Apigenin intervenes in liver fibrosis by regulating PKM2-HIF-1α mediated oxidative stress.

Apigenin (API) is a natural flavonoid compound with antioxidant, anti fibrotic, anti-inflammatory and other effects, but there is limited research on the effect of API on liver fibrosis. This study aims to explore the effect and potential mechanism of API on liver fibrosis induced by CCl4 in mice. The results indicate that API reduces oxidative stress levels, inhibits hepatic stellate cell (HSC) activation, and exerts anti liver fibrosis effects by regulating the PKM2-HIF-1α pathway. We observed that API alleviated liver tissue pathological damage and collagen deposition in CCl4 induced mouse liver fibrosis model, promoting the recovery of liver function in mice with liver fibrosis. In addition, the API inhibits the transition of Pyruvate kinase isozyme type M2 (PKM2) from dimer to tetramer formation by regulating the EGFR-MEK1/2-ERK1/2 pathway, thereby preventing dimer from entering the nucleus and blocking PKM2-HIF-1α access. This change leads to a decrease in malondialdehyde (MDA) and Catalase (CAT) levels and an increase in glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) levels, as well as total antioxidant capacity (T-AOC) in the liver of liver fibrosis mice. At the same time, API downregulated the expression of α-smooth muscle actin (α-SMA), Vimentin and Desmin in the liver tissue of mice with liver fibrosis, inhibited the activation of HSC, and reduced collagen deposition. These results indicate that API can inhibit HSC activation and alleviate CCl4 induced liver fibrosis by inhibiting the PKM2-HIF-1α pathway and reducing oxidative stress, laying an important foundation for the development and clinical application of API as a novel drug for treating liver fibrosis.

Immune Regulation Patterns in Response to Environmental Pollutant Chromate Exposure-Related Genetic Damage: A Cross-Sectional Study Applying Machine Learning Methods.

Exposure to hexavalent chromium damages genetic materials like DNA and chromosomes, further elevating cancer risk, yet research rarely focuses on related immunological mechanisms, which play an important role in the occurrence and development of cancer. We investigated the association between blood chromium (Cr) levels and genetic damage biomarkers as well as the immune regulatory mechanism involved, such as costimulatory molecules, in 120 workers exposed to chromates. Higher blood Cr levels were linearly correlated with higher genetic damage, reflected by urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and blood micronucleus frequency (MNF). Exploratory factor analysis revealed that both positive and negative immune regulation patterns were positively associated with blood Cr. Specifically, higher levels of programmed cell death protein 1 (PD-1; mediated proportion: 4.12%), programmed cell death ligand 1 (PD-L1; 5.22%), lymphocyte activation gene 3 (LAG-3; 2.11%), and their constitutive positive immune regulation pattern (5.86%) indirectly positively influenced the relationship between blood Cr and urinary 8-OHdG. NOD-like receptor family pyrin domain containing 3 (NLRP3) positively affected the association between blood Cr levels and inflammatory immunity. This study, using machine learning, investigated immune regulation and its potential role in chromate-induced genetic damage, providing insights into complex relationships and emphasizing the need for further research.

Relationships between blood chromium exposure and liver injury: Exploring the mediating role of systemic inflammation in a chromate-exposed population.

Hexavalent chromium and its compounds are prevalent pollutants, especially in the work environment, pose a significant risk for multisystem toxicity and cancers. While it is known that chromium accumulation in the liver can cause damage, the dose-response relationship between blood chromium (Cr) and liver injury, as well as the possible potential toxic mechanisms involved, remains poorly understood. To address this, we conducted a follow-up study of 590 visits from 305 participants to investigate the associations of blood Cr with biomarkers for liver injury, including serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), and direct bilirubin (DBIL), and to evaluate the mediating effects of systemic inflammation. Platelet (PLT) and the platelet-to-lymphocyte ratio (PLR) were utilized as biomarkers of systemic inflammation. In the linear mixed-effects analyses, each 1-unit increase in blood Cr level was associated with estimated effect percentage increases of 0.82% (0.11%, 1.53%) in TBIL, 1.67% (0.06%, 3.28%) in DBIL, 0.73% (0.04%, 1.43%) in ALT and 2.08% (0.29%, 3.87%) in AST, respectively. Furthermore, PLT mediated 10.04%, 11.35%, and 10.77% increases in TBIL, DBIL, and ALT levels induced by chromate, respectively. In addition, PLR mediated 8.26% and 15.58% of the association between blood Cr and TBIL or ALT. These findings shed light on the mechanisms underlying blood Cr-induced liver injury, which is partly due to worsening systemic inflammation.

