接铅组比较Ｐ＜０．００１。ＳＯＤ活性三组间无差别。     

空气负离子对白噪声及窄带噪声听力损伤的保护作用

本研究的目的为探索预防性吸入空气负离子对强噪声性听力损伤的保护作用和听力恢复规律。选用豚鼠暴露于１１８ｄＢ ＳＰＬ １ｈ的白噪声及２ｋＨｚ和４ｋＨｚ的窄带噪声，暴露前吸入空气负离子浓度０．９６×１０＾６￣０．９９×１０＾６／ｃｍ＾８ ２ｈ／ｄ １１￣１３ｄ。动态测定实验过程中豚鼠的皮层听觉反应阈指标。预先吸入空气负离子可减少白噪声性听力损失１７．９ｄＢ（噪声暴露停止后８ｈ与对照组比Ｐ〈０．０１），     

上海地区正常成人瞬态诱发耳声发射测试

目的了解上海地区正常成年人瞬态诱发耳声发射（ＴＥＯＡＥ）的基本特点及影响测试结果的因素。方法采用耳声发射分析仪Ｃｅｌｅｓｔａ５０３对１２０名上海地区正常成年人进行ＴＥＯＡＥ测试。结果由８０ｄＢＳＰＬ短声非线性方式诱发的ＴＥＯＡＥ检出率为１００％,平均幅值９．８１±４．３２ｄＢＳＰＬ（ｘ±ｓ）;６０ｄＢＳＰＬ短声线性方式诱发的检出率为９１％,平均幅值６．７１±４．５１ｄＢＳＰＬ（ｘ±ｓ）;６０ｄＢＳＰＬ短声非线性方式诱发的检出率为８９％,平均幅值５．３８±４．２３ｄＢＳＰＬ（ｘ±ｓ）。频谱范围分布在０．５～５ＫＨｚ之间,１～２ＫＨｚ范围的反应幅值和检出率最高。测试耗时平均２．４分钟。结论ＴＥＯＡＥ具有快速、灵敏、客观等特点。对于高刺激声（８０ｄＢＳＰＬ）正常人均能够引出ＴＥＯＡＥ,正常引出ＴＥＯＡＥ还与探头的放置、刺激声的强度和性质、叠加次数、测试环境等因素有关。     

不同水氟浓度对人群生化指标的影响

对饮水氟浓度分别为０．５９ｍｇ／Ｌ、０．９０ｍｇ／Ｌ、１．５９ｍｇ／Ｌ、１．９０ｍｇ／Ｌ、３．３７ｍｇ／Ｌ的五组人群用氯胺Ｔ氧化法测血清羟脯氨酸（ＨＹＰ）；用赖氏法测血清谷丙转氨酶（ＳＧＰＴ）；用４—氨基安替比林法测血清碱性磷酸酶（ＡＫＰ）。结果：五组人群ＨＹＰ均值依次为０．０８１ｍｇ／ｍｌ、０．２１０ｍｇ／ｍｌ、０．１５８ｍｇ／ｍｌ、０．１７９ｍｇ／ｍｌ；五组人群ＡＫＰ均依次为２．２７金氏单位／ｄ１，１０．５０金氏单位／ｄ１，１２．２１金氏单位／ｄｌ，９．６９金氏单位／ｄｌ，７．５金氏单位／ｄｌ；五组人群ＳＧＰＴ均值依次为１９．６１卡门氏单位／ｄｌ、１７．３５卡门氏单位／ｄｌ、２０．２２卡门氏单位／ｄｌ、２２．７１卡门氏单位／ｄｌ、１１．２２卡门氏单位／ｄｌ。上述结果提示：五组人群ＨＹＰ均值随水氟浓度的增高而增高；当水氟浓度在１．５９ｍｇ／Ｌ以上时，ＡＫＰ活性随水氟浓度增加而随低；当水氟浓度在０．５９ｍｇ／Ｌ～３．３７ｍｇ／Ｌ范围内，暂未看出对ＳＧＰＴ的影响。     

