Nanotoxicity of tungsten trioxide nanosheets containing oxygen vacancy to human umbilical vein endothelial cells.

Because of the excellent performance in photochemistry, WO3 is increasingly applied in the field of biology and medicine. However, little is known about the mechanism of WO3 cytotoxicity. In this work, WO3 nanosheets with oxygen vacancy are synthesized by solvothermal method, then characterized and added to culture medium of human umbilical vein endothelial cells (HUVECs) with different concentrations. We characterized and analyzed the morphology of nano-WO3 by transmission electron microscopy and calculated the specific data of oxygen vacancy by XPS. It is the first time the effect of WO3-x on cells that WO3-x can cause oxidative stress in HUVEC cells, resulting in DNA damage and thus promoting apoptosis. Transcriptome sequencing is performed on cells treated with low and high concentrations of WO3-x, and a series of key signals affecting cell proliferation and apoptosis are detected in differentially expressed genes, which indicates the research direction of nanotoxicity. The expression levels of key genes are also verified by quantitative PCR after cell treatment with different concentrations of WO3-x. This work fills the gap between the biocompatibility of nano WO3-x materials and molecular cytology and paves the way for investigating the mechanism and risks of oxygen vacancy in cancer therapy.

Acute inhalation of tungsten particles results in early signs of cardiac injury.

Epidemiological studies have established that exposure to tungsten increases the risk of developing cardiovascular diseases. However, no studies have investigated how tungsten affects cardiac function or the development of cardiovascular disease. Inhalation of tungsten particulates is relevant in occupational settings, and inhalation of particulate matter has a known causative role in driving cardiovascular disease. This study examined if acute inhalation to tungsten particulates affects cardiac function and leads to heart tissue alterations. Female BALB/c mice were exposed to Filtered Air or 1.5 ± 0.23 mg/m3 tungsten particles, using a whole-body inhalation chamber, 4 times over the course of two weeks. Inhalation exposure resulted in mild pulmonary inflammation characterized by an increased percentage and number of macrophages and metabolomic changes in the lungs. Cardiac output was significantly decreased in the tungsten-exposed group. Additionally, A', an indicator of the amount of work required by the atria to fill the heart was elevated. Cardiac gene expression analysis revealed, tungsten exposure increased expression of pro-inflammatory cytokines, markers of remodeling and fibrosis, and oxidative stress genes. These data strongly suggest exposure to tungsten results in cardiac injury characterized by early signs of diastolic dysfunction. Functional findings are in parallel, demonstrating cardiac oxidative stress, inflammation, and early fibrotic changes. Tungsten accumulation data would suggest these cardiac changes are driven by systemic consequences of pulmonary damage.

In vivo toxicity evaluation of a polyoxotungstate nanocluster as a promising contrast agent for computed tomography.

In this study, we demonstrate for the first time, that a discrete metal-oxo cluster α-/ß-K6P2W18O62 (WD-POM) exhibits superior performance as a computed tomography (CT) contrast agent, in comparison to the standard contrast agent iohexol. A toxicity evaluation of WD-POM was performed according to standard toxicological protocols using Wistar albino rats. The maximum tolerable dose (MTD) of 2000 mg/kg was initially determined after oral WD-POM application. The acute intravenous toxicity of single WD-POM doses (1/3, 1/5, and 1/10 MTD), which are at least fifty times higher than the typically used dose (0.015 mmol W kg-1) of tungsten-based contrast agents, was evaluated for 14 days. The results of arterial blood gas analysis, CO-oximetry status, electrolyte and lactate levels for 1/10 MTD group (80% survival rate) indicated the mixed respiratory and metabolic acidosis. The highest deposition of WD-POM (0.6 ppm tungsten) was found in the kidney, followed by liver (0.15 ppm tungsten), for which the histological analysis revealed morphological irregularities, although the renal function parameters (creatinine and BUN levels) were within the physiological range. This study is the first and important step in evaluating side effects of polyoxometalate nanoclusters, which in recent years have shown a large potential as therapeutics and contrast agents.

Tungsten toxicity on kidney tubular epithelial cells induces renal inflammation and M1-macrophage polarization.