Hexavalent chromium caused DNA damage repair and apoptosis via the PI3K/AKT/FOXO1 pathway triggered by oxidative stress in the lung of rat.

Hexavalent chromium [Cr(VI)] is an occupational carcinogen that accumulates in the lungs and causes lung injury and even lung cancer. 36 SD male rats received inhalable intratracheal instillation of Cr(VI) (0.05, 0.25 mg Cr/kg) or the same volume (3 ml/kg) of normal saline weekly for 28 days (total 5 times). After 28 days of exposure, half of the rats in each group were sacrificed for investigation, and the rest stopped exposure and began to be self-repaired for two weeks. Histopathology analyses revealed that Cr(VI) induced slight dilatation and hemorrhage of perialveolar capillaries, pulmonary bronchodilation, and congestion with peripheral flaky-like necrosis accompanied by inflammatory cell infiltration, especially the 0.25 mg Cr/kg group. Cr(VI) exposure caused the increase of blood Cr, urinary Cr, MDA, urinary 8-hydroxy-2' -deoxyguanosine (8-OHdG), and the decrease of GSH and MDA, while two-week repair only reduced urinary Cr. Exposure to Cr(VI) significantly upregulated FOXO1 and downregulated p-AKT and p-FOXO1 for two weeks. PI3K in the 0.25 mg Cr/kg group was inhibited after two weeks of repair. Cr(VI) exposure mainly promoted GADD45a and CHK2 in the exposure group, promoted Bim, Bax/Bcl-2, and suppressed Bcl-2 and Bcl-xL in the repair group. These results demonstrate that Cr(VI) may induce DNA damage repair and apoptosis in the lung by activating the PI3K/AKT/FOXO1 pathway. Two-week repair may alleviate oxidative stress and DNA damage induced by Cr(VI) exposure but couldn't eliminate its effects. This study provides a new perspective for exploring the Cr(VI) induced lung cancer mechanism.

Blood leukocyte count as a systemic inflammatory biomarker associated with a more rapid spirometric decline in a large cohort of iron and steel industry workers.

OBJECTIVE: Iron and steel industry workers are exposed to high levels of inhalable dust particles that contain various elements, including metals, and cause occupational lung diseases. We aim to assess the relationship between occupational dust exposure, systemic inflammation, and spirometric decline in a cohort of Chinese iron and steel workers. METHODS: We studied 7513 workers who participated in a Health Surveillance program at Wugang Institute for Occupational Health between 2008 and 2017. Time-weighted exposure intensity (TWEI) of dust was quantified based on self-reported dust exposure history, the experience of occupational hygienists, and historical data of dust exposure for workers with certain job titles. A linear mixed-effects model was used for association analyses. RESULTS: The average annual change of lung function was - 50.78 ml/year in forced expiratory volume in 1 s (FEV1) and - 34.36 ml/year in forced vital capacity (FVC) in males, and - 39.06 ml/year in FEV1 and - 26.66 ml/year in FVC in females. Higher TWEI prior to baseline was associated with lower longitudinal measurements of FEV1 and FVC but not with their decline rates. Higher WBC and its differential at baseline were associated with lower longitudinal measurements and a more rapid decline of FEV1 and FVC in a dose-dependent monotonically increasing manner. Moreover, the increase of WBC and its differential post-baseline was also associated with a more rapid decline of FEV1 and FVC. CONCLUSIONS: Our findings support the important role of systemic inflammation in affecting the temporal change of lung function in iron and steel industry workers.

Chronic exposure to diesel exhaust may cause small airway wall thickening without lumen narrowing: a quantitative computerized tomography study in Chinese diesel engine testers.

BACKGROUND: Diesel exhaust (DE) is a major source of ultrafine particulate matters (PM) in ambient air and contaminates many occupational settings. Airway remodeling assessed using computerized tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural changes of small airways caused by chronic DE exposure is unknown. Wall and lumen areas of 6th and 9th generations of four candidate airways were quantified using end-inhalation CT scans in 78 diesel engine testers (DET) and 76 non-DETs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response relationship. RESULTS: Environmental monitoring and CCAM showed a much higher PM exposure in DETs, which was associated with higher wall area and wall area percent for 6th generation of airways. However, no reduction in lumen area was identified. No study subjects met spirometry diagnosis of airway obstruction. This suggested that small airway wall thickening without lumen narrowing may be an early feature of airway remodeling in DETs. The effect of DE exposure status on wall area percent did not differ by lobes or smoking status. Although the trend test was of borderline significance between categorized CCAM and wall area percent, subjects in the highest CCAM category has a 14% increase in wall area percent for the 6th generation of airways compared to subjects in the lowest category. The impact of DE exposure on FEV1 can be partially explained by the wall area percent with mediation effect size equal to 20%, Pperm = 0.028). CONCLUSIONS: Small airway wall thickening without lumen narrowing may be an early image feature detected by CT and underlie the pathology of lung injury in DETs. The pattern of changes in small airway dimensions, i.e., thicker airway wall without lumen narrowing caused by occupational DE exposure was different to that (i.e., thicker airway wall with lumen narrowing) seen in our previous study of workers exposed to nano-scale carbon black aerosol, suggesting constituents other than carbon cores may contribute to such differences. Our study provides some imaging indications of the understanding of the pulmonary toxicity of combustion derived airborne particulate matters in humans.

