Prevalence and its risk factors for low back pain among operation and maintenance personnel in wind farms.

BACKGROUND: With the increasingly severe energy shortage and climate change problems, developing wind power has become a key energy development strategy and an inevitable choice to protect the ecological environment worldwide. The purpose of this study was to investigate the prevalence of low back pain (LBP) and analyze its risk factors among operation and maintenance personnel in wind farms (OMPWF). METHODS: A cross-sectional survey of 151 OMPWF was performed, and a comprehensive questionnaire, which was modified and combined from Nordic Musculoskeletal Questionnaires (NMQ), Washington State Ergonomics Tool (WSET) and Syndrome Checklist-90(SCL-90) was used to assess the prevalence and risk factors of LBP among OMPWF. RESULTS: The prevalence of LBP was 88.74 % (134/151) among OMPWF. The multivariable model highlighted four related factors: backrest, somatization, squatting and lifting objects weighing more than 10 lb more than twice per minute. CONCLUSIONS: The prevalence of LBP among OMPWF appears to be high and highlights a major occupational health concern.

[Genotoxic effects of oral-exposed TiO2 nanoparticles on bone marrow cells in young rats].

OBJECTIVE: To explore the genotoxic effects of oral-exposed TiO2 nanoparticles on bone marrow cells in young rats. METHODS: Twenty-eight SD male young rats (4 weeks old) were randomly divided into 4 groups, which were exposed to TiO2 nanoparticles ((75 ± 15) nm, anatase) through intragastric administration at 0, 10, 50 and 200 mg/kg body weight (bw) every day for 30 days. The bone marrow cells were collected for micronuclei and γ-H2AX immunofluorescence analysis. RESULTS: The percentage of γ-H2AX foci-positive cells (37.4 ± 10.0)% in the 50 mg/kg bw dose group were significantly higher than that in the control group (19.8 ± 3.1)% (t value was -17.59, P < 0.01). No significantly difference was found in polychromatic erythrocyte/normochromatic erythrocyte (PCE/NCE) ratio and PCE micronucleus rate between three experimental groups and control group. CONCLUSION: TiO2 nanoparticles can increase the frequency of DNA double-strand breaks in bone marrow cells, but has no effect on micronucleus of bone marrow cells in young rats.

Susceptibility of young and adult rats to the oral toxicity of titanium dioxide nanoparticles.

Titanium dioxide nanoparticles (TiO2 NPs) have potential applications as food additives, but concerns persist about their safety. Children are identified as having the highest exposure and may face the greatest health risks. However, the toxicological sensitivity of TiO2 NPs in different ages is not clear. Here, a comparative toxicity study of TiO2 NPs in 3-week (youth) and 8-week (adult) old Sprague-Dawley rats is reported following oral exposure at doses of 0, 10, 50, 200 mg kg(-1) body weight per day for 30 days. The organ mass and histology, blood biochemistry and redox state, intestinal function, and biodistribution of NPs are characterized. The results show that TiO2 NPs induce different toxic effects on young and adult rats. The liver edema, heart injuries and non-allergic mast cell activation in stomach tissues are found in young rats. On the other hand, only slight injury in the liver and kidney and decreased intestinal permeability and molybdenum contents are found in adult rats. Furthermore, TiO2 NP exposure can provoke reductive stress (i.e., increased reduced glutathione (GSH)/oxidized glutathione (GSSG) ratios) in plasmas through enhancing the glucose and GSH levels in young rats or reducing the glutathione peroxidase (GSH-Px) acitivity and GSSG levels in adult rats. These results suggest that different ages may require different biomarkers for identifying and monitoring oral toxicity of nanoparticles.

Alteration of Th1/Th2/Th17 cytokine profile and humoral immune responses associated with chromate exposure.

