工伤保险行业差别费率确定方法探讨

制定合理的行业差别费率对于工伤保险基金的稳定、促进企业改善安全生产状况具有积极作用.我国工伤保险制度处于起步阶段,有些地区对行业差别费率厘定进行了探索,但费率与风险的关联性不强,影响了低风险企业参加工伤保险统筹的积极性.本文针对工伤统计数据缺乏的现状,分析了现阶段工伤保险行业差别费率确定方法的研究现状,重点讨论了确定行业风险等级的3种方法,即聚类分析法、风险系数测评和模糊风险评估法的应用过程以及优缺点;另外,强调了在确定行业风险指数时,应注意根据不同事故类别的严重度来确定各风险因素指标的权重大小.最后,应用风险评估理论分析工伤保险行业差别费率的运作机理,提出应用工伤赔付支出费用计算行业差别费率的数学公式,此公式原理清晰、操作方便,且有利于各统筹地区根据实际情况划分行业差别费率.     

Ecological selection of bacterial taxa with larger genome sizes in response to polycyclic aromatic hydrocarbons stress

Polycyclic aromatic hydrocarbons(PAHs) are ubiquitous priority pollutants that cause great damage to the natural environment and health. Average genome size in a community is critical for shedding light on microbiome’s functional response to pollution stress within an environment. Here, microcosms under different concentrations were performed to evaluate the selection of PAHs stress on the average genome size in a community. We found the distinct communities of significantly larger genome size w...     

Evaluation of potential toxic effects of occupational inhalation exposure to licorice root dust

Licorice, a plant indigenous to southern Europe, the Middle East, and northern China, exhibits several pharmacological properties, including estrogenic, anti-tumoral, anti-inflammatory, anti-allergenic, and anti-tussive activities. Prolonged use of licorice is known to produce headaches, hypertension, cardiac arrhythmias, edema, lethargy, dyspnea, sodium retention and loss of potassium in humans. However, to date, the potential adverse health effects due to occupational inhalation exposure of licorice root dust remains unknown. This study was, therefore, undertaken to address this issue. In this cross-sectional study, individuals (30 workers) occupationally exposed to licorice root dust at a licorice producing plant in Shiraz, Iran were recruited. Similarly, 30 healthy male unexposed employees at a telecommunications industry, with identical demographic and socioeconomic status, without any past or current exposure to licorice dust or habitual ingestion of this compound, served as the referent group. Systolic and diastolic blood pressures were measured. Further, individuals underwent electrocardiography, clinical examination and blood chemistry tests. To assess the extent to which subjects were exposed to licorice root dust, atmospheric concentrations of this compound were also measured in the plant. There were no differences in age, weight, height and duration of exposure to licorice dust or length of employment between exposed and referent groups. Atmospheric measurement of licorice dust showed that concentration exceeded the permissible limit of 5 mg m^?3. Systolic and diastolic blood pressures of exposed subjects were significantly higher than those of the referent group. Similarly, blood analysis revealed that serum concentrations of potassium and platelet counts were significantly lower in exposed subjects than in referent individuals. Questionnaire data demonstrated that symptoms such as headaches, lethargy, and vertigo were more common in exposed subjects. No abnormal changes were noted in the electrocardiographs of exposed or referent subjects. Our findings provide evidence that inhalation exposure to high concentrations of licorice dust is associated with an increased prevalence of headache, lethargy, and vertigo, as well as hypertension and hypokalemia. None of these changes resulted in increased morbidity and mortality in exposed workers.     

Determination of F2-isoprostanes in cultured human lung epithelial cells after exposure to metal oxide and silica nanoparticles by high-performance liquid chromatography/tandem mass spectrometry