Carbon content in airway macrophages and genomic instability in Chinese carbon black packers.

Carbon black (CB) particulates as virtually pure elemental carbon can deposit deep in the lungs of humans. International Agency for Research on Cancer classified CB as a Group 2B carcinogen due to inconclusive human evidence. A molecular epidemiological study was conducted in an established cohort of CB packers (CBP) to assess associations between CB exposure and genomic instability in peripheral lymphocytes using cytokinesis-block micronucleus assay (CBMN). Carbon content in airway macrophages (CCAM) was quantified as a bio-effective dosimeter for chronic CB exposure. Dose-response observed in CBPs was compared to that seen in workers exposed to diesel exhaust. The association between CB exposure status and CBMN endpoints was identified in 85 CBPs and 106 non-CBPs from a 2012 visit and replicated in 127 CBPs and 105 non-CBPs from a 2018 visit. The proportion of cytoplasm area occupied by carbon particles in airway macrophages was over fivefold higher in current CBPs compared to non-CBPs and was associated with CBMN endpoints in a dose-dependent manner. CB aerosol and diesel exhaust shared the same potency of inducing genomic instability in workers. Circulatory pro-inflammatory factors especially TNF-α was found to mediate associations between CB exposure and CBMN endpoints. In vitro functional validation supported the role of TNF-α in inducing genomic instability. An estimated range of lower limits of benchmark dose of 4.19-7.28% of CCAM was recommended for risk assessment. Chronic CB exposure increased genomic instability in human circulation and this provided novel evidence supporting its reclassification as a human carcinogen.

[Association between single nucleotides polymorphism of catalase gene and susceptibility to noise-induced hearing loss in occupational population].

OBJECTIVE: To investigate the relationship between single nucleotides polymorphism of catalase(CAT) gene and susceptibility to noise-induced hearing loss(NIHL) in occupational noise exposed population. METHODS: A case-control study of 1∶1 was conducted to select 286 workers with binaural high frequency average hearing threshold ≥40 dB(HL), from 2006 to 2015 in a cohort study of occupational noise exposure workers in Henan Province. According to the type of work, the age difference was not more than 5 years and the length of exposure to noise was not more than 2 years. The polymorphism of 8 single nucleotides in CAT gene was detected by medium SNPscanTM, and the relationship between 8 single nucleotides polymorphism of CAT gene and NIHL susceptibility was analyzed by multivariate conditional logistic regression. RESULTS: Under the dominant model of rs208679 locus of CAT gene [(GA GG)/AA], the risk of NIHL in individuals carrying GA or GG genotype was 1. 431 times higher than that in individuals carrying AA genotype(95%CI 1. 020-2. 009), and P=0. 038. CONCLUSION: G, a mutant at rs208679 site of CAT gene, may be one of the risk factors for NIHL susceptibility.

Effect of GRM7 polymorphisms on the development of noise-induced hearing loss in Chinese Han workers: a nested case-control study.