Tungsten is widely used in medical, industrial, and military applications. The environmental exposure to tungsten has increased over the past several years, and few studies have addressed its potential toxicity. In this study, we evaluated the effects of chronic oral tungsten exposure (100 ppm) on renal inflammation in male mice. We found that 30- or 90-day tungsten exposure led to the accumulation of LAMP1-positive lysosomes in renal tubular epithelial cells. In addition, the kidneys of mice exposed to tungsten showed interstitial infiltration of leukocytes, myeloid cells, and macrophages together with increased levels of proinflammatory cytokines and p50/p65-NFkB subunits. In proximal tubule epithelial cells (HK-2) in vitro, tungsten induced a similar inflammatory status characterized by increased mRNA levels of CSF1, IL34, CXCL2, and CXCL10 and NFkB activation. Moreover, tungsten exposure reduced HK-2 cell viability and enhanced reactive oxygen species generation. Conditioned media from HK-2 cells treated with tungsten induced an M1-proinflammatory polarization of RAW macrophages as evidenced by increased levels of iNOS and interleukin-6 and decreased levels of the M2-antiinflammatory marker CD206. These effects were not observed when RAW cells were exposed to conditioned media from HK-2 cells treated with tungsten and supplemented with the antioxidant N-acetylcysteine (NAC). Similarly, direct tungsten exposure induced M1-proinflammatory polarization of RAW cells that was prevented by NAC co-treatment. Altogether, our data suggest that prolonged tungsten exposure leads to oxidative injury in the kidney ultimately leading to chronic renal inflammation characterized by a proinflammatory status in kidney tubular epithelial cells and immune cell infiltration.

Comparative pulmonary toxicity assessment of tungsten trioxide and tungsten trioxide hydrate nanoparticles.

Tungsten trioxide (WO3)-based nanoparticles (NPs) are gaining popularity because of their exciting potential for photocatalytic applications; however, the toxic potential of WO3-based NPs remains a concern. In this study, we evaluated the toxic risk of WO3 NPs and hydrated WO3 NPs (WO3·H2O NPs) using lung cells and explored the underlying mechanism. WO3 NPs and WO3·H2O NPs significantly decreased the number of viable cells (59.5 %-85.8 % of control) and promoted apoptosis in human alveolar basal epithelial A549 cells after a 24-h exposure. Both WO3 NPs and WO3·H2O NPs reduced the expression of heme oxygenase-1 (0.15-0.33 folds of control) and superoxide dismutase 2 (0.31-0.66 folds of control) and increased reactive oxygen species production (1.4-2.6 folds of control) and 8-hydroxy-2'-deoxyguanosine accumulation (1.22-1.43 folds of control). The results showed that WO3 NPs have higher cytotoxicity and oxidative potential than WO3·H2O NPs. In addition, the WO3 NP cellular uptake rate was significantly higher than the WO3·H2O NPs uptake rate in pulmonary cells. The greater extent of oxidative adverse effects induced by WO3-based NPs appears to be related to the enhanced particle uptake. WO3 NPs and WO3·H2O NPs exposure led to the secretion of inflammatory factor interleukin 6 (1.63-3.42 folds of control). Decreases in serpin family A member 1 gene expression (0.28-0.58 folds of control) and increases in the oxidation of neutrophil elastase inhibitor (1.34-1.62 folds of control) in pulmonary cells also suggest that exposure to WO3 NPs and WO3·H2O NPs raises the risk of developing chronic obstructive pulmonary disease. Taken together, our findings indicate that the toxic risk of WO3 NPs and WO3·H2O NPs must be considered when manufacturing and applying WO3-based NPs.

Valorization of Waste Tungsten Filament into mpg-C3N4-WO3 Photocatalyst: A Sustainable e-Waste Management and Wastewater Treatment.

The waste of tungsten filament materials in the environment is one of the reasons for environmental pollution, and it is very dangerous to animals and plants. To date, not much attention has been given to its utility or recyclability. Herein, the present work reported the synthesis of tungsten trioxide nanoparticles (WO3 NPs) by the utilization of cost-free waste tungsten filament by a simple calcination method. A mesoporous graphitic carbon nitride-tungsten trioxide (mpg-C3N4-WO3) composite designed from the WO3 NPs produced from tungsten filament waste and thiourea as a carbon and nitrogen precursor by a one-step calcination method. The synthesized samples were characterized and confirmed by different characterization techniques. The photocatalytic behavior of the synthesized mpg-C3N4-WO3 composite was assessed, with respect to the effect of initial pH, amount of photocatalyst, dye concentration, and reaction time, as well for the degradation of Methylene Blue (MB) dye under sunlight. The best photocatalytic performance (92%) was achieved using mpg-C3N4-WO3 with experimental condition ([photocatalyst] = 100 mg/L, [MB]0 = 10 mg/L, pH 8, and time = 120 min) under sunlight irradiation with excellent photostability than that of isolated mpg-C3N4 and WO3 NPs. The histotoxicological studies also showed that the photodegraded products of MB were found to be nontoxic and did not structurally changes in the gill architecture as well as brain tissues of freshwater fish Labeo rohita.