血浆纤维蛋白原和Ｄ 二聚体与急性缺血性脑卒中 病情进展及出院结局的关系研究

摘要：目的　探讨急性缺血性脑卒中（ａｃｕｔｅｉｓｃｈｅｍｉｃｓｔｒｏｋｅ,ＡＩＳ）不同病情进展及出院结局患者血浆纤维 蛋白原和Ｄ 二聚体的动态变化。方法　连续纳入浙江衢化医院住院治疗的ＡＩＳ患者３３５例,比较进展性脑 梗死（ｐｒｏｇｒｅｓｓｉｖｅｉｓｃｈｅｍｉｃｓｔｒｏｋｅ,ＰＩＳ）和出院结局不良组患者与对照组患者血浆纤维蛋白原和Ｄ 二聚体 的差异,并分析患者一般临床资料。采用ＳＰＳＳ１７．０ 处理,计量资料采用狋检验,计数资料采用χ ２ 检验, 犘＜０．０５为差异有统计学意义。结果　１０４例患者纳入ＰＩＳ组,ＰＩＳ的发生率为３１．０４％。发病初始（２４ｈ 内）,ＰＩＳ患者血浆纤维蛋白原（４．４２±１．０６）ｇ／Ｌ 和Ｄ 二聚体水平（１３７６．９±４１６．６）μｇ／Ｌ 高于非ＰＩＳ患 者血浆纤维蛋白原（４．０５±０．９５）ｇ／Ｌ 和Ｄ 二聚体水平（８２０．０±３２４．５）μｇ／Ｌ （犘＜０．０５）,并在住院７ｄ 内呈进行性升高,然后逐渐降低;同一住院时间点比较,ＰＩＳ 患者纤维蛋白原和Ｄ 二聚体水平均高于非 ＰＩＳ组,两组间差异有统计学意义（犘＜０．０５）。７６例患者纳入到结局不良组,结局不良发生率为２２．６９％。 结局不良组患者入院时（２４ｈ）及住院过程中（３～１４ｄ） 血浆纤维蛋白原（２４ｈ、３ｄ、７ｄ、１０ｄ、１４ｄ） 和Ｄ 二聚体水平（２４ｈ、３ｄ、７ｄ、１０ｄ、１４ｄ）均高于结局良好组（犘＜０．０５）。ＰＩＳ组患者合并糖尿病和 冠心病史的发病率高于非ＰＩＳ组（χ ２＝６．２７６、５．６７４,犘＜０．０５）,结局不良组患者的年龄及合并糖尿病、 冠心病、房颤的发病率高于结局良好组（χ ２＝６．７６９、５．１３２、４．８００,犘＜０．０５）。结论　血浆纤维蛋白原、 Ｄ 二聚体入院时和住院期间维持较高水平可能预示着急性缺血性脑卒中患者病情进展和出院不良结局,但 可能会受到其他因素的影响。 关键词：缺血性脑卒中;纤维蛋白原;Ｄ 二聚体;病情进展;出院结局 中图分类号：Ｒ７４３．３　　文献标识码：Ａ　　文章编号：１００９ ６６３９ （２０１７）０４ ０２８１ ０５     