BACKGROUND: Noise-induced hearing loss (NIHL) is a complex, irreversible disease caused by the interaction of genetic and environmental factors. In recent years, a great many studies have been done to explore the NIHL susceptibility genes among humans. So far, high powerful detections have been founded that genes of potassium ion channel genes (KCNQ4 and KCNE1), catalase (CAT), protocadherin 15 (PCDH15), myosin 14 (MYH14) and heart shock protein (HSP70) which have been identified in more than one population may be associated with the susceptibility to NIHL. As for metabolic glutamate receptor7 gene (GRM7), a lot of researches mainly focus on age-related hearing loss (ARHL) and the results have shown that the polymorphisms of GRM7 are linked to the development of ARHL. However, little is known about the association of GRM7 and the susceptibility to NIHL. Therefore, the aim of this study was to explore the effect of GRM7 polymorphisms on the susceptibility to NIHL. METHODS: A nested case-control study based on the cohort in a Chinese steel factory was implemented in 292 cases and 584 controls matched with the same sex, the age difference ≤ 5 years old, the same type of work, duration of occupational noise exposure ≤2 years. Five single nucleotide polymorphisms (SNPs) of GRM7 were gained through selecting and genotyping SNPs. Conditional logistic regression analysis was used to assess the main effect of GRM7 polymorphisms on the susceptibility to NIHL and the gene-by-environment interaction. Furthermore, the gene-by-gene interactions were analyzed by generalized multiple dimensionality reduction (GMDR). RESULTS: This research discovered for the first time that the mutant allele C in rs1485175 of the GMR7 may decrease individuals' susceptibility to NIHL. The interaction between rs1485175 and cumulative noise exposure (CNE) at high level was found after the stratification according to CNE (p/p bon = 0.014/0.007, OR = 0.550, 95% CI: 0.340-0.891). Permutation test of GMDR suggested that rs1920109, rs1485175 and rs9826579 in GRM7 might interact with each other in the process of developing NIHL (p = 0.037). CONCLUSIONS: The results suggest that the mutant allele C of rs1485175 in GRM7 may reduce the susceptibility to NIHL in Chinese Han population.

[Relationship between GRM7 gene polymorphisms and the susceptbility to noise-induced hearing loss].

OBJECTIVE: To investigate the relationship between metabolic glutamate receptor 7 gene( GRM7) polymorphisms and the susceptibility to noise-induced hearing loss( NIHL) in Chinese Han occupational population. METHODS: Using a nested case-control study with a 1 ∶ 1 matching, a total of 277 cases of contacting noise workers were selected from a cohort in a steel factory. According to the matching criteria: the same sex, the same type of work, the age difference ≤ 5 years, contact noise length ≤ 2 years, 277 controls were selected. The 8 single nucleotide polymorphisms( SNPs) of the GRM7 gene, rs3749380, rs11928865, rs9877154, rs3828472, rs9819783, rs11920109, rs1485175 and rs9826579, were detected by SNPscanTMmethod. The 4 gene models, the additive model, dominant model, recessive model, codominant model, were constructed to explore the biological association with NIHL susceptibility. The possible diplotype of each subject was constructed using Phase 2. 0. 2 to analyze its relationship with NIHL. According to the layered cumulative noise exposure( CNE), the interactions between the influencing factor were analyzed. The relationship between the GRM7 gene and NIHL was analyzed by single factor and multivariate factors conditional logistic regression analysis. RESULTS: The comparison of general demographic characteristics between the hearing loss group and control group showed that smoking could increase the risk of developing NIHL by 2. 051 times( 95 % CI 1. 456-2. 891, P< 0. 001). No statistically significant difference was found in the analysis of GRM7 polymorphisms and the susceptibility to NIHL. CONCLUSION: Smoking may increase the risk of NIHL. The relationship between GRM7 polymorphisms and the susceptibility to NIHL has not been found in this study.

Genetic variation in EYA4 on the risk of noise-induced hearing loss in Chinese steelworks firm sample.

OBJECTIVES: Noise-induced hearing loss is one of the most serious occupational diseases worldwide. It is caused by interactions between environmental and genetic factors. The purpose of this study was to examine the association between the genetic susceptibility of the eye absent homolog 4 (EYA4) gene and the risk of developing noise-induced hearing loss in China. METHODS: A case-control association study was carried out with 326 hearing loss cases and 326 controls matched with age and duration of noise exposure, drawn from a cohort of steel workers. Five single nucleotide polymorphisms (SNPs) in the EYA4 were selected and genotyped. Logistic regression was performed to analyse the main effect of genotypes and interactions between genotypes and individual/environmental factors adjusted for confounding factors. Moreover, generalised multiple dimensionality reduction was applied to further detect interaction among the 5 selected SNPs. RESULTS: Analysis revealed that locus polymorphism of rs3813346 was associated with the risk of developing noise-induced hearing loss in the dominance model, the codominance model and the addictive model (p=0.004, 0.009 and 0.003, respectively). A significant interaction between rs9321402 and cumulative noise exposure was found (p=0.002). A significant main effect p value (p=0.006) was obtained in the high-level exposure group (cumulative noise exposure ≥98 dB(A)). Generalised multiple dimensionality reduction indicated that the combined interaction of the 2 loci-rs3813346 and rs9493627-significantly affected the incidence of noise-induced hearing loss. CONCLUSIONS: The research suggests that EYA4 genetic variant and its interaction with noise levels may modify the susceptibility to develop noise-induced hearing loss in Chinese population.

