本文選題：生產(chǎn)性粉塵 + 標(biāo)化死亡比��； 參考：《華中科技大學(xué)》2012年博士論文

【摘要】：在生產(chǎn)過程中,勞動者長期吸入石英含量10%的生產(chǎn)性粉塵可導(dǎo)致以慢性肺纖維化為主要病理改變的職業(yè)病——矽肺,其纖維化的病變具有不可逆性,且目前無法治愈,是我國最嚴(yán)重的職業(yè)病。因此研究石英粉塵導(dǎo)致矽肺纖維化的發(fā)生及發(fā)展,對于矽肺的早期診斷、治療及預(yù)防具有十分重要的意義。 越來越多的研究表明,石英粉塵引發(fā)的氧化活性及肺部炎性反應(yīng)是導(dǎo)致機(jī)體損傷的關(guān)鍵因素。最近,體內(nèi)外實驗研究表明石英粉塵誘導(dǎo)產(chǎn)生高水平的IL-1p,但I(xiàn)L-1β作用模式及其導(dǎo)致的健康損害仍不清楚。 為探討不同粉塵引發(fā)炎性反應(yīng)的程度和誘發(fā)炎性反應(yīng)的機(jī)制及影響因素,我們收集了3個企業(yè)(江西的1個陶瓷廠和1個鎢礦,廣西的1個錫礦)作業(yè)點的生產(chǎn)性粉塵,以及不同粒徑的標(biāo)準(zhǔn)石英粉塵,選取PMA誘導(dǎo)THP-1單核細(xì)胞株分化的巨噬細(xì)胞作為靶細(xì)胞,采用體外細(xì)胞實驗的方法分析各廠礦粉塵毒性及致炎作用,結(jié)合接塵工人的健康狀況,綜合評價粉塵的致病能力,本研究主分為三個部分：(1)不同廠礦粉塵的化學(xué)組分及對接塵工人健康的影響；(2)粉塵致對巨噬細(xì)胞損傷和炎性反應(yīng)及其接塵工人健康損害的關(guān)系；(3)IL-1β在石英粉塵導(dǎo)致巨噬細(xì)胞炎性反應(yīng)中的作用。 第一部分不同廠礦粉塵的化學(xué)組分及對接塵工人健康的影響 目的：探討粉塵的化學(xué)組分及其對接塵工人健康的影響。 方法：生產(chǎn)性粉塵樣本來自上述3個企業(yè),采用焦磷酸質(zhì)量法測定粉塵中游離二氧化硅的含量,采用原子吸收光譜法和原子熒光光譜法測定粉塵中化學(xué)元素的含量。本部分以上述3個企業(yè)1960年1月1日至1974年12月31日期間在冊且工作一年以上的所有接塵工人為研究對象建立隊列,追訪至2003年底,以衛(wèi)生部發(fā)布的全國城市居民年齡別平均死亡率(1973-2003年)為對照計算標(biāo)化死亡比。 結(jié)果：(1)瓷廠和錫礦粉塵中游離二氧化硅含量接近,分別為43.39%、43.60%；而鎢礦粉塵中游離二氧化硅含量高于瓷廠和錫礦粉塵,達(dá)到57.51%。 (2)陶瓷廠中除鋁元素的含量最高(10.64%)以外,其他元素的含量都很低；鎢礦粉塵中鐵元素的含量最高,達(dá)到3.47%,鋅元素的含量最低,為0.09%；錫礦粉塵中鈣、鋅、砷元素的含量最高,分別為9.62%、0.33%、0.34%,鋁元素的含量最低,為2.80%。 (3)陶瓷廠隊列人數(shù)為907人,塵肺人數(shù)為148人,發(fā)病率為2.82‰。全死因標(biāo)化死亡比(SMR)為1.15,塵肺、惡性腫瘤及肺癌標(biāo)化死亡率比分別為85.26、0.58、0.77；鎢礦廠隊列人數(shù)為2350人,塵肺人數(shù)為788人,發(fā)病率為8.44‰。全死因標(biāo)化死亡比(SMR)為1.24,塵肺、惡性腫瘤及肺癌標(biāo)化死亡率比分別為101.80、0.67、0.73；錫礦隊列人數(shù)為3108人,塵肺人數(shù)為466人,發(fā)病率為2.42%o。全死因標(biāo)化死亡比(SMR)為1.07,塵肺、惡性腫瘤及肺癌標(biāo)化死亡率比分別為48.67、1.44、2.43。 粉塵中游離二氧化硅含量是影響塵肺發(fā)病的關(guān)鍵性因素。陶瓷廠粉塵中鋁元素含量高于其它2類金屬礦山,可能是造成陶瓷廠工人累積接矽塵量高而塵肺發(fā)病相對較低的主要原因。錫礦惡性腫瘤的升高與粉塵中砷的含量存在一定關(guān)聯(lián)。 