GSTM1和CYP2D6基因多态性与肺癌敏感性的关系

采用病例－对照研究方法,应用ＰＣＲ技术检测５９例肺癌患者、５９例住院对照和７３例健康对照的ＧＳＴＭ１（－）型频率,分别为５７．６％、４９．２％和４９．３％,差异无显著性;经病理分型后,在腺癌中ＧＳＴＭ１（－）的频率（７６．９％）高出２个对照组（平均４９．２％）３．４２～３．４５倍,差异有显著性（Ｐ＝０．０１５～０．０１７）,提示ＧＳＴＭ１（－）型可能是肺腺癌的敏感性标记。应用ＰＣＲ－ＲＦＬＰ技术检测肺癌组和住院对照组的ＣＹＰ２Ｄ６Ｃｈ（Ｔ１８８／Ｔ）基因型频率,分别为３５．６％和４７．５％,差异无显著性;经吸烟指数分层后在不吸烟者中,肺癌组的Ｔ１８８／Ｔ型频率（１９％）显著低于住院对照组（４７．１％）,ＯＲ＝３．７８,Ｐ＝０．０３６,提示在不吸烟者中Ｔ１８８／Ｔ型可能是肺癌的一个保护因子。联合分析未见ＧＳＴＭ１和ＣＹＰ２Ｄ６Ｃｈ有协同关系。     

铸造作业职业危害研究进展

铸造作业的职业危害早已受到关注,由于新工艺、新材料的引进,使铸造作业职业有害因素更加复杂。我们就国内外该行业职业有害因素及其职业危害方面的研究现状作一综述。一、作业场所职业有害因素现状１．矽尘和其他金属粉尘：引进树脂砂后,粉尘浓度明显下降,平均水平为（１．３±０．８）ｍｇ／ｍ３,游离ＳｉＯ２为５９．８％～７６．７％［１］。东风公司３个铸造厂平均粉尘浓度分别从１９．９、１４．０、３３．６ｍｇ／ｍ３下降为２．２、３．０、２．７ｍｇ／ｍ３,游离ＳｉＯ２含量为２７．７９％～２９．２３％［２］。２．金属烟…     

燃煤对儿童免疫功能的影响研究

目的：探讨不同生活燃料对儿童免疫功能的影响。方法：配对选择燃煤和燃气各41名小学生作为研究对象,监测不同燃料导致的室内空气污染水平,同时对研究对象进行了免疫功能7项指标包括IgA、IgG、IgM、补体C3、血清溶菌酶和CD4、CD8的检测.结果：燃煤家庭的室内SO2、CO2、NO2及IP均显著高于燃气家庭,但两组儿童的各项免疫指标未见显著性差异。结论：南方由于住房结构尤其是通风状况,导致燃料所产生的室内空气污染物扩散稀释速度快,在室内停留时间短,儿童实际暴露水平低,因此未见明显的免疫功能损害。     

广州市不同家庭燃料致室内空气污染状况调查

对广州市燃煤和燃气家庭的室内空气进行了监测,了解燃煤对南方城市室内空气的污染状况以及污染物在室内的消长情况。结果发现,不论燃煤还是燃气,燃烧时都可导致室内空气污染物水平显著高于室外。燃煤导致的室内空气污染状况比燃气家庭严重,前者以ＳＯ２、ＣＯ和ＩＰ污染为主,后者则以ＮＯ２污染为主。无论是燃煤还是燃气,均以餐中时段室内污染物浓度最高;餐后０．５ｈ,各污染物浓度即迅速下降接近餐前水平。与北方城市存在很     

室内空气中氮氧化物污染水平及其影响因素的探讨

为制定我国室内空气中氮氧化物（ＮＯｘ）卫生标准，采用现场监测和实验室模拟相结合的方法，对室内空气中ＮＯｘ的污染水平及其影响因素进行研究。结果表明，冬季燃烧原煤的厨房、卧室空气中ＮＯｘ日平均浓度分别为０．１５９ｍｇ／ｍ３、０．１３２ｍｇ／ｍ３，燃烧煤气的厨房、卧室空气中ＮＯｘ日平均浓度分别为０．０９１ｍｇ／ｍ３、０．０７８ｍｇ／ｍ３，燃烧液化气分别为０．０７０ｍｇ／ｍ３、０．０６４ｍｇ／ｍ３。冬季与夏季室内空气中ＮＯｘ日平均浓度有显著性差异，冬季比夏季严重，厨房比卧室严重，未使用排油烟机的比使用排油烟机的严重     

Risk of male lung cancer attributed to coal combustion indoors in Shanghai.