Long-term impact of the Tyrnyauz tungsten-molybdenum mining and processing factory waste on environmental pollution and children's population.

We studied the consequences of the long-term impact of remediated tailing ponds from the Tyrnyauz tungsten-molybdenum mining and processing factory on the environmental pollution and children living in the area. For more than 60 years, the factory has been engaged in the development of tungsten-molybdenum deposits by open-pit and mine methods and the enrichment of the extracted ore. More than 252,771 thousand tons of waste accumulated in its dumps and tailings ponds. This 170-hectare tailing pond contains more than 125 million tons of waste with arsenic, tungsten, molybdenum and other metals. To examine the possible accumulation of potentially toxic elements in children's bodies, we determined the content of heavy metals in drinking water and in the hair of children. An exfoliated buccal micronucleus test was used to determine the cytogenetic status of children. We did not find significant differences in the content of heavy metals inherent of a tailing pond in children's hair from polluted area compared to the control zone. In buccal cells of children living in the vicinity of the tailings pond, the total number of cytogenetic abnormalities was increased by 4.1 times, the total index of proliferation by 1.5 times, early destruction of the nucleus by 2 times and apoptosis by 1.2 times compared to the clean zone. Thus, we identified a genotoxic and cytotoxic effect on children living in the vicinity of the tailing ponds, which led to an increase in the number of children belonging to the medium- and high-risk groups. No correlations were found between the content of heavy metals in children's hair and the frequency of cells with cytogenetic abnormalities. Weak positive correlation was found between the content of manganese, zinc and copper in children's hair and the indicators of buccal epithelial cell proliferation.

Pulmonary toxicity, genotoxicity, and carcinogenicity evaluation of molybdenum, lithium, and tungsten: A review.

Molybdenum, lithium, and tungsten are constituents of many products, and exposure to these elements potentially occurs at work. Therefore it is important to determine at what levels they are toxic, and thus we set out to review their pulmonary toxicity, genotoxicity, and carcinogenicity. After pulmonary exposure, molybdenum and tungsten are increased in multiple tissues; data on the distribution of lithium are limited. Excretion of all three elements is both via faeces and urine. Molybdenum trioxide exerted pulmonary toxicity in a 2-year inhalation study in rats and mice with a lowest-observed-adverse-effect concentration (LOAEC) of 6.6 mg Mo/m3. Lithium chloride had a LOAEC of 1.9 mg Li/m3 after subacute inhalation in rabbits. Tungsten oxide nanoparticles resulted in a no-observed-adverse-effect concentration (NOAEC) of 5 mg/m3 after inhalation in hamsters. In another study, tungsten blue oxide had a LOAEC of 63 mg W/m3 in rats. Concerning genotoxicity, for molybdenum, the in vivo genotoxicity after inhalation remains unknown; however, there was some evidence of carcinogenicity of molybdenum trioxide. The data on the genotoxicity of lithium are equivocal, and one carcinogenicity study was negative. Tungsten seems to have a genotoxic potential, but the data on carcinogenicity are equivocal. In conclusion, for all three elements, dose descriptors for inhalation toxicity were identified, and the potential for genotoxicity and carcinogenicity was assessed.

A sensitive electrochemical sensor for environmental toxicity monitoring based on tungsten disulfide nanosheets/hydroxylated carbon nanotubes nanocomposite.