Long-term exposure to diesel engine exhaust induces primary DNA damage: a population-based study.

OBJECTIVES: Diesel engine exhaust (DEE) is a ubiquitous environmental pollutant and is carcinogenic to humans. To seek early and sensitive biomarkers for prediction of adverse health effects, we analysed the components of DEE particles, and examined the genetic and oxidative damages in DEE-exposed workers. METHODS: 101 male diesel engine testing workers who were constantly exposed to DEE and 106 matched controls were enrolled in the present study. The components of DEE were analysed, including fine particulate matter (PM2.5), element carbon (EC), nitrogen dioxide (NO2), sulfur dioxide (SO2) and polycyclic aromatic hydrocarbons (PAHs). Postshift urine samples were collected and analysed for 1-hydroxypyrene (1-OHP), an internal exposure marker for DEE. Levels of DNA strand breaks and oxidised purines, defined as formamidopyrimidine-DNA glycosylase (FPG) sites in leucocytes, were measured by medium throughput Comet assay. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was also used to determine the level of oxidative stress. RESULTS: We found higher levels of PM2.5, EC, NO2, SO2 and PAHs in the diesel engine testing workshop and significantly higher urinary 1-OHP concentrations in exposed subjects (p<0.001). Compared with controls, the levels of parameters in normal Comet and FPG-Comet assay were all significantly higher in DEE-exposed workers (p<0.001), and in a dose-dependent and time-dependent manner. There were no significant differences between DEE-exposed workers and controls in regard to leucocyte FPG sensitive sites and urinary 8-OHdG levels. CONCLUSIONS: These findings suggest that DEE exposure mainly induces DNA damage, which might be used as an early biomarker for risk assessment of DEE exposure.

Associations between DNA methylation in DNA damage response-related genes and cytokinesis-block micronucleus cytome index in diesel engine exhaust-exposed workers.

Recently, diesel engine exhaust (DEE) was reclassified as a known carcinogen to humans. DNA methylation alterations in DNA damage response (DDR)-related genes have the potential to affect DEE exposure-related cancer risk. However, the evidence regarding the association between DEE exposure and methylation alterations in DDR-related genes is limited. In 117 DEE-exposed workers and 112 non-DEE-exposed workers, we measured urinary concentrations of six mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs). We also determined the methylation levels of three DDR-related genes (p16, RASSF1A, and MGMT) and LINE-1 by bisulfite-pyrosequencing assay. We found that DEE-exposed workers exhibited significantly lower mean promoter methylation levels of p16, RASSF1A, and MGMT than non-DEE-exposed workers (all p < 0.001). In all study subjects and non-smoking workers, increasing quartiles of urinary summed OH-PAHs was associated with hypomethylation of p16, RASSF1A, and MGMT (all p < 0.05). In non-smoking workers, methylation in p16, RASSF1A, and MGMT decreased by 0.36 % [95 % confidential interval (CI): -0.60, -0.11 %], 0.46 % (95 % CI: -0.79, -0.14 %), and 0.55 % (95 % CI: -0.95, -0.15 %), respectively, in association with highest versus lowest quartile of urinary summed OH-PAHs. In addition, p16, RASSF1A, MGMT, and LINE-1 methylation levels showed negative correlations with cytokinesis-block micronucleus cytome index which was previously measured in the same workers (all p < 0.05). In conclusion, our results clearly indicated that DEE exposure and increased genetic damage were associated with hypomethylation of p16, RASSF1A, and MGMT. Future studies with larger sample size are needed to confirm these associations.

Cytotoxicity of diesel engine exhaust among the Chinese occupational population: a complement of cytokinesis-block micronucleus cytome.

Diesel engine exhaust (DEE), a ubiquitous environmental pollutant, has been associated with adverse health effects. Revelation of cellular and molecular changes is critical for understanding environmental exposure-related diseases. Although the molecular-level effects of DEE exposure have been investigated, whether it is associated with aberrant changes at cellular level is largely unknown at the population level. In the present study, we measured urinary concentrations of 6 mono-hydroxylated PAHs (OH-PAHs) and cytotoxicity-related endpoints including apoptosis and necrosis frequencies, and nuclear division cytotoxicity index (NDCI) in peripheral blood lymphocytes (PBLs) of 79 DEE-exposed workers and 59 non-DEE-exposed workers. We found that DEE-exposed workers had significantly higher necrosis frequency and lower NDCI than did non-DEE-exposed workers (both p < 0.001). In all study subjects and nonsmoking workers, urinary summed OH-PAHs was associated with increased necrosis frequency and reduced NDCI. In nonsmoking workers, an interquartile range increase in urinary summed OH-PAHs was associated with 105.03% increase in necrosis frequency and 8.70% decrease in NDCI. Taking advantage of the previous measure of micronucleus frequency, we observed that micronucleus frequency was positively correlated with apoptosis and necrosis frequencies (r = 0.277, p = 0.047 and r = 0.452, p = 0.001, respectively) and negatively correlated with NDCI (r = -0.477, p < 0.001). In conclusion, our results suggested that DEE exposure was associated with increased necrosis frequency and further with reduced NDCI in PBLs, providing evidence of DEE exposure-induced cytotoxicity in humans.