第二部分粉塵致巨噬細(xì)胞損傷和炎性反應(yīng)及其接塵工人健康損害的關(guān)系 第一節(jié)石英誘導(dǎo)巨噬細(xì)胞產(chǎn)生IL-1β的模型篩選 目的：探討石英粉塵激活巨噬細(xì)胞產(chǎn)生IL-1p的作用條件、時間效應(yīng)及劑量效應(yīng)。 方法：以PMA誘導(dǎo)THP-1單核細(xì)胞株分化的巨噬細(xì)胞作為靶細(xì)胞,選取三個粒徑的標(biāo)準(zhǔn)石英DQ12(DQ12-PM1,1μm；DQ12-PM3-5,3～5μm；DQ12-PM5,5μm),配制成900,600,300,150,75,37.5μg/m6個濃度,分別染毒巨噬細(xì)胞3、6、12、18、24h,測定巨噬細(xì)胞釋放IL-1p的水平。 結(jié)果：(1)三種粒徑的標(biāo)準(zhǔn)石英在3、6、12、18、24h這5個時間點均能誘導(dǎo)巨噬細(xì)胞釋放IL-1p的水平升高,IL-1p的水平變化較明顯且較早的時間點為6h,呈現(xiàn)明顯的劑量反應(yīng)關(guān)系。 (2)當(dāng)粉塵濃度在75～300μg/ml之間時,三種粒徑標(biāo)準(zhǔn)石英誘導(dǎo)巨噬細(xì)胞釋放IL-1p的水平有明顯的劑量反應(yīng)關(guān)系,且粉塵濃度在300gμg/ml時,釋放的IL-1p基本都達(dá)到了最高水平。在后續(xù)的實驗中我們選擇了37.5、75、150、300gg/ml作為染毒的濃度組。 第二節(jié)節(jié)不同粒徑石英粉塵致巨噬細(xì)胞損傷及炎性因子變化 目的：探討不同粒徑石英粉塵對巨噬細(xì)胞的損傷及炎性反應(yīng)作用,從而評價粒徑在粉塵致炎性及纖維化反應(yīng)途徑中的作用。 方法：以PMA誘導(dǎo)THP-1單核細(xì)胞株分化的巨噬細(xì)胞作為靶細(xì)胞,選取兩種不同粒徑的標(biāo)準(zhǔn)石英(DQ12-PM1,1μm；DQ12-PM3～5,3～5μm),以細(xì)胞空白為陰性對照,將粉塵配制成300,150,75,37.5μg/m14個濃度,與巨噬細(xì)胞共培養(yǎng)6h,測定細(xì)胞活力(MTT)、活性氧(ROS)的釋放量及IL-1β、TNF-α、IL-6、IL-β1、IL-18、IL-33的水平。 結(jié)果：不同粒徑的石英粉塵均能損傷巨噬細(xì)胞的細(xì)胞活力,且隨粉塵濃度的升高,巨噬細(xì)胞的細(xì)胞活力也逐漸下降,均能誘導(dǎo)巨噬細(xì)胞釋放活性氧(ROS)及炎性細(xì)胞因子的表達(dá)。在較低濃度組(37.5、75、150μg/ml),粒徑為PM1的標(biāo)準(zhǔn)石英誘導(dǎo)巨噬細(xì)胞釋放IL-1p、TNF-α、IL-6、IL-33的水平略高于粒徑為PM3-5的標(biāo)準(zhǔn)石英；在最高濃度組300μg/ml,粒徑為PM3-5的標(biāo)準(zhǔn)石英粉塵的作用能力較強(qiáng)。 第三節(jié)生產(chǎn)性粉塵致巨噬細(xì)胞的損傷及炎性因子變化及其與接塵工人健康損害的關(guān)聯(lián) 目的：分析生產(chǎn)性粉塵致巨噬細(xì)胞炎性因子的反應(yīng),評價炎性因子變化與接塵工人健康損害之間的可能關(guān)聯(lián)。 方法：上述企業(yè)作業(yè)點的呼吸性粉塵作為本次試驗粉塵,以標(biāo)準(zhǔn)石英為陽性對照組,其他方法同第二部分第一節(jié)。 結(jié)果：瓷廠、鎢礦及錫礦粉塵均可導(dǎo)致巨噬細(xì)胞的細(xì)胞存活率下降、釋放炎性細(xì)胞因子(IL-1β、TNF-α、IL-6、IL-18、IL-33)及抗炎細(xì)胞因子(TGF-β1)水平升高,并隨粉塵濃度的升高有一定的劑量反應(yīng)關(guān)系。瓷廠粉塵致巨噬細(xì)胞活力下降的程度最顯著,錫礦粉塵次之,鎢礦粉塵最弱；鎢礦和錫礦粉塵誘導(dǎo)巨噬細(xì)胞產(chǎn)生前炎性細(xì)胞因子(IL-1β、TNF-α(?)