BACKGROUND: The role of chromate exposure in the deregulation of total lymphocyte and other immune factors is largely unclear. OBJECTIVES: We aimed to examine alteration of the Th1/Th2/Th17 cytokine profile and humoral indicators caused by occupational chromate exposure. METHODS: A cross-sectional study was conducted in two similar workshops (groups 1 and 2) with 106 male occupational workers and 50 matched local controls. Environmental and biological exposures were assessed by measuring chromium concentrations in workplace air, and in whole blood and urine samples of the workers. Cytokines in serum (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17A) were determined by CBA assay, while immunoglobin (IgA, IgM, IgG, IgE) and complement (C3, C4) were evaluated by immunonephelometric and ELISA methods. Micronucleus analysis was also used to explore the relationship between genotoxicity and immunotoxicity. RESULTS: Compared with the control group, environmental chromate exposure in groups 1 and 2 was much higher, and the mean values of IL-6, IL-10, IFN-γ, IL-17A and IFN-γ/IL-4 were significantly decreased in group 1. In group 2, IgA and IgG levels were reduced, while C3 and C4 were increased. Levels of IFN-γ, IgG and IgA were all inversely associated with whole blood chromium, while C3 and C4 were positively associated with whole blood chromium (p<0.05). Both IL-10 and IL-17A were inversely associated with urine chromium. Correlations were also found between IL-10, IL-17A and micronucleus (r=-0.329, r=-0.312, respectively). CONCLUSIONS: Occupational exposure to chromate could downregulate the cellular and humoral factors of the immune system.

[Evidence-based study of chromate exposed workers' health surveillance indexes].

OBJECTIVE: The health surveillance proposal for chromate exposed workers was provided and analyzed on the evidence-based study and then to be improved. METHOD: Firstly, the related literatures were searched about liver damage, micronuclei, urinary chromium and hexavalent chromium exposure in Evidence Based Medicine Reviews such as Cochran library, OVID Medline, Web of knowledge in December 2011; and then, these literatures were reviewed in according to inclusion and exclusion criteria; 22 articles totally were retrieved, evaluated and classified in according to the grading standard by Oxford Centre for Evidence-based Medicine.Finally, field epidemiological investigation was further adopted to confirm the efficiency and feasibility of this proposal, combined with cost-effectiveness analysis:the ratio of total cost divided survival years was used to express the cost-effectiveness. RESULT: Only the glutamic pyruvic transaminase test could not reflect liver damage caused by chromate exposure well; Urinary chromium correlated well with the index reflecting body damage caused by chromate exposure; Binucleated cells micronucleus index in peripheral blood lymphocyte could reflect the genetic damage caused by chromate exposure. As for health economic evaluation of chromate lung cancer, the value of cost/effectiveness was ¥42 321.61 per year that was far below the value of common people (¥252 868.97 per year) . CONCLUSION: It was suggested that serum glutamic pyruvic transaminase test should be replaced by liver function test, urinary chromium should be classified as a compulsory index and binucleated cells micronucleus index in peripheral blood lymphocyte should be supplied as a recommended index.

[Dynamic observation of pulmonary ventilation function in workers contacting chromate].

OBJECTIVE: To explore changes of pulmonary ventilation function of chromate exposed workers. METHODS: Ninety-five chromate exposed workers were used as exposure group, and forty-two workers without chromate exposure as control group. Pulmonary ventilation function was performed two times in the winter of 2010 and 2011 respectively in one chromate manufactured factory in Henan Province. RESULTS: In 2010, pulmonary ventilation function of chromate exposed group compared with the control group, forced vital capacity [FVC, (75.38±15.23) L vs. (83.99±26.52)L], forced expiratory volume in one second [FEV1,(82.13±16.51)L vs.(91.24±30.03)L], FEV1/FVC(112.10±13.23 vs. 116.18±11.32), peak expiratory flow [PEF,(74.31±28.09) L/s vs.(78.13±28.34)L/s], maximal expiratory flow [MEF,(101.23±46.37) L/s vs. (110.02±41.40)L/s], maximum ventilation volume [MVV,(90.82± 16.89)L/min vs. (99.95±22.61)L/min]were significantly decreased(P<0.05). In 2011, pulmonary ventilation function of chromate exposed group compared with the control group, FVC[(72.34±14.18)L vs.(81.01±20.79)L], FEV1[(76.04±16.20)L vs.(86.71±24.53)L], FEV1/FVC(109.10±16.18 vs.114.08±10.79), PEF[(71.35±24.87 )L/s vs.(75.36±20.67)L/s], MEF[(96.51±30.17)L/s vs.(107.11±34.81)L/s], MVV[(84.85±21.22)L/min vs. (96.77±22.63)L/min] were also significantly decreased(P<0.05). 2011 compared with 2010, pulmonary ventilation function of chromate exposed group FEV1[(76.04±16.20)L vs.( 82.13±16.51)L], MEF[(96.51±30.17)L/s vs. (101.23±46.37)L/s], MVV[(84.85±21.22)L/min vs. (90.82±16.89)L/min] were significantly decreased(P<0.05). Comparing the classification and category of pulmonary dysfunction based on FVC, FEV1, FVC/ FEV1, no difference was found for classification between the two groups and the category of pulmonary dysfunction almost belongs to limit type, which did not change with exposed time. CONCLUSION: Chronic chromate exposure can cause significant effects on pulmonary function of the workers, and the types of work in production can affect the results.