There has been growing concern about the toxic effects of pollutants in the aquatic environment. In this study, a novel cell-based electrochemical sensor was developed to detect the toxicity of contaminants in water samples. A screen-printed carbon electrode, which was low-cost, energy-efficient, and disposable, was modified with tungsten disulfide nanosheets/hydroxylated multi-walled carbon nanotubes (WS2/MWCNTs-OH) to improve electrocatalytic performance and sensitivity. The surface morphology, structure, and electrochemical property of WS2/MWCNTs-OH composite film were characterized by emission scanning electron microscopy, transmission electron microscopy, energy dispersive spectroscopy, X-ray diffraction, Raman spectroscopy, and electrochemical impedance spectroscopy. Grass carp kidney cell line was utilized as the sensor biorecognition element to determine the electrochemical signals and evaluate cell viability. The sensor was used to detect the toxicity of one typical contaminant (2,4,6-trichlorophenol) and two emerging contaminants (bisphenol AF and polystyrene nanoplastics). The 48 h half inhibitory concentration (IC50) values were 169.96 µM, 21.88 µM, and 123.01 µg mL-1, respectively, which were lower than those of conventional MTT assay, indicating the higher sensitivity of the proposed sensor. Furthermore, the practical application of the sensor was evaluated in chemical wastewater samples. This study provides an up-and-coming tool for environmental toxicity monitoring.

Subchronic oral exposure of tungsten induces myofibroblast transformation and various markers of kidney fibrosis.

Tungsten is a naturally occurring transition element used in a broad range of applications. As a result of its extensive use, we are increasingly exposed to tungsten from our environment, including potable water, since tungsten can become bioaccessible in ground sources. The kidneys are particularly susceptible to tungsten exposure as this is the main site for tungsten excretion. In this study, we investigated the prolonged effects of tungsten on the kidneys and how this may impact injury and function. When mice were exposed to tungsten in their drinking water for 1 mo, kidney function had not significantly changed. Following 3-mo exposure, mice were presented with deterioration in kidney function as determined by serum and urine creatinine levels. During 3 mo of tungsten exposure, murine kidneys demonstrated significant increases in the myofibroblast marker α-smooth muscle actin (αSMA) and extracellular matrix products: fibronectin, collagen, and matricellular proteins. In addition, Masson's trichrome and hematoxylin-eosin (H&E) staining revealed an increase in fibrotic tissue and vacuolization of tubular epithelial cells, respectively, from kidneys of tungsten-treated mice, indicative of renal injury. In vitro treatment of kidney fibroblasts with tungsten led to increased proliferation and upregulation of transforming growth factor ß1 (TGFß1), which was consistent with the appearance of fibroblast-to-myofibroblast transition (FMT) markers. Our data suggest that continuous exposure to tungsten impairs kidney function that may lead to the development of chronic kidney disease (CKD).

Inhalation of Tungsten Metal Particulates Alters the Lung and Bone Microenvironments Following Acute Exposure.

Inhalation of tungsten particulates is a relevant route of exposure in occupational and military settings. Exposure to tungsten alloys is associated with increased incidence of lung pathologies, including interstitial lung disease and cancer. We have demonstrated, oral exposure to soluble tungsten enhances breast cancer metastasis to the lungs through changes in the surrounding microenvironment. However, more research is required to investigate if changes in the lung microenvironment, following tungsten particulate exposure, can drive tumorigenesis or metastasis to the lung niche. This study examined if inhalation to environmentally relevant concentrations of tungsten particulates caused acute damage to the microenvironment in the lungs and/or systemically using a whole-body inhalation system. Twenty-four female BALB/c mice were exposed to Filtered Air, 0.60 mg/m3, or 1.7 mg/m3 tungsten particulates (<1 µm) for 4 h. Tissue samples were collected at days 1 and 7 post-exposure. Tungsten accumulation in the lungs persisted up to 7 days post-exposure and produced acute changes to the lung microenvironment including increased macrophage and neutrophil infiltration, increased levels of proinflammatory cytokines interleukin 1 beta and C-X-C motif chemokine ligand 1, and an increased percentage of activated fibroblasts (alpha-smooth muscle actin+). Exposure to tungsten also resulted in systemic effects on the bone, including tungsten deposition and transient increases in gene expression of proinflammatory cytokines. Taken together, acute whole-body inhalation of tungsten particulates, at levels commonly observed in occupational and military settings, resulted in changes to the lung and bone microenvironments that may promote tumorigenesis or metastasis and be important molecular drivers of other tungsten-associated lung pathologies such as interstitial lung disease.

Cobalt-related interstitial lung disease or hard metal lung disease: A case series of Chinese workers.