(?)IL-6)的作用能力強(qiáng)于瓷廠,在低濃度組(37.5、75μg/ml),鎢礦和錫礦粉塵誘導(dǎo)巨噬細(xì)胞產(chǎn)生IL-1β的能力顯著強(qiáng)于標(biāo)準(zhǔn)石英,而在最高濃度組(300μg/ml),標(biāo)準(zhǔn)石英誘導(dǎo)產(chǎn)生IL-1β的能力顯著強(qiáng)于瓷廠、鎢礦及錫礦粉塵。鎢礦和錫礦粉塵在各濃度組誘導(dǎo)巨噬細(xì)胞釋放TNF-α的水平顯著高于標(biāo)準(zhǔn)石英。但鎢礦粉塵幾乎未能誘導(dǎo)巨噬細(xì)胞產(chǎn)生TGF-β1,,錫礦粉塵幾乎未能誘導(dǎo)巨噬細(xì)胞產(chǎn)生IL-18及IL-33。 鎢礦和錫礦粉塵作用于巨噬細(xì)胞后誘導(dǎo)產(chǎn)生前炎性細(xì)胞因子(IL-1β、TNF-α和IL-6)的能力都較強(qiáng),而抗炎細(xì)胞因子(TGF-β1)的表達(dá)卻很低；瓷廠粉塵誘導(dǎo)巨噬細(xì)胞釋放前炎性細(xì)胞因子的能力最弱,但抗炎細(xì)胞因子的水平卻相對較高,與接塵工人患矽肺危險度也是鎢礦和錫礦的較高,瓷廠的最低相對應(yīng)。本部分研究提示IL-1β對評價生產(chǎn)性粉塵致纖維化的有一定的預(yù)測作用。 第三部分IL-1β在石英導(dǎo)致巨噬細(xì)胞炎性反應(yīng)中的作用 目的：探討IL-1β在石英引發(fā)的炎性反應(yīng)中的作用。 方法：以PMA誘導(dǎo)THP-1單核細(xì)胞株分化的巨噬細(xì)胞作為靶細(xì)胞,將重組的IL-1β配制1600,800,400,200,100pg/m15個濃度,染毒巨噬細(xì)胞6h或24h；用50ng/ml的LPS預(yù)處理巨噬細(xì)胞6h,將標(biāo)準(zhǔn)石英粉塵配制成300,150,75,37.5μg/ml4個濃度,與LPS預(yù)處理的巨噬細(xì)胞共培養(yǎng)6h；用2.5μg/ml IL-1β單克隆抗體預(yù)處理細(xì)胞,按300,150,75,37.5μg/ml4個濃度的不同粒徑的標(biāo)準(zhǔn)石英染毒巨噬細(xì)胞6h或24h,均測定細(xì)胞培養(yǎng)液上清中IL-1β、TNF-α、IL-6的水平。 結(jié)果：(1)重組IL-1β作用于巨噬細(xì)胞6h和24h后,均可誘導(dǎo)其釋放TNF-α、IL-6的水平升高,有明確的劑量反應(yīng)關(guān)系；并隨時間的延長,TNF-α、IL-6的水平也逐漸增高；但未能誘導(dǎo)其釋放IL-1β,反而重組IL-1β本身的水平呈現(xiàn)下降的趨勢,并隨時間的延長其下降的趨勢越明顯。 (2)標(biāo)準(zhǔn)石英作用于LPS預(yù)處理的巨噬細(xì)胞6h后,能誘導(dǎo)其分泌IL-1β、TNF-α、IL-6的水平均隨粉塵濃度的增加而逐漸上升,有明顯的劑量反應(yīng)關(guān)系,且三種炎性細(xì)胞因子的水平明顯高于未用LPS預(yù)處理的巨噬細(xì)胞。 (3)IL-1β抗體能明顯降低高濃度組(150、300μg/m1)標(biāo)準(zhǔn)石英誘導(dǎo)巨噬細(xì)胞產(chǎn)生IL-1β的水平,且IL-1β抗體阻斷小粒徑的標(biāo)準(zhǔn)石英(PM1)誘導(dǎo)釋放的IL-1β作用更為顯著；IL-1β抗體幾乎完全阻斷兩種粒徑的標(biāo)準(zhǔn)石英誘導(dǎo)巨噬細(xì)胞釋放TNF-α、IL-6。
[Abstract]:In the process of production, the long-term inhalation of 10% of the productive dust of quartz can lead to the occupational disease of silicosis with chronic pulmonary fibrosis as the main pathological change, which is irreversible and can not be cured at present. It is the most serious occupational disease in our country. Development is of great importance for early diagnosis, treatment and prevention of silicosis.
More and more studies have shown that the oxidation activity induced by quartz dust and the inflammatory response of the lungs are the key factors that lead to the injury of the body. Recently, the experimental study in vitro and in vivo showed that the quartz dust induced the high level of IL-1p, but the mode of action of IL-1 beta and the health damage caused by it are still unclear.
In order to investigate the degree of inflammatory reaction caused by different dust and the mechanism and influencing factors of induced inflammatory reaction, we collected the productive dust of 3 enterprises (1 ceramic factories in Jiangxi and 1 tungsten mines, 1 tin mines in Guangxi), and standard quartz dust with different particle sizes, and selected PMA to induce macrophage fines in the differentiation of the mononuclear cell lines. As a target cell, cell test in vitro was used to analyze the toxic and inflammatory effects of dust dust in various factories, combined with the health status of the dust exposed workers and comprehensively evaluate the pathogenic ability of dust. This study was divided into three parts: (1) the chemical composition of dust in different factories and the health of dusts, and (2) dust caused to macrophage damage. The relationship between injury and inflammatory reaction and the health damage of workers exposed to dust; (3) the role of IL-1 beta in the inflammatory reaction of macrophages induced by quartz dust.
The first part is about the chemical composition of dust from different factories and the health of workers exposed to dust.
