The debate on tungsten (W) is fostered by its continuous usage in military munitions. Reports demonstrate W solubilizes in soil and can migrate into drinking water supplies and, therefore, is a potential health risk to humans. This study evaluated the reproductive, systemic and neurobehavioral effects of sodium tungstate (NaW) in rats following 70 days of daily pre-and postnatal exposure via oral gavage to 5, 62.5 and 125 mg/kg/day of NaW through mating, gestation and weaning (PND 0-20). Daily administration of NaW produced no overt evidence of toxicity and had no apparent effect on mating success or offspring physical development. Distress vocalizations were elevated in F(1) offspring from the high dose group, whereas righting reflex showed unexpected sex differences where males demonstrated faster righting than females; however, the effects were not dose-dependent. Locomotor activity was affected in both low and high-dose groups of F(1) females. Low-dose group showed increased distance traveled, more time in ambulatory movements and less time in stereotypic behavior than controls or high dose animals. The high-dose group had more time in stereotypical movements than controls, and less time resting than controls and the lowest exposure group. Maternal retrieval was not affected by NaW exposure. Tungsten analysis showed a systemic distribution of NaW in both parents and offspring, with preferential uptake within the immune organs, including the femur, spleen and thymus. Histopathological evidence suggested no severe chronic injury or loss of function in these organs. However, the heart showed histological lesions, histiocytic inflammation from minimal to mild with cardiomyocyte degeneration and necrosis in several P(0) animals of 125 mg NaW dose group. The result of this study suggests that pre and postnatal exposure to NaW may produce subtle neurobehavioral effects in offspring related to motor activity and emotionality.

 

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The potential for adverse health effects of using tungsten and its alloys in military munitions are an important concern to both civilians and the US military. The toxicological implications of exposure totungsten, its alloys, and the soluble tungstate (Na(2)WO(4)) are currently under investigation. To examine tungstate toxicity, a series of experiments to determine its in vitro effects on cells of the immune system were performed. We identified alterations in isolated human peripheral blood lymphocytes (PBL) treated in vitro with sodium tungstate (0.01, 0.1, 1.0, and 10 mM). Analyses of apoptosis with annexin V and propidium iodide revealed a dose- and time-dependent increase in the quantity of cells in early apoptosis after tungstate exposure. Reductions in the number of cells entering into the cell cycle were also noted. Exposure of PBL to tungstate (1 mM) and Concanavalin A (ConA) for 72 h reduced the number of cells in S and G(2)/M phases of the cell cycle. There were alterations in the numbers of cells in G(0)/G(1), S, and G(2)/M phases of the cell cycle in long-term THP-1 (acute leukemic monocytes) cultures treated with tungstate (0.01, 0.1, 1.0, and 10 mM). Gel electrophoresis,silver staining, and LC-MS/MS showed