Establishment of a reference value for chromium in the blood for biological monitoring among occupational chromium workers.

The concentration of chromium in the blood (CrB) has been confirmed as a biomarker for occupational chromium exposure, but its biological exposure indices (BEIs) are still unclear, so we collected data from the years 2006 and 2008 (Shandong Province, China) to analyze the relationship between the concentration of chromium in the air (CrA) of the workplaces and CrB to establish a reference value of CrB for biological monitoring of occupational workers. The levels of the indicators for nasal injury, kidney (ß2 microglobulin (ß2-MG)), and genetic damages (8-hydroxy-deoxyguanosine (8-OHdG) and micronucleus (MN)) were measured in all subjects of the year 2011 (Henan Province, China) to verify the protective effect in this reference value of CrB. Compared with the control groups, the concentrations of CrA and CrB in chromium exposed groups were significantly higher (P < 0.05). Positive correlations were found between CrA and CrB in chromium exposed groups (r 2006 = 0.60, r 2008 = 0.35) in the years 2006 and 2008. According to the occupational exposure limitation of CrA (50 µg/m(3), China), the reference value of CrB was recommended to 20 µg/L. The levels of nasal injury, ß2-MG, 8-OhdG, and MN were not significantly different between the low chromium exposed group (CrB ≤ 20 µg/L) and the control group, while the levels of ß2-MG, 8-OHdG, and MN were statistically different in the high chromium exposed group than that in the control group. This research proved that only in occupational workers, CrB could be used as a biomarker to show chromium exposure in the environment. The recommended reference value of CrB was 20 µg/L.

[Analysis of relationship between shift-work and occupational stress among workers from different companies].

OBJECTIVE: To investigate the relationship between work in shifts and occupational stress. METHODS: A total of 5338 employees from 13 companies were investigated by cluster sampling, and occupational stress measuring tools, job content questionnaire, and effort-reward imbalance questionnaire were used to investigate occupational stress factors, stress reaction, and the condition of work in shifts. RESULTS: The employees who worked in shifts accounted for 46.6%. The condition of work in shifts varied significantly across different companies, employees with different individual features (including sex, job title, degree of education, age, working years, smoking, and drinking), and employees with different weekly working times(P<0.01 or P<0.05); health status was associated with work in shifts(P<0.01); compared with the employees who did not work in shifts, those who worked in shifts had significantly lower scores of technology utilization, work control level, psychological need, reward, social support, and job satisfaction(P<0.01 or P<0.05), as well as significantly higher scores of physical demands, effort, depressive symptoms, and negative affectivity(P<0.01). CONCLUSION: Work in shifts can affect health status, and is associated with occupational stress.

[Prevalence and influence factors of hypertension among the workers exposed to noise in steel making and steel rolling workshop of an iron and steel plant].