[Impact of specimen collection and storage consumable products on trace element quantitative analysis].

OBJECTIVE: This study aimed to explore the impact of specimen collection and storage consumable products on trace element quantitative analysis. METHODS: Devices and consumable products of different brands used in specimen collection or storage were selected and treated separately as below:urine collection and storage tubes (Brand A, B, C and D, 2 samples for each brand) were treated with 1% of HNO(3) volume fraction for 2 - 4 h; blood taking device (Brand O, P and Q, 3 samples for each brand) were used for ultra-pure water samples collecting as simulation of blood sampling;dust sampling filters (Brand X, Y and Z, 2 samples for each brand) were cold digested by nitric acid for 12 h, followed by microwave digestion. Then cadmium, cobalt, chromium, copper, iron, manganese, molybdenum, nickel, lead, selenium, stannum, titanium, vanadium and zinc concentrations in the solutions obtained during the course of collect or storage were quantified by inductively coupled plasma mass spectrometer. RESULTS: For the urine collection and storage consumable products, background values of elements were described as mean of parellel samples. The consentration of 14 quantified elements were relatively low for 5 ml cryogenic vials (brand B) with background values range of 0.001 - 0.350 ng/ml. The background values of copper of 50 ml centrifuge tubes (brand A), chromium of 5 ml cryogenic vials (brand C) and zinc of 1.5 ml centrifuge tubes (brand D) were relatively high, which were 1.900, 1.095 and 1.368 ng/ml, respectively. Background values of elements in blood sampling devices were described as x(-) ± s. Background values of chromium for brand O, P and Q were (0.120 ± 0.017), (0.337 ± 0.093) and (0.360 ± 0.035) ng/ml; for copper were (0.050 ± 0.001), (0.017 ± 0.012) and (0.103 ± 0.015) ng/ml; for lead were (0.057 ± 0.072), (0.183 ± 0.118) and (0.347 ± 0.006) ng/ml; for titanium were (7.883 ± 0.145), (8.863 ± 0.190) and (8.613 ± 0.274) ng/ml; zinc were (2.240 ± 0.573), (42.140 ± 22.756) and (8.850 ± 3.670) ng/ml. There were statistically differences of background values for chromium, copper, lead, titanium and zinc among the above three brands of blood sampling devices (all P values < 0.05). For air sampling filters, background values of elements were described as mean of parellel samples. Background values of chromium and nickel of sampling filters (brand X) were lowest, which were 17.000 and 15.400 ng per piece, respectively; while background values for other elements were relatively high, the quantification of cadmium, cobalt, copper, iron, manganese, molybdenum, lead, selenium, stannum, titanium, vanadium and zinc were 0.250, 0.550, 48.500, 690.000, 25.500, 0.900, 6.500, 10.550, 7.950, 10.500, 0.850, 370.000 ng per piece, respectively. Background values of chromium and nickel of sampling filters (brand Z) were highest, which were 171.000 and 29.850 ng per piece. CONCLUSION: Background values of trace elements varied among products of different brands, and the most noticable differences were found in chromium, manganese, nickel, lead, stannum and zinc.

