Dust ; Humans ; Silicon Dioxide ; adverse effects ; Silicosis ; etiology

Dust ; Humans ; Maximum Allowable Concentration ; Occupational Exposure ; adverse effects ; Research Report ; Silicon Dioxide ; toxicity

Dust ; Humans ; Inflammation ; metabolism ; Intercellular Signaling Peptides and Proteins ; metabolism ; Silicon Dioxide ; adverse effects ; Silicosis ; metabolism

Animals ; Inflammation ; chemically induced ; Lung ; drug effects ; Oligodeoxyribonucleotides ; pharmacology ; Pulmonary Alveoli ; drug effects ; pathology ; Silicon Dioxide ; adverse effects

Bronchoalveolar Lavage Fluid ; Humans ; Interleukin-1beta ; metabolism ; Macrophages, Alveolar ; cytology ; drug effects ; metabolism ; Silicon Dioxide ; adverse effects ; Silicosis ; metabolism

Adult ; Construction Materials ; adverse effects ; Dust ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; Retrospective Studies ; Silicon Dioxide ; adverse effects ; Silicosis ; etiology

OBJECTIVEMeta-analysis is applied to process a systematic, comprehensive evaluation on the relationship between silica exposure and lung cancer in order to provide scientific evidences for controlling measures and offer a case for EBOM.

METHODSAccording to established entrance standards, the collected original articles on silica exposure and lung cancer were classified and put in order, then fixed effects model and random effects model were used which suited to analyze occupational epidemiology and occupational tumor materials, and their correlation intensity were analyzed. First, combined SMR and 95% CI values for case-control study and cohort study were calculated respectively. Then all case-control studies and cohort studies were combined according to different study designs, mixed factors adjusted and stratification analysis processed, and their SMR and 95% CI calculated respectively. In order to lessen bias or errors, fail safe number was calculated.

RESULTSWhen combining all the cohort study and all the case-control study respectively, corresponding combination SMR(cohort) = 1.93, 95% CI is 0.55 - 6.92; SMR case = 1.73, 95% CI is 1.01 - 2.99; SMR(sum) = 2.19, 95% CI is 1.45 - 3.31. Statistical test showed a statistically significant relationship lied between silica exposure and lung cancer, with P < 0.05.

CONCLUSIONMiddle intensity relation is drawn between silica exposure and lung cancer incidence at worksite. This result is consistent with a lot of public reports.

Case-Control Studies ; Cohort Studies ; Humans ; Lung Neoplasms ; epidemiology ; Occupational Diseases ; epidemiology ; Occupational Exposure ; adverse effects ; Silicon Dioxide

OBJECTIVETo study the effect of dust exposure and smoking on mortality.

METHODSBased on the Guangzhou Occupational Health Surveillance Record System established in 1989-1992, 61,648 factory workers, aged > or = 30, occupationally exposed to dust and non-exposure to dust or any other hazardous substances(controls), were included in a prospective cohort study.

RESULTS(1) 28 were lost to follow-up. Malignant neoplasm was most common among 1,186 deaths. (2) Most subjects were male workers, aged 35 to 44, with secondary education, and married. 42.2% had ever smoked and 32.8% were ever-drinkers. (3) To compare with non-exposure, non-smoking + non-smoking and non-exposure respectively, the adjusted RR of death from all causes, malignant neoplasm and respiratory diseases were 1.24, 1.34 and 1.96 respectively for dust exposed workers(compared to control, P < 0.01), 1.16, 1.37 and 1.63 respectively for those smoking(compared to non-smoker except RR of death from respiratory diseases, P < 0.01), and 1.48, 1.85 and 3.12 respectively for those smoking and dust exposure, which were far greater than those either smoked or exposed to dust alone(P < 0.01). (4) The influence of dust exposure on death was mainly showed in occupational exposure to silica dust and wood dust.

CONCLUSIONBoth dust exposure and smoking may increase the mortality, and they had synergistic effect.