The environmental impact of nanotechnology has caused a great concern. Many in vitro studies showed that many types of nanoparticles were cytotoxic. However, whether these nanoparticles caused cell membrane damage was not well studied. F₂-isoprostanes are specific products of arachidonic acid peroxidation by nonenzymatic reactive oxygen species and are considered as reliable biomarkers of oxidative stress and lipid peroxidation. In this article, we investigated the cytotoxicity of different nanoparticles and the degree of cellular membrane damage by using F₂-isoprostanes as biomarkers after exposure to nanoparticles. The human lung epithelial cell line A549 was exposed to four silica and metal oxide nanoparticles: SiO₂ (15 nm), CeO₂ (20 nm), Fe₂O₃ (30 nm), and ZnO (70 nm). The levels of F₂-isoprostanes were determined by using high-performance liquid chromatography/mass spectrometry. The F₂-isoprostanes’ peak was identified by retention time and molecular ion m/z at 353. Oasis HLB cartridge was used to extract F₂-isoprostanes from cell medium. The results showed that SiO₂, CeO₂, and ZnO nanoparticles increased F₂-isoprostanes levels significantly in A549 cells. Fe₂O₃ nanoparticle also increased F₂-isoprostanes level, but was not significant. This implied that SiO₂, CeO₂, ZnO, and Fe₂O₃ nanoparticles can cause cell membrane damage due to the lipid peroxidation. To the best of our knowledge, this is the first report on the investigation of effects of cellular exposure to metal oxide and silica nanoparticles on the cellular F₂-isoprostanes levels.     

Effects of benzo(a)pyrene on blood components,tumor markers,and oxidative status in mice

This study was carried out to investigate the effect of long-term exposure to benzo(a)pyrene (B(a)P) in mice. Hemogram, tumor markers, oxidative status, and B(a)P residues in liver tissue were evaluated. Sixty albino Swiss mice were randomly distributed equally into three groups; the control was given 0.1?mL corn oil once a week for 8 weeks. The other two groups were given 20 and 40?mg B(a)P per kg body weight once a week orally for the same period. B(a)P-treated mice suffered from depression and ascites, and macrocytic normochromic anemia was recorded at the 16th and 30th week. There was marked leukocytosis with lymphocytosis at the early stage of the experiment, followed by leukopenia, lymphopenia, and neutropenia at the end of the experiment. Monocytes and arginase activity were elevated throughout the experiment. Alpha feto-protein was detected only in the experimental groups in the 30th week of the experiment. A marked increase in lipid peroxides associated with a decrease in reduced glutathione and glutathione-S-transferase (GST) activity was observed in liver homogenate of the B(a)P-exposed animals. Residues of B(a)P were detected in liver tissue with a concentration parallel to the B(a)P dose level. In conclusion, B(a)P caused abnormal changes in the hemogram, evidence of tumor formation through B(a)P-induced oxidative stress, and it was accumulated in the liver tissue of mice.     

Oxidative stress mediated cytotoxicity of TiO2 nano anatase in liver and kidney of Wistar rat

This study examined the adverse effects of TiO₂ nanoparticle (nano-TiO₂) on the kidney and liver of Wistar rats. Changes of serum biochemical parameters and pathological lesions indicated that liver and kidney were significantly affected in animals treated with 50?mg?kg^?1 of nano-TiO₂. The inverse relationship between the level of reactive oxygen species and the activities of superoxide dismutase, catalase, and glutathione peroxidase indicates that nano-TiO₂ induces oxidative stress. A significant increase in the apoptosis of liver and kidney in a dose-dependent manner was also observed. The ultrastructural observations confirmed the internalization of nano-TiO₂ and their direct involvement in the mitochondria-mediated cytotoxicity. Data indicated that nano-TiO₂ induce oxidative stress which produces genotoxicity such as oxidative DNA damage, micronuclei (MN) induction, and cell apoptosis in liver and kidney.     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

Smoke alleviates adverse effects induced by stress on rice

Smoke and salinity are environmental hazards. Smoke produced DNA damage, inflammatory, and oxidative stress in humans while salinity reduced plant yield. However, smoke from plants is beneficial towards plant growth. In this study, smoke of two plants, Buhania varegata (1:1000 and 1:5000 dilutions (v/v)) and Cymbopogon jwarancusa (1:500 and 1:1000), were used to determine effects on different physiological and biochemical parameters in rice Basmati-385 (B-385) and Shaheen Basmati under different saline concentrations (control: 50, 100, and 150 mM). With increasing salinity, germination%, seedling growth, K⁺, Ca⁺, cell membrane stability, and total nitrogen and protein contents were decreased while Na⁺ content increased. However, seeds primed with different dilution of smoke significantly diminished the adverse effects of salinity and shown to produce positive responses in all of the above parameters. The most effective dilutions were 1:5000 for Buhania varegata and C-500 for Cymbopogon jwarancusa. It seems that priming with plant smoke solution is a potent stimulant for plant growth exerting a significant role in physiology and biochemistry of rice plants under saline condition.