Lung cancer is now the leading cause of death among all male cancers in Shanghai. Besides the smoking habit, the indoor air pollution from coal combustion may also make some contribution. The purpose of our study is to explore the risk of lung cancer death in male residents who live in coal-using families. Stratified by two extreme levels of ambient sulphur dioxide (SO2) and inhalable particulate (IP) concentrations, 4 areas were chosen in the city proper: Area A (low SO2, low IP); Area B (high SO2, low IP); Area C (low SO2, high IP) and Area D (high SO2, high IP). Within each of these areas, two neighboring residential groups were chosen, one of which uses coal as fuel (group 1), with the other using coal gas or liquified petroleum gas as fuel (group 0). The percentages of smokers and the ambient environment of the two chosen groups within each area are comparable. Total person-years observed is 117,039 from 1 January 1978 to 31 December 1987 for all males in the 8 groups. The mortalities (per 100,000 person-years) of male lung cancer in the 8 groups are as follows: A0-22.33, A1-37.64; B0-27.14, B1-30.72; C0-41.77, C1-54.99; D0-49.97, D1-78.11. The result shows that male lung cancer mortality in the coal-using group is higher than that in the coal-gas-using group within each area. Mantel-Haenszel's Relative Risk (RRMH) of male lung cancer in coal-using groups is 1.44 stratified by ambient SO2 and IP and smoking levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Estimation of respirable dust exposure among coal miners in South Africa

The use of retrospective occupational hygiene data for epidemiologic studies is useful in determining exposure-outcome relationships, but the potential for exposure misclassification is high. Although dust sampling in the South African coal industry has been a legal requirement for several decades, these historical data are not readily adequate for estimating past exposures. This study describes the respirable coal mine dust levels in three South African coal mines over time. Each of the participating mining operations had well-documented dust sampling information that was used to describe historical trends in dust exposure. Investigator-collected personal dust samples were taken using standardized techniques from the face, backbye (underground jobs not at the coal face), and surface from 50 miners at each mine, repeated over three sampling cycles. Job histories and exposure information was obtained from a sample of 684 current miners and 188 ex-miners. Linear models were developed to estimate the exposure levels associated with work in each mine, exposure zone, and over time using a combination of operator-collected historical data and investigator-collected samples. The estimated levels were then combined with work history information to calculate cumulative exposure metrics for the miner cohort. The mean historical and investigator-collected respirable dust levels were within international norms and South African standards. Silica content of the dust samples was also below the 5% regulatory action level. Mean respirable dust concentrations at the face, based on investigator-collected samples, were 0.9 mg/m(3), 1.3 mg/m(3), and 1.9 mg/m(3) at Mines 1, 2, and 3, respectively. The operator-collected samples showed considerable variability across exposure zones, mines, and time, with the annual means at the face ranging from 0.4 mg/m(3) to 2.9 mg/m(3). Statistically significant findings were found between operator- and investigator-collected dust samples. Model-based arithmetic mean dust estimates at the face were 1.2 mg/m(3), 2.0 mg/m(3), and 0.9 mg/m(3) for Mines 1, 2, and 3, respectively. Using these levels, the mean cumulative exposure for the cohort was 56.8 mg-years/m(3). Current miners had a mean cumulative exposure of 66.5 mg-years/m(3), compared with ex-miners of 26.8 mg-years/m(3). Improvements in dust management or the use of different sampling equipment could account for the significant differences seen between operator- and investigator-collected data. Regression modeling for estimating mean dust levels over time using combined historical and investigator-collected data seems a reasonable method and useful in constructing models to describe cumulative exposures in a cohort of current and ex-miners.     