Objective: To explore the chemical composition of dust and its influence on the health of workers exposed to dust.
Methods: the sample of productive dust came from the above 3 enterprises. The content of free silica in dust was determined by pyrophosphoric acid mass spectrometry. The content of chemical elements in dust was determined by atomic absorption spectrometry and atomic fluorescence spectrometry. The 3 enterprises in this section were published and worked for one year from January 1, 1960 to December 31, 1974. All the dust workers above set up a cohort for the study, followed by the end of 2003. The average mortality rate (1973-2003 years) of the national average age of urban residents (1973-2003 years) issued by the Ministry of health was calculated as a comparison of the standardized mortality ratio.
Results: (1) the content of free silica in the dust of porcelain and tin ore is close to 43.39% and 43.60%, respectively, while the free silica content in tungsten dust is higher than that of the porcelain factory and the tin dust, reaching 57.51%..
(2) the content of other elements is very low in the ceramic factory except for the highest content of aluminum (10.64%), the content of iron in tungsten dust is the highest, the content of the zinc element is the lowest, and the lowest is 0.09%. The content of calcium, zinc and arsenic in tin dust is the highest, which is 9.62%, 0.33%, 0.34%, and the content of aluminum is the lowest, 2.80%.
(3) the number of workers in the ceramic factory was 907, the number of pneumoconiosis was 148, the incidence was 2.82 per thousand. The standardized death ratio (SMR) was 1.15, the mortality ratio of pneumoconiosis, malignant tumor and lung cancer was 85.26,0.58,0.77, the number of wolfram coal mines was 2350, the number of pneumoconiosis was 788, the incidence was 8.44 per thousand. The ratio of death to death was 1.24, and the ratio of death to the standardized death ratio (SMR) was 1.24, The mortality ratio of pneumoconiosis, malignant tumor and lung cancer was 101.80,0.67,0.73, the number of tin mines was 3108, and the number of pneumoconiosis was 466, the incidence of the incidence was 1.07 of the 2.42%o. total death ratio (SMR), and the mortality ratio of pneumoconiosis, malignant tumor and lung cancer was 48.67,1.44,2.43., respectively.
The content of free silica in dust is the key factor affecting the incidence of pneumoconiosis. The content of aluminum in the dust of the ceramic factory is higher than that of the other 2 types of metal mines, which may be the main cause of the high accumulation of silica dust in the ceramic factory workers and the relatively low incidence of pneumoconiosis.
The second part is the relationship between dust induced macrophage injury and inflammatory reaction and the health damage of workers exposed to dust.
Model selection of silica induced macrophage producing IL-1 beta
Objective: To explore the effects, time effects and dose effects of silica dust on macrophages producing IL-1p.
Methods: the macrophages differentiated from THP-1 mononuclear cells were used as target cells by PMA. The standard quartz DQ12 (DQ12-PM1,1 mu m, DQ12-PM3-5,3 ~ 5 m, DQ12-PM5,5 u m) was selected as 900600300150,75,37.5 mu g/m6 concentration, and macrophage 3,6,12,18,24h was poisoned, and the level of macrophage release was measured.
Results: (1) the standard quartz of three particle sizes could induce the increase of the level of macrophage releasing IL-1p at the 5 time points of 3,6,12,18,24h. The level of IL-1p was significantly changed and the earlier time point was 6h, showing a significant dose response relationship.
(2) when the dust concentration is 75~300 g/ml, there is a significant dose response relationship between three kinds of standard quartz induced macrophages to release IL-1p. And when the dust concentration is 300g mu g/ml, the release of IL-1p basically reaches the highest level. In the follow-up experiment, we selected 37.5,75150300gg/ml as the concentration group.
Macrophage injury and inflammatory factor changes induced by second different size quartz dust
Objective: To investigate the effect of different particle size quartz dust on the damage and inflammatory reaction of macrophages, and to evaluate the effect of particle size on the inflammatory and fibrotic reaction pathways of dust.
