[Analysis of spirometer data of 5272 coal dust-exposed miners].

Objective: To analyze the spirometer data of coal mine workers, explore the impact of coal dust on the lung function of coal mine workers. Methods: From June to December 2018, 5272 male coal mine dust-exposed workers who underwent occupational health examinations at the Xinjiang Uygur Autonomous Region Occupational Disease Prevention and Treatment Hospital were selected as the research subjects. The basic information and spirometer data of the workers were collected and analyzed for different ages, years of service and the degree of lung function injury of workers exposed to dust and its influencing factors. Results: The total detection rate of lung function injury among dust-exposed workers was 33.9% (1785/5272) . The type of injury was mainly restrictive ventilatory dysfunction (66.7%, 1190/1785) , followed by mixed ventilatory dysfunction (31.4%, 561/1785) , obstructive ventilatory dysfunction (1.9%, 34/1785) . The detection rate of mild lung function impairment was 21.0% (1105/5272) , The detected rate of moderate or higher lung injury was 12.9% (680/5272) . The abnormal detection rate of chest radiography was 3.4% (179/5272) . The logistic regression analysis of the factors affecting lung function damage showed that employees aged 40-<50 were more likely to detect overall lung function injury and the moderate or higher lung injury (P<0.05) , and that they had been working for 35 to 45 years and excavators were more likely to detect overall function injury and different degree of lung injury (P<0.05) . Conclusion: The lung function injury of coal mine dust-exposed workers is related to their age, dust-exposed working years and type of work, mainly with mild injury and restrictive ventilation dysfunction.

[The effects of methylprednisolone on NLRP3 inflammasome in rats with acute lung injury Induced by Phosgene].

Objective: To investigate the effects of methylprednisolone on NOD-like receptor hot protein domain-associated protein 3 (NLRP3) inflammasome in phosgene-induced acute lung injury. Methods: Rats were randomly divided into four groups, 10 rats in Air group (inhalation of air of the same volume as the phosgene group) , 10 rats in Phosgene group (inhalation of 8.33 mg/L with 100% purity phosgene for 5 min) , 10 rats in Saline control group (inhalation of the same dose of phosgene and 2 mg/kg saline via tail vein injection one hour later) , 10 rats in MP group (inhalation of the same dose of phosgene and 2 mg/kg MP via tail vein injection one hour later) . The specimens of serum, bronchoalveolar lavage fluid (BALF) and lung tissue were collected after 6h. Morphological changes were observed by HE staining. The expression of NLRP3 in the lung of four groups was detected by immunohistochemistry. NLRP3、ASC and caspase-1 expression in the lung tissue was quantified by Western blot. Reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the expression of NLRP3、ASC and caspase-1 mRNA in the lung tissue. The concentrations of IL-1ß、IL-18 and IL-33 in the serum and BALF were measured by enzyme-linked immunosorbent assay. Results: We successfully replicated the model of phosgene-induced ALI in rats. Morphological of HE staining after phosgene exposure to 6 h observed inflammatory cell infiltration in lung tissue in Phosgene group. Immunohistochemical staining results showed that there were many NLRP3 positive cells in lung tissue in Phosgene group. The levels of NLRP3, caspase-1 mRNA and protein expression in lung were significantly increased (P<0.05) in Phosgene group compared with Air group; compared with Phosgene group, The levels of NLRP3 and caspase-1 mRNA and protein expression in MP group were significantly decreased (P<0.05) . Compared with Air group, The levels IL-1ß、IL-18 and IL-33 mRNA protein expression in the serum and BALF were significantly increased (P<0.05) in Phosgene group. Compared with Phosgene group, The levels IL-1ß、IL-18 and IL-33 mRNA protein expression in the serum and BALF were significantly decreased (P<0.05) in MP group. Conclusion: Methylprednisolone can effectively protect the rats from phosgene-induced acute lung injury by inhibiting the expression of the NLRP3 inflammasome and reducing the release of inflammatory factors such as interleukin-1ß (IL-1ß) mediated by it.

[Comparison of knowledge and behavior toward hearing protection among workers in different workplaces and its influence factors].

Objective: To compare the knowledge and behavior toward hearing protection among workers in different workplaces and investigate its influence factors. Methods: 2 manufacturing companies with obvious noise hazard in workplace were selected into the study. Health management level was distinguished through field investigation and verification. Questionnaire focus on basic knowledge of hearing health, acceptance level of noise hazard, comfort of wearing hearing protectors and atmosphere in workplace was designed and was used to investigate the knowledge and behavior toward hearing protection. Results: Hearing protectors that meet the level of protection are distributed throughout the workplaces. Although company A has a lower noise hazards level, the health management system was poorly executed. The proportion of workers persisting in wearing hearing protectors throughout the work shift in company A was lower than B (P<0.01) . Workers in company A intended to underestimate the noise level (P<0.01) and the health effect of hearing loss (P<0.01) . All the workers were worry about suffering from hearing loss (P>0.05) , but those in company B had more positive attitude toward the protection of hearing protector (P<0.01) and relied on the protector (P<0.01) . The awareness of protection, in turn, help workers adapt attitude and get used to wearing hearing protectors consciously in workplace (P<0.01) . Conclusion: Health management performance play a key role in help workers form good knowledge and behavior. To protect workplace health, employers need to creative a healthy supportive environment for workers.

[Significance of the NLRP3 inflammasome expression in rats with acute lung injury induced by phosgene].