家用燃料气态燃烧产物对室内空气污染的初步评估

目的 初步评估天然气、液化石油气和蜂窝煤的气态燃烧产物对室内空气污染的影响程度和特征.方法 在特别设计的3间实验房间内分别使用天然气、液化石油气和蜂窝煤在室内进行定量燃烧,同时根据国家标准方法采集空气样品并测定SO2、NO2、CO和甲醛的浓度,对其排放量和排放特征进行分析.结果 3种燃料的气态燃烧产物(SO2、NO2、CO、甲醛)中,均以CO和NO2的排放量最高.在日均用量下,蜂窝煤的CO和NO2排放量远高于天然气和液化石油气.使用蜂窝煤的家庭CO单位排放量高达30 136 mg/kg,明显高于液化石油气(8 725 mg/kg)和天然气(2 755 mg/kg);液化石油气的NO2单位排放量(42.69 mg/kg)则明显高于蜂窝煤(20.01 mg/kg)和天然气(11.87 mg/m3).在通风不良的室内,均可使室内CO和NO2浓度均超过GB/T 18883-2002<室内空气质量标准>.结论 厨房室内燃烧天然气或液化石油气,能造成CO和NO2的污染.     

3种民用燃料的燃烧颗粒物的含量及其粒径组成

目的了解天然气、液化石油气和蜂窝煤3种民用燃料定量燃烧所产生的各粒径颗粒物(PN25，PM10和TSP)的含量及构成比情况，并根据普通家庭各民用燃料的实际使用量推算居民对各粒径颗粒物的日暴露量。方法对北京地区常用的蜂窝煤、天然气和液化石油气3种民用燃料同时进行定量燃烧后，采集和测定燃烧产物中不同粒径颗粒物的含量及构成比。结果3种燃料燃烧生成的颗粒物均以PM10为主，分别占TSP的95．73％，85．98％和77．87％；但在PM10中，PM25和PM25-10构成比有所不同，天然气依次为95．73％和4．27％，液化石油气为51．52％和48．48％，蜂窝煤为93．56％和6．44％；在日平均用量下，蜂窝煤所产生的各粒径颗粒物的量远远高于天然气和液化石油气，其中蜂窝煤产生的PM25约为后2种燃料的13和30倍。结论该研究为深人研究和比较3种民用燃料燃烧产物的毒性及其对室内空气污染的贡献大小提供基础资料。     

Occupational exposure to crystalline silica dust in the United States, 1988-2003

The purposes of this study were a) to summarize measurements of airborne (respirable) crystalline silica dust exposure levels among U.S. workers, b) to provide an update of the 1990 Stewart and Rice report on airborne silica exposure levels in high-risk industries and occupations with data for the time period 1988-2003, c) to estimate the number of workers potentially exposed to silica in industries that the Occupational Safety and Health Administration (OSHA) inspected for high exposure levels, and d) to conduct time trend analyses on airborne silica dust exposure levels for time-weighted average (TWA) measurements. Compliance inspection data that were taken from the OSHA Integrated Management Information System (IMIS) for 1988-2003 (n = 7,209) were used to measure the airborne crystalline silica dust exposure levels among U.S. workers. A second-order autoregressive model was applied to assess the change in the mean silica exposure measurements over time. The overall geometric mean of silica exposure levels for 8-hr personal TWA samples collected during programmed inspections was 0.077 mg/m3, well above the applicable American Conference of Governmental Industrial Hygienists threshold limit value of 0.05 mg/m3. Surgical appliances supplies industry [Standard Industrial Classification (SIC) 3842] had the lowest geometric mean silica exposure level of 0.017 mg/m3, compared with the highest level, 0.166 mg/m3, for the metal valves and pipe fitting industry (SIC 3494), for an 8-hr TWA measurement. Although a downward trend in the airborne silica exposure levels was observed during 1988-2003, the results showed that 3.6% of the sampled workers were exposed above the OSHA-calculated permissible exposure limit.     