Methods: the macrophages differentiated by PMA THP-1 mononuclear cells were used as target cells, and two different particle sizes of standard quartz (DQ12-PM1,1 mu m; DQ12-PM3 to 5,3 ~ 5 m) were selected as negative control, and the dust was prepared into 300150,75,37.5 u g/m14 concentration and co cultured with macrophage cells for 6h, and the activity oxygen (MTT) and reactive oxygen species were measured. ROS release and IL-1 beta, TNF- alpha, IL-6, IL- beta 1, IL-18, IL-33 levels.
Results: the quartz dust with different particle sizes could damage the cell viability of macrophages, and the cell viability of macrophages decreased with the increase of dust concentration, which could induce the release of reactive oxygen species (ROS) and the expression of inflammatory cytokines in macrophages. In a lower concentration group (37.5,75150 mu g/ml), a standard quartz with a particle size of PM1 was induced to induce macrophages. The level of IL-1p, TNF- alpha, IL-6 and IL-33 was slightly higher than the standard quartz with the particle size of PM3-5, and the standard quartz dust with a particle size of PM3-5 was stronger than the standard quartz with the highest concentration of PM3-5 in the highest concentration group.
Third sections of dust induced macrophage injury and inflammatory factors and their relationship with health damage of exposed workers
Objective: to analyze the reaction of inflammatory cytokines in macrophages induced by productive dust, and to evaluate the possible correlation between the changes of inflammatory factors and the health damage of workers exposed to dust.
Methods: respirable dust at the above operation points was taken as the dust in this experiment. The standard quartz was used as the positive control group, and the other methods were the first part of the second part.
Results: porcelain factory, tungsten ore and tin dust can lead to the decrease of cell survival rate of macrophage, the release of inflammatory cytokines (IL-1 beta, TNF- a, IL-6, IL-18, IL-33) and anti-inflammatory cytokine (TGF- beta 1) level, and the increase of the concentration of dust has a certain anti response relationship. The degree of the decrease of macrophage vitality caused by the dust of porcelain factory is the most obvious At the same time, tungsten dust is the weakest, tungsten ore dust is the weakest; IL-1 beta, TNF- alpha (?) IL-6) induced by tungsten and tin dust is stronger than porcelain factory. In low concentration group (37.5,75 mu g/ml), the ability of tungsten ore and tin dust to induce the production of IL-1 beta in megagocytic cells is stronger than that of standard quartz, but at the highest concentration Group (300 g/ml), the ability of standard quartz to induce the production of IL-1 beta was significantly stronger than that of porcelain factory, tungsten ore and tin dust. The level of TNF- alpha released by macrophages in each concentration group was significantly higher than that of standard quartz. But tungsten dust could hardly induce macrophage to produce TGF- beta 1, and tin dust almost failed to induce macrophage. Producing IL-18 and IL-33.
The ability of tungsten ore and tin dust to induce proinflammatory cytokines (IL-1, TNF- A and IL-6) after the action of macrophages is strong, but the expression of anti-inflammatory cytokine (TGF- beta 1) is very low, and the ability of porcelain factory dust to induce macrophage to release inflammatory cytokines is the weakest, but the level of anti-inflammatory cytokines is relatively high, and the dust is connected to the dust. The risk of silicosis in workers is also higher than that of tungsten ores and tin mines, and the lowest in porcelain factories. This part of this study suggests that IL-1 beta has a certain predictive effect on evaluating the fibrosis of productive dust.
The third part is the role of IL-1 beta in the inflammatory response of macrophages induced by quartz.
Objective: To investigate the role of IL-1 beta in the inflammatory reaction induced by quartz.