Assessing the suitability of 8-OHdG and micronuclei as genotoxic biomarkers in chromate-exposed workers: a cross-sectional study.

OBJECTIVES: We aimed to investigate suitable conditions of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and micronucleus (MN) as genotoxic biomarkers at different levels of occupational chromate exposure. DESIGN: A cross-sectional study was used. PARTICIPANTS: 84 workers who were exposed to chromate for at least 1 year were chosen as the chromate exposed group, while 30 non-exposed individuals were used as controls. MAIN OUTCOME MEASURES: Environmental and biological exposure to chromate was respectively assessed by measuring the concentration of chromate in the air (CrA) and blood (CrB) by inductively coupled plasma mass spectrometer (ICP-MS) in all participants. MN indicators, including micronucleus cell count (MNCC), micro-nucleus count (MNC), nuclear bridge (NPB) and nuclear bud (NBUD) were calculated by the cytokinesis-block micronucleus test (CBMN), while the urinary 8-OHdG was measured by the ELISA method and normalised by the concentration of Cre. RESULTS: Compared with the control group, the levels of CrA, CrB, MNCC, MNC and 8-OHdG in the chromate-exposed group were all significantly higher (p<0.05). There were positive correlations between log(8-OHdG) and LnMNCC or LnMNC (r=0.377 and 0.362). The levels of LnMNCC, LnMNC and log (8-OHdG) all have parabola correlations with the concentration of CrB. However, there was a significantly positive correlation between log (8-OHdG) and CrB when the CrB level was below 10.50 µg/L (r=0.355), while a positive correlation was also found between LnMNCC or LnMNC and CrB when the CrB level was lower than 9.10 µg/L (r=0.365 and 0.269, respectively). CONCLUSIONS: MN and 8-OHdG can be used as genotoxic biomarkers in the chromate-exposed group, but it is only when CrB levels are lower than 9.10 and 10.50 µg/L, respectively, that they can accurately reflect the degree of genetic damage.

Effects of repeated Cr(VI) intratracheal instillation on club (Clara) cells and activation of nuclear factor-kappa B pathway via oxidative stress.

Hexavalent chromium [Cr(VI)] exposure is known to induce respiratory inflammation and contribute to lung cancer development, but little is known about its target cell type in lung. In the current study, we investigated the effects of repeated Cr(VI) intratracheal instillation on club (Clara) cells and club (Clara) cell secretory protein (CC16) in rats and explored whether the nuclear factor-kappa B (NF-κB) related pathway was involved. We also studied the role of orally delivered Zn against Cr-induced adverse health effects. For four weeks, sixty Sprague-Dawley male rats received weekly intratracheal instillation of potassium dichromate (K2Cr2O7) at 0, 0.063 and 0.630mgCr/kg with or without daily intragastric administration of zinc sulfate (ZnSO4) at 10mg Zn/kg. Results showed that exposure to Cr(VI) significantly increased the organ coefficient of lung (organ weight as a percentage of body weight), albumin and total protein level in bronchoalveolar lavage fluid (BALF), indicating lung injury and compromised bronchoalveolar/blood barrier (BA/BB) integrity. With increasing Cr(VI) dose, the secretion of CC16 decreased in a dose-dependent manner, suggesting that CC16 can serve as a peripheral biomarker for club cell damage during early lung injury induced by Cr(VI). Increased expression of NF-κB were observed in club cells in both Cr-exposed groups, indicating upregulation of NF-κB, which can be induced by reactive oxygen species (ROS) generated by club cells during Cr reduction with repetitive Cr(VI) exposure. Cr-induced DNA damage was also observed, as significant increase of 8-OHdG was found with Cr exposure at 0.630mg/kg week. Oral Zn supplementation did not alleviate changes in serum CC16 level under Cr(VI) exposure, indicating its failure in protecting against Cr(VI)-induced club cell damage.

Genotoxic evaluation of titanium dioxide nanoparticles in vivo and in vitro.