Objective: To investigate changes of NLRP3 signal transduction pathway of acute lung injury induced by phosgene to analyze NLRP3-mediated IL-1ß release inflammatory process in rats. Methods: Rats were randomly divided into two groups, 10 rats in the Air group that consists of the rats with air exposure, 10 rats in the Psg group that consists of the rats with phosgene exposure at 8.33 g/m(3) for 5 min. The specimens of serum, bronchoalveolar lavage fluid (BALF) and lung were collected after 6h. Morphological changes were observed by HE staining. The expression of NLRP3 in the lung of two groups was detected by immunohistochemistry. NLRP3、ASC and caspase-1 expression in the lung tissue was quantified by Western blot. Reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the expression of NLRP3、ASC and caspase-1 mRNA in the lung tissue. The concentrations of IL-1ß、IL-18 and IL-33 in the serum and BALF were measured by enzyme-linked immunosorbent assay. RT-PCR were used to detect the expression of IL-1ß、IL-18 and IL-33 mRNA in the lung tissue. Results: We successfully replicated the model of phosgene-induced ALI in rats. Morphological of HE staining after phosgene exposure to 6 h observed inflammatory cell infiltration in lung tissue in Phosgene group. Immunohistochemical staining results showed that there were many NLRP3 positive cells in lung tissue in Phosgene group. The levels of NLRP3 and caspase-1 mRNA and protein expression in lung were significantly increased (P<0.05) in Phosgene group, but no significant change was observed in lung ASC mRNA and protein expression (P>0.05) . Compared with Air group, the serum, BALF and lung tissue of IL-1ß、IL-18 and IL-33 mRNA and protein expression were significantly increased (P<0.01) in Phosgene group. Conclusion: NLRP3-mediated inflammatory response probably involved in the process of the phosgene, so it maybe one of the pathogenesis of acute lung injury.

[HSP70 gene polymorphism on genetic susceptibility to the coal worker's penumoconiosis of han nationality in Xinjiang, China.]

Objective: To explore the influence of heat shock protein 70 (HSP70) gene genetic susceptibility of coal worker's pneumoconiosis among the han nationality in xinjiang. Methods: 156 coal worker's pneumoconiosis patients and 96 mine workers were randomly selected from the han coal worker's pneumoconiosis patients and attend the health check retirement mine workers from March to December, 2014 in Xinjiang Uygur Autonomous Region of Occupational Disease Hospital. Using TaqMan genotyping methods to detect HSP70 genotype distribution in the two groups. Results: The HSP70-1+190 loci GC genotype occurrence frequencies of coal worker's pneumoconiosis was significantly higher than the control group (χ2=6.75, P<0.05) , the risk of coal worker's pneumoconiosis armed with HSP70-1+190 GC genotype individual was 2.21 times of CC genotype individual (95%CI: 1.03~4.75) , and HSP70-2+1267 and HSP70-hom+2437 loci polymorphism were no significant difference between the two groups (HSP70-2+1267: χ2=3.30, P=0.19; HSP70-hom+2437: χ2=0.12, P=0.94) . Conclusion: HSP70-1+190 GC genotypes may be a susceptible genotype, the genotype individual may be more likely to suffer from coal worker's pneumoconiosis.

Gamma-diketone peripheral neuropathy III. Neurofilament gene expression.

Evidence suggests the morphologic hallmark of gamma-diketone neuropathy is axon atrophy and that this effect is associated with reduced neurofilament (NF) subunit protein content (Toxicol Appl Pharmacol 2000;165:141-7). To investigate the mechanism of diminished NF content, subunit (NF-L, -M and -H) gene expression was quantified in dorsal root ganglion (DRG) of slightly affected and moderately intoxicated groups of rats exposed to 2,5-hexanedione (HD) at one of three daily dosing rates (175, 250 and 400 mg/kg per day). Results show that sensory ganglia from slightly affected rats exhibited no changes in gene expression, whereas at a moderate level of neurotoxicity, each dosing protocol was associated with small but significant reductions (approximately 20%) in mean NF subunit mRNA. This was not a generalized effect on expression of cytoskeletal components in sensory ganglia since tubulin message levels were not affected. Although the observed reduction in NF gene expression might be related to diminished levels of subunit proteins in peripheral nerve, the actual contribution is likely to be minimal. The magnitude of effect was small and did not correspond to the dose-rate dependent effect of HD on respective isotype proteins. The mechanism of gamma-diketone-induced axon atrophy is unknown but might involve local changes in axonal NF phosphorylation and degradation.

gamma-diketone peripheral neuropathy. II. Neurofilament subunit content.

Quantitative morphometric analyses have demonstrated that axon atrophy is the primary neuropathic alteration in peripheral nerve of 2,5-hexanedione (HD)-intoxicated rats (Lehning et al., Toxicol. Appl. Pharmacol. 165, 127-140, 2000). Research suggests that axon caliber is regulated by neurofilament (NF) content and density. Therefore, as a possible mechanism of atrophy, NF subunit (NF-L, -M, and -H) proteins were quantitated in moderately affected rats intoxicated with HD at three daily dosing rates (175, 250, and 400 mg/kg/day). Analyses of subunit protein contents in proximal sciatic nerves indicated uniformly small decreases, which corresponded to minimal changes in axon area occurring in this region. In distal tibial nerve, subunit proteins were decreased substantially (40-70%) when rats were exposed to the 175 and 250 mg/kg/day doses. These reductions in NFs corresponded to significant decreases (approximately 50%) in tibial axon area induced by lower dosing rates. In contrast, 400 mg/kg/day produced similar changes in caliber but smaller reductions (18-25%) in NF-L, -M, and -H levels. This suggests that a decrement in axonal NF content is unlikely to be solely responsible for gamma-diketone-induced axon atrophy and that the corresponding mechanism probably involves additional changes in factors regulating NF density. Analysis of NF content in peripheral nerve also identified the presence of anomolous higher molecular weight NF-H proteins. However, the neurotoxicological significance of these abnormal subunits is uncertain based on their limited occurrence and inconsistent spatiotemporal expression.