Methods: the macrophages differentiated from THP-1 mononuclear cells were used as target cells by PMA, and the recombinant IL-1 beta was prepared for 1600800400200100pg/m15 concentration, 6h or 24h of macrophages, and 6h of macrophages was pretreated with 50ng/ml LPS, and the standard quartz dust was prepared into 300150,75,37.5 um g/ml4 concentration, and the macrophage pretreated with LPS. 6h was co cultured. The cells were pretreated with 2.5 g/ml IL-1 beta monoclonal antibody, and 6h or 24h of macrophages were infected by standard quartz with different particle sizes of 300150,75,37.5 mu g/ml4. The level of IL-1 beta, TNF- alpha and IL-6 in the supernatant of cell culture liquid was measured.
Results: (1) the effect of recombinant IL-1 beta on macrophage 6h and 24h could induce the release of TNF- alpha, the level of IL-6 increased, and there was a definite dose response relationship; and the level of TNF- alpha and IL-6 increased gradually with the prolongation of time, but failed to induce the release of IL-1 beta, instead, the level of IL-1 beta itself showed a downward trend, and with time. The more obvious the trend of prolonging its decline.
(2) standard quartz can induce the secretion of IL-1 beta, TNF- alpha and IL-6 after the effect of LPS pretreated macrophage 6h. The level of the standard quartz increases with the increase of dust concentration, and there is a significant dose response relationship, and the level of the three inflammatory cytokines is significantly higher than that of the macrophages without the LPS pretreated.
(3) IL-1 beta antibody could significantly reduce the level of IL-1 beta in the standard quartz induced macrophages in the high concentration group (150300 g/m1), and the IL-1 beta antibody blocked the IL-1 beta induced by the standard quartz (PM1) induced by the small size of the quartz (PM1), and the IL-1 beta antibody almost completely blocked the release of TNF- a by two kinds of standard quartz induced macrophages. IL-6.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2012
【分類號】：R131

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 陳鏡瓊,陳衛(wèi)紅,魯嘉模,傅長漢,戴啟瓷,宋小明,唐錄生,陳仲軒,劉興泰;陶工塵肺危險度及其防制措施評價[J];工業(yè)衛(wèi)生與職業(yè)病;1999年04期

2 陳衛(wèi)紅,陳鏡瓊,楊劍,張華生,盧小春,余利貞,文加團(tuán);廣西錫礦工人肺癌病例對照研究[J];工業(yè)衛(wèi)生與職業(yè)病;1999年04期

3 楊海兵,楊磊,張鈞岳,陳鏡瓊;塵肺疾病過程與接塵工人健康監(jiān)護(hù)的關(guān)系[J];工業(yè)衛(wèi)生與職業(yè)病;2005年05期

4 陳鏡瓊，魯嘉模，，陳榮安，陳安珞，張鈞岳;金屬礦山和陶瓷廠接塵工人的死亡率[J];工業(yè)衛(wèi)生與職業(yè)病;1994年01期

5 王燕;康現(xiàn)江;穆淑梅;;納米二氧化鈦的毒理學(xué)研究進(jìn)展[J];中國藥理學(xué)與毒理學(xué)雜志;2008年01期

6 王小慧;劉學(xué)軍;;IL-1β及其Ⅰ型受體在大鼠肺纖維化發(fā)生過程中的動態(tài)表達(dá)[J];中國醫(yī)藥導(dǎo)報;2010年09期

7 謝妮,董靜,金一和;石英粉塵粒徑與肺損傷作用關(guān)系的實驗研究[J];中國公共衛(wèi)生;2004年06期

8 高竹;郭新彪;;大氣PM_(10)與PM_(2．5)的健康效應(yīng)比較[J];中國衛(wèi)生工程學(xué);2006年01期

9 陳衛(wèi)紅;;塵肺防制的研究進(jìn)展與展望[J];中華勞動衛(wèi)生職業(yè)病雜志;2006年09期

10 William E.Wallace;陳鏡瓊;王海椒;陳衛(wèi)紅;;瓷廠與錫礦及鎢礦石英粉塵表面鋁硅酸鹽包裹的測定和分析[J];中華勞動衛(wèi)生職業(yè)病雜志;2006年09期

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