With the extensive application of titanium dioxide (TiO2) nanoparticles (NPs) in food industry, there is a rising debate concerning the possible risk associated with exposure to TiO2 NPs. The purpose of this study is to evaluate the genotoxicity of TiO2 NPs using in vivo and in vitro test systems. In vivo study, the adult male Sprague-Dawley rats were exposed to anatase TiO2 NPs (75 ± 15 nm) through intragastric administration at 0, 10, 50 and 200mg/kg body weight every day for 30 days. The γ-H2AX assay showed TiO2 NPs could induce DNA double strand breaks in bone marrow cells after oral administration. However, the micronucleus test revealed that the oral-exposed TiO2 NPs did not cause damage to chromosomes or mitotic apparatus observably in rat bone marrow cells. In vitro study, Chinese hamster lung fibroblasts (V79 cells) were exposed to TiO2 NPs at the dose of 0, 5, 10, 20, 50 and 100 µg/mL. Significant decreases in cell viability were detected in all the treated groups after 24h and 48h exposure. Significant DNA damage was only observed at the concentration of 100 µg/mL after 24h treatment using the comet assay. The obvious gene mutation was observed at the concentration of 20 and 100 µg/mL after 2h treatment using hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene mutation assay. This study presented a comprehensive genotoxic evaluation of TiO2 NPs, and TiO2 NPs were shown to be genotoxic both in vivo and in vitro tests. The gene mutation and DNA strand breaks seem to be more sensitive genetic endpoints for the detection of TiO2 NPs induced genotoxic effects.

Association of folate deficiency and selected tumor marker concentrations in long-term hexavalent chromium exposed population.

Both hexavalent chromium [Cr (VI)] exposure and folate deficiency have been associated with increased cancer risks. Our previous studies have found folate deficiency in Cr (VI) exposed population. Here the relationship between some tumor markers and folate status in long-term Cr (VI) exposure was investigated carefully to show the multiple aspects of Cr (VI) carcinogenesis. A group of 115 workers occupationally exposed to chromate and 60 matched, unexposed controls in Shandong province of China were recruited. Environmental and biological exposure assessments including personal exposure to airborne Cr and Cr contents in erythrocytes were performed. Serum folate, plasma total homocysteine (tHcy) and plasma carcinoembryonic antigen (CEA), neuron specific enolase (NSE), squamous cell carcinoma antigen (SCC), cytokeratin fragment antigen 21-1 (CYFRA 21-1), cancer antigen 72-4 (CA72-4), as well as α-fetoprotein (AFP) were measured. Smoking index (SI) was also calculated to discriminate possible confounding effects of smoking status. Serum folate level decreased significantly, while plasma tHcy, CEA, NSE, SCC, CYFRA21-1, CA72-4 and AFP concentrations increased significantly after Cr (VI) exposure. Meanwhile, plasma CEA, NSE and SCC were negatively correlated with serum folate. SI was negatively correlated with serum folate but positively correlated with plasma tHcy, CEA and NSE levels. Present study suggests that folate deficiency was associated with increased cancer risks and might be affected by smoking in Cr (VI) exposed population. Folate might play a key role in Cr (VI) carcinogenesis although further detailed investigations are needed to clarify the mechanism of this process.

Oxidative DNA damage and global DNA hypomethylation are related to folate deficiency in chromate manufacturing workers.

Exposure to hexavalent chromium [Cr (VI)] can cause DNA damage, genetic instability and increase the risk of cancer development. Folate deficiency affects DNA methylation and reduces the stability of the genetic material. However, the correlation between folate deficiency and DNA damage has never been clearly elucidated in chromate workers. In this study, we recruited one hundred and fifteen workers from chromate producing facilities as testing subjects and sixty local residents without chromium exposure history served as controls. The results showed an evident accumulation of Cr in peripheral red blood cells accompanied by a significantly decreased serum folate in chromate exposed workers. The decreased serum folate was associated with an increased urinary 8-hydroxy-2'-deoxyguanosine, DNA strand breaks and global DNA hypomethylation. These findings suggest that chronic occupational chromate exposure could induce folate depletion, which may further promote DNA damages and global DNA hypomethylation. Adequate folate supplement may provide benefit to chromate sufferers in stabilization of genetic material and reduce the risk of cancer development.