Hard metal lung disease (HMLD) is rarely diagnosed and is caused by the occupational inhalation of hard metal dust, mainly cobalt. The diagnosis of HMLD is based on a thorough occupational dust exposure combined with clinical-radiological-histological findings. We present a series of four Chinese workers who had occupational exposure to cobalt acid lithium or cobalt and tungsten dust. Four patients all complained of intermittent cough, chest tightness, or shortness of breath on exertion. High-resolution computed tomography scans presented bilateral ground-glass attenuation, consolidations, and/or reticular opacities with diffuse small nodules. Histologic findings showed that interstitial inflammation and fibrotic lesions distributed peribronchioles. The infiltrations by macrophages as well as visible multinucleated giant cells indicated giant cell interstitial pneumonia (GIP). Cobalt was detectable in the lung tissues of two patients measured by inductively-coupled plasma mass spectrometry. The first patient was diagnosed with cobalt-related interstitial lung disease (ILD), while the others were HMLD. GIP is the classic pathology of cobalt-related ILD or HMLD. One of the patients showed spontaneous remission after the cessation of exposure, while the other three recovered within 6-32 weeks after avoiding occupational exposure and using corticosteroids. At follow-up, all four patients showed no recurrence. A multidisciplinary diagnostic panel including occupational cobalt exposure evaluation is beneficial to recognize cobalt-related ILD or HMLD and to indicate the necessity of prevention.

Toxicological assessment of commercial monolayer tungsten disulfide nanomaterials aqueous suspensions using human A549 cells and the model fungus Saccharomyces cerevisiae.

The utilization of tungsten disulfide (WS2) nanomaterials in distinct applications is raising due to their unique physico-chemical properties, such as low friction coefficient and high strength, which highlights the necessity to study their potential toxicological effects, due to the potential increase of environmental and human exposure. The aim of this work was to analyze commercially available aqueous dispersions of monolayer tungsten disulfide (2D WS2) nanomaterials with distinct lateral size employing a portfolio of physico-chemical and toxicological evaluations. The structure and stoichiometry of monolayer tungsten disulfide (WS2-ACS-M) and nano size monolayer tungsten disulfide (WS2-ACS-N) was analyzed by Raman spectroscopy, whereas a more quantitative approach to study the nature of formed oxidized species was undertaken employing X-ray photoelectron spectroscopy. Adenocarcinomic human alveolar basal epithelial cells (A549 cells) and the ecotoxicology model Saccharomyces cerevisiae were selected as unicellular eukaryotic systems to assess the cytotoxicity of the nanomaterials. Cell viability and reactive oxygen species (ROS) determinations demonstrated different toxicity levels depending on the cellular model used. While both 2D WS2 suspensions showed very low toxicity towards the A549 cells, a comparable concentration (160 mg L-1) reduced the viability of yeast cells. The toxicity of a nano size 2D WS2 commercialized in dry form from the same provider was also assessed, showing ability to reduce yeast cells viability as well. Overall, the presented data reveal the physico-chemical properties and the potential toxicity of commercial 2D WS2 aqueous suspensions when interacting with distinct eukaryotic organisms, showing differences in function of the biological system exposed.

Cytotoxic and genotoxic assessment of tungsten oxide nanoparticles in Allium cepa cells by Allium ana-telophase and comet assays.

Tungsten oxide nanoparticles or nanopowder (WO3NPs) is commonly used in various industries and also in biomedical applications such as additives, pigments, and biomedical sensors. Non-judicious excessive use of these nanoparticles (NPs) could be a serious human health concern. Therefore, the current study aimed to explore the cytotoxic and genotoxic assessment of WO3NPs through Allium cepa anaphase-telophase and comet assays. Nanoparticles were characterized through the scanning and transmission electron microscopy (TEM), zetasizer, and energy-dispersive X-ray spectroscopy. The mean size and the average diameter of WO3NPs were determined as 21.57 ± 2.48 nm and 349.42 ± 80.65 nm using TEM and a Zetasizer measurement system, respectively. Five concentrations (12.5 mg/L, 25 mg/L, 50 mg/L, 75 mg/L, and 100 mg/L) of WO3NPs were employed on the Allium cepa (A. cepa) roots for 4 h. Significant (p ≤ 0.05) decrease in mitotic index (MI) was shown by WO3NPs at all concentrations. The increase of chromosomal aberrations (CAs) was also observed in a concentration-dependent manner due to the WO3NPs exposure. There was a significant increase (p ≤ 0.05) in DNA damage at all concentrations of WO3NPs on the A. cepa cells. It was concluded that WO3NPs had cytotoxic and genotoxic effects on A. cepa meristematic cells. Moreover, further cytogenetic effects of WO3NPs should be investigated at the molecular level to assess its safety margin.