中国人群慢性阻塞肺病相关危险因素的Meta分析

目的 探讨影响中国人群慢性阻塞肺病相关危险因素的Meta分析。 方法 收集2000-2015年我国公开发表的关于中国人群慢性阻塞肺病相关危险因素的研究文献资料共14篇。应用RevMan 5.0软件进行Meta分析。 结果 吸烟、有被动吸烟史、BMI、职业粉尘或化学品暴露、家族呼吸道疾病史、儿童时期呼吸道疾病史、受教育程度、使用煤及柴草燃料及厨房通风情况与慢性阻塞肺病OR值之间存在关联,且均为危险因素。根据其OR估计值的大小,吸烟3.08(95％CI:2.26,4.21)、使用煤及柴草燃料3.10(95％CI:1.77,3.71)、家族呼吸道疾病史3.42(95％CI:2.76,3.98)与慢性阻塞肺病OR值呈较强的关联强度, 被动吸烟1.46(95％CI:1.15,1.98)、职业粉尘或化学品暴露1.57(95％CI:1.17,2.45)、厨房通风情况1.28(95％CI:1.82,2.43)与慢性阻塞肺病OR值呈较弱关联, 其他因素均呈中等强度关联。男性、高龄与慢性阻塞肺病OR值无相关。采用固定效应模型和随机效应模型分别计算慢性阻塞肺病发病危险因素的OR合并值及95%CI,结果两种模型分析结果基本相似。 结论 吸烟、有被动吸烟史、BMI、职业粉尘或化学品暴露、家族呼吸道疾病史、儿童时期呼吸道疾病史、受教育程度、使用煤及柴草燃料及厨房通风情况是影响中国人群慢性阻塞肺病发病的危险因素。     

2003至2008年某矿务集团煤工尘肺发病情况分析

目的 分析某煤矿2003至2008年尘肺病检出情况,探讨该矿尘肺发病特点,为尘肺病的防治提供科学依据.方法 收集1949年以来井下粉尘监测数据及2003至2008年的健康监护资料和尘肺诊断资料,分析尘肺发病情况,根据不同年代的粉尘接触水平结合工种和工龄推算安全总粉尘累积剂量.结果 2003至2008年该矿务集团在岗工人职业性健康监护率呈逐年提高趋势,共新检出煤工尘肺病例296例,总检出率为0.57%,平均年检出率为0.32%;Ⅰ期煤工尘肺268例,占全部病例的90.59%,87.20%(258例)的煤工尘肺患者为采掘工;新发病例的接尘工龄最短为3年,最长38年;每年总粉尘累积剂量为86.1～4926.0mg/m3.用百分位数法(第99%百分位数)推算煤矿井下工人每年安全总粉尘累积剂量为120.6 mg/m3.结论 尘肺病防治的重点工种是采掘工,在现有工作条件下井下采掘作业工龄不应超过13年.

Abstract：

Objective Analyzed associations among the incidence of coal workers' pneumoconiosis from 2003 to 2008, jobs, exposure years and cumulative total dust exposure levels(CTE ) and found the current characteristics of the mine incidence of pneumoconiosis disease. Methods collected the health care information of the new diagnosed pneumoconiosis of underground mine workers from 2003 to 2008 and the dust monitoring data of underground mine from 1949 and estimated the personnel cumulative total dust exposure levels (CTE); analyzed the incidence features of the new diagnosed pneumoconiosis. Results The rates of health surveillance of workers were gradually improved from 2003 to 2008 and 296 new coal workers pneumoconiosis were diagnosed. The total incidence was 0.57%, and the average annual rate was 0.32%. Among the new diagnosed cases, phase I accounted for 90.5% and the 87.2% from coal mine drillers. The shortest exposure period was 3 years and the longest was 38 years, and the cumulative total dose of dust was varied between 86. 1 and 4926 mg/m3 per year. The total dust accumulated limited dose was calculated by the percentile method to prevent 99% of miners from pneumoconiosis, which was 120.6 mg/m3 per year, so we suggested that the exposure years should be shorter than 13 years under the current working conditions. Conclusions Preventive coal workers' pneumoconiosis should be focused on mine drillers and their limited exposure years should be within 13 years.