OBJECTIVE: To investigate the prevalence and influence factors of hypertension among the workers exposed to noise in steel making and steel rolling workshop of an iron and steel plant. METHODS: Using cluster sampling method, 3 150 workers exposed to noise participated in this study. According to do questionnaire survey and blood pressure measurement, 2 924 workers were tested, among which 1 313 workers were from steel making workshop and 1 611 workers were from steel rolling workshop. The relationships between different demographic characteristics, different habits, and different cumulative noise exposures of workers exposed to noise and hypertension were analyzed. RESULTS: For the hypertension prevalence rate, the total prevalence rate was 27.43% (802/2 924), the male was higher than the female (29.88 % (753/2 520) vs 12.13% (49/404), χ² = 55.13, P < 0.001), married ones were higher than the unmarried (29.84% (718/2 406) vs 16.22% (84/518), χ² = 39.76, P < 0.001), the smoking subjects were higher than the no smoking (30.31% (438/1 445) vs 24.61% (364/1 479), χ² = 11.93, P = 0.001), drinking ones were higher than the no drinking (31.53% (541/1 716) vs 21.61% (261/1 208), χ² = 35.05, P < 0.001). The hypertension prevalence rates among the subjects with education background in junior high school and below, high school (secondary) and university and above were separately 44.96%(125/278), 29.95%(455/1 519) and 19.70%(222/1 127) (χ² = 81.65, P < 0.001), among cumulative exposure groups 77-89, 90-94, 95-99, 100-104 and 105-113 were separately 8.43% (14/166), 14.48% (53/366), 24.28% (297/1 223), 36.65% (335/914) and 40.39%(103/255) (χ² = 127.58, P < 0.001). Multivariate logistic regression analysis showed that workers who exposed to cumulative noise in 95-99, 100-104 and 105-113 dB(A) ·year had the higher risk of hypertension, the OR (95%CI) were 1.84 (95% CI: 1.35-2.51), 1.74 (95% CI: 1.24-2.45) and 1.68 (95% CI: 1.09-2.58). Drinking (OR = 1.60, 95% CI: 1.32-1.95) and BMI ≥ 24.0 kg/m² (OR = 1.26, 95% CI: 1.22-1.30) were the risk factors for hypertension as well. CONCLUSION: Cumulative noise exposure, alcohol consumption and above normal BMI may affect the hypertension prevalence rate of the workers exposed to noise.

[Effects of occupational stress and related factors on depression symptoms in train drivers].

OBJECTIVE: To explore the influence of occupational stress and related factors on depression symptoms in train drives. METHODS: In March 2012, by using cluster sampling method, a cross-sectional epidemiological study was conducted in 1 402 train drivers in China. Questionnaires was investigation was conducted by face to face interview. Sample with missing variables on demographic characteristics questionnaire with missed survey variables, and occupational stress related factors and with over 3 item missing in depression symptoms self-rating scale were exclued. Depression symptoms were measured by Center for Epidemiological Survey Depression Scale. The occupational stress related actors were measured by the revised effort-reward imbalance (ERI) model questionnaires and occupational stress measurement scale. Chi-square test was carried out to analyze the differences of the incidence of depressive symptoms among different general characteristics groups, and multivariate logistic regression analysis was conducted to analyze the influence of occupational stress and related factors on depression symptoms in train drivers. RESULTS: The study showed that the average age of 1 402 subjects was (34.95±9.20) years, the length of service were (13.28±9.78) years, the score of depressive symptoms was (24.14±5.98) scores. 902 subjects (64.3%,902/1 402) were classified as people with depressive symptoms, the incidence of depressive symptoms in EMU or high-speed train drivers were the highest (68.0%,51/75); Incidence of depressive symptoms showed that were statistically significant differences in two groups of technical secondary school and college, and incidence of depressive symptoms in the junior college and above group (68.1%,352/517) was higher than that in the senior high school and below group (62.1%, 550/885) (χ(2)=5.02, P=0.025). The results of the multiple logistic regression analysis revealed that high levels of education (OR=1.63, 95%CI: 1.12-2.19), role conflict (OR=1.65, 95% CI: 1.21-2.24), role ambiguity (OR=1.99, 95% CI: 1.45-2.73), negative emotion(OR=2.87, 95%CI: 2.15-3.82), daily tension(OR=2.86, 95%CI: 2.11-3.86), poor colleagues and family support (OR=1.55, 95% CI: 1.11-2.16 and OR=1.75, 95% CI: 1.27-2.41) were risk factors of depressive symptoms, but positive emotion (OR=0.72, 95% CI: 0.53-0.96), self-esteem (OR=0.22, 95% CI: 0.16-0.30), and job itself satisfaction (OR=0.48, 95%CI: 0.35-0.65) were protective factors of depressive symptoms in train drivers. CONCLUSION: Train drivers, in particular EMU or high-speed train drivers who were prone to depressive symptoms. To arrange reasonably job roles and tasks, increase support from superiors, colleagues, and family, bring up healthy and coordinated personality, keep a good mood, promote job satisfaction, reduce the daily tension have positive effects on reducing the occurrence of depressive symptoms for train drivers.

[The effect of occupational stress on depression symptoms among 244 policemen in a city].