Adult ; Cohort Studies ; Dust ; Female ; Humans ; Male ; Occupational Exposure ; adverse effects ; Prospective Studies ; Silicon Dioxide ; Smoking ; mortality ; Wood

OBJECTIVETo evaluate the diagnostic value of spirometrically controlled quantitative CT in silica-exposed workers.

METHODSWhole lung spiral scans at 50% vital capacity (VC) and image with high resolution CT(HRCT) at 10% VC and 90% VC level and 5 cm above/below carina were performed in 62 silica-exposed workers and 54 healthy adults. Automatic evaluation software, Pulmo, was used to evaluate the quantitative parameters and compared with clinical pulmonary function tests.

RESULTS9 workers with emphysema were detected by CT scans from 62 silica-exposed workers. The quantitative parameters of 10% VC and 90% VC were significantly different between the silica-exposed workers and the controls (P < 0.05). With the increasing of length of exposure to silica dust, the difference showed a ladder-like rising.

CONCLUSIONSpirometrically controlled quantitative CT is a sensitive, accurate and objective method. It is superior to conventional CT and pulmonary function tests for the early detection in silica-exposed workers, espicially for detecting early stage of small airway disease.

Humans ; Occupational Exposure ; Respiratory Function Tests ; Sensitivity and Specificity ; Silicon Dioxide ; adverse effects ; Spirometry ; Tomography, X-Ray Computed ; methods ; Vital Capacity

Objective: To investigate the effect of asiaticoside for fibrosis in lung tissues of rats exposed to silica and to explore its possible mechanism. Methods: 144 SD male rats were randomly divided into control group, model group, positive drug control group, asiaticoside high-dose group, medium-dose group and low-dose group, each group included 24 rats. Rats in the control group were perfused with 1.0 ml of normal saline, and the other groups were given 1.0 ml 50 mg/ml SiO(2) suspension. Gavage of herbal was given from the next day after model establishment, once a day. Rats in the positive drug control group were administration with 30 mg/kg tetrandrine and rats in the low-dose group, medium-dose group and high-dose group were given 20 mg/kg, 40 mg/kg and 60 mg/kg asiaticoside for fibrosis respectively. Rats in the control group and the model group were given 0.9% normal saline. The rats were sacrificed in on the 14th, 28th and 56th day after intragastric administration and collect the lung tissues to detect the content of hydroxyproline, TGF-β(1) and IL-18, observe the pathological changes of the lung tissues by HE and Masson staining and determine the expressions of Col-I, a-SMA, TGF-β in lung tissues by Western Blot. Results: On the 14th day, 28th day and 56th day after model establishment, the lung tissues of rats in the model group showed obvious inflammatory response and accumulation of collagen fibers, and the degree of inflammation and fibrosis increased with time. The intervention of asiaticoside could effectively inhibit the pathological changes of lung tissues. The contents of hydroxyproline, IL-18 and TGF-β1 in lung tissues of model group were higher than those in the control group (P<0.05) , while the level of hydroxyproline, IL-18 and TGF-β1 in asiaticoside groups were significantly decreased, and the difference was statistically signicant (P<0.05) . Compared with the control group, the expression levels of Col-I, TGF-β1and α-SMA in lung tissue of model group were increased (P<0.05) , while the expression level of Col-I, TGF-β1 and α-SMA were decreased after the intervention of asiaticoside, and the difference was statistically signicant (P<0.05) . Conclusion: Asiaticoside can inhibit the increase of Col-I, TGF-β1 and α-SMA content in the SiO(2)-induced lung tissues of rats, reduce the release of TGF-β1 and IL-18 inflammatory factors in lung tissue, and then inhibit the synthesis and deposition of extracellular matrix in rat lung tissue, and improve silicosis fibrosis.
Animals ; Dust ; Lung ; Male ; Pulmonary Fibrosis/metabolism* ; Rats ; Silicon Dioxide/adverse effects* ; Silicosis/metabolism* ; Transforming Growth Factor beta1/metabolism*