Tungsten Increases Sex-Specific Osteoclast Differentiation in Murine Bone.

Tungsten is a naturally occurring metal that is increasingly used in industry and medical devices, and is labeled as an emerging environmental contaminant. Like many metals, tungsten accumulates in bone. Our previous data indicate that tungsten decreases differentiation of osteoblasts, bone-forming cells. Herein, we explored the impact of tungsten on osteoclast differentiation, which function in bone resorption. We observed significantly elevated osteoclast numbers in the trabecular bone of femurs following oral exposure to tungsten in male, but not female mice. In order to explore the mechanism(s) by which tungsten increases osteoclast number, we utilized in vitro murine primary and cell line pre-osteoclast models. Although tungsten did not alter the adhesion of osteoclasts to the extracellular matrix protein, vitronectin, we did observe that tungsten enhanced RANKL-induced differentiation into tartrate-resistant acid phosphatase (TRAP)-positive mononucleated osteoclasts. Importantly, tungsten alone had no effect on differentiation or on the number of multinucleated TRAP-positive osteoclasts. Enhanced RANKL-induced differentiation correlated with increased gene expression of differentiated osteoclast markers Nfatc1, Acp5, and Ctsk. Although tungsten did not alter the RANK surface receptor expression, it did modulate its downstream signaling. Co-exposure of tungsten and RANKL resulted in sustained positive p38 signaling. These findings demonstrate that tungsten enhances sex-specific osteoclast differentiation, and together with previous findings of decreased osteoblastogenesis, implicate tungsten as a modulator of bone homeostasis.

Spectroscopic investigation on photocatalytic degradation of methyl orange using Fe2O3/WO3/FeWO4 nanomaterials.

In this study, iron oxide (Fe2O3), tungsten oxide (WO3) and iron-tungstate oxide (FeWO4) nanoparticles (NPs) were synthesized by simple precipitation, acid precipitation, and hydrothermal method respectively. All the spectroscopic analysis reveals that as-synthesized NPs are crystalline with a z-average size of 342, 313 and 373 d.nm respectively. The element compositions, shape and size of the NPs were identified with the help of SEM with EDX analysis. FTIR analysis concluded that the presence of functional groups on the surface of NPs and which responsible for capping and formation of NPs. Besides, the as-synthesized NPs have been used as a photocatalyst for the degradation of Methyl Orange (MO) dye under visible irradiation. FeWO4 NPs (98%) show more effective in the degradation of MO as compared to other NPs. Moreover, the degraded MO and its by-products were used to assess their toxicity on Vigna radiata and RAW 264.7 cell line and which were confirmed that degraded by-products were non-hazardous.

Effect of tungsten-resistant bacteria on uptake of tungsten by lettuce and tungsten speciation in plants.

Tungsten is an emerging contaminant because of its potential toxicity to humans. However, tungsten-plant-microbe interactions remains unknown. The objective of the study was to evaluate the effect of tungsten-resistant bacteria on tungsten species in plants and microbial community structure in soil. Although bacterial inoculation did not affect lettuce (Lactuca sativa L.) growth or tungsten uptake via root, tungsten-resistant bacteria increased translocation of tungsten from root to shoot. Bacterial inoculation slightly oxidized tungsten in lettuce based on tungsten L3 x-ray absorption near-edge structure (XANES). Tungsten in lettuce roots and shoots grown in tungsten(VI)-spiked soil existed as a mixture of tungsten(IV) and tungsten(VI). Tungsten accumulated as polytungstate in the root and monotungstate in the shoot. Inoculation with tungsten-resistant bacteria and plant growth increased microbial diversity in tungsten-contaminated soil. In tungsten-spiked soils without plants, metal-resistant or reducing bacteria were found while bacteria growing in rhizosphere were detected in soils supporting plant growth. These results indicate a role of the bacteria and plants in phytoremediation of tungsten-contaminated soil.