OBJECTIVE: To explore the influence of occupational stress related factors on depression symptoms among 244 policemen in a city in China. METHODS: In May 2011, 287 policemen from a city public security bureau were recruited to this survey by cluster sampling method. We deleted questionnaires which include missing variables on demographic characteristics and factors associated with occupational stress questionnaires which include over 3 missing items. 244 policemen were included in this study. Depression symptoms and occupational stressors were measured using Chinese version of depression self-reported questionnaire, job content questionnaire, Chinese version of effort-reward imbalances questionnaire, job hazard scale and occupational stress inventory. Depression symptom scores and the relationship between the variables and occupational stress were analyzed by Spearman correlation analysis and multiple regression analysis. RESULTS: The Median (P25-P75) of depression symptom scores of all respondents was 16.50 (11.00-25.00). 144 were policemen with no depression symptoms and 100 were with depression symptoms. The median (P25-P75) of depression symptoms scores among policemen with length of serves <10, 10-19, 20-29 and ≥30 was 17.00 (8.00-26.00), 16.00 (11.00-24.50), 19.00 (12.00-27.00), and 12.00 (6.25-15.00), respectively. The difference of scores was significant among length of serves groups (χ2=9.52, P=0.023). The scores of psychological demands, sleep disorder, daily life stress and negative affectivity among policemen with depression symptoms were 17.00 (8.00-26.00), 16.00 (11.00-24.50), 19.00 (12.00-27.00), and 12.00 (6.25-15.00), respectively, which were higher than those with no depression symptoms (24.00 (22.00-25.00), 8.00 (5.00-13.00), 8.00 (6.00-10.00), 1.00 (0-2.75)), and the differences were significant (Z=3.82, 5.39, 5.15, 6.41, P<0.001). Spearman correlation analysis revealed that depression symptoms score was positively related to sleep disorder, commitment effort, psychological demands, daily life stress, negative affectivity and job hazards scores. Correlations coefficient were 0.44, 0.28, 0.28, 0.33, 0.38, 0.44, and 0.38, respectively (P<0.001). Multiple linear regression analysis indicated that self-esteem, daily life stress and negative affectivity had bigger contribution on the depression symptoms scores. The standard regression coefficient was -0.46, 0.19 and 0.13, respectively (P<0.001, P=0.001, P=0.030). CONCLUSION: Sleep disorder, commitment effort, psychological demands, daily life stress, negative affectivity and job hazards scores were the inducement of depression symptoms for policemen. To reduce the daily life stress, negative affectivity and improve the quality of sleep, add to self-esteem, reward and social support have positive effects on reducing the occurrence of depressive symptoms for police.

[Effects on cell proliferation capacity and genome stability in periphery lymphocytes of occupational diesel exhaust exposed workers].

OBJECTIVE: To investigate the cell proliferation and genome stability in workers with occupational exposure to diesel exhaust (DE). METHODS: In 2012, 117 DE-exposed workers and 106 control workers were recruited by cluster sampling in this study. The demographic data were obtained by questionnaire survey. The airborne fine particle and enriched polycyclic aromatic hydrocarbons (PAHs) at different workplaces were collected and analyzed. The concentrations of main PAHs monohydroxy metabolites in the urine were determined by high performance liquid chromatography-mass spectrometry (LC-MS), which could reflect the internal exposure level of DE. The cell proliferation capacity and genome stability in the periphery lymphocytes of workers were evaluated by cytokinesis-block micronucleus (CBMN) cytome assay. RESULTS: The concentrations (median (P5-P95)) of total PAHs monohydroxy metabolites in the urine of exposed group and control group were 12.96 (4.73-28.10), 4.76 (0.90-15.00) µg/L, respectively, and the exposed group was higher than that of controls (Z = -8.77, P < 0.001). The nuclear division index (NDI) of exposed group and control group was 1.68±0.13, 1.85±0.16, respectively, and the NDI of exposed group showed significantly decreased (t = 8.86, P < 0.001), while the genome instability index calculated by micronucleus, nuclear bridges and nuclear buds, of exposed group and control group was 13.27±6.26, 4.83±3.38, respectively, and the exposed group had statistically significant increase (Z = -10.08, P < 0.001). The tertiles of total PAHs monohydroxy metabolites in the urine were categorized into low, medium and high groups (<5.96, 5.96-12.46, >12.46 µg/L). With the NDI decreased, 1.81±0.17, 1.79±0.17, 1.68±0.14 (F = 13.14, P < 0.001), genome instability index began to increase 5.80±4.15, 9.97±7.14, 11.99±6.61 (/1 000), respectively (χ(2) = 36.74, P < 0.001). With the increase of total PAHs monohydroxy metabolites level in corresponding groups. In addition, the NDI was negatively correlated with the frequencies of micronucleus, nuclear bridges, nuclear buds and genome instability index, respectively, and the difference was statistically significant (P < 0.001). CONCLUSIONS: DE exposure lead to inhibition of cell proliferation capacity and increase genome instability in the peripheral lymphocytes of occupational-exposed population, providing important clues and evidence for early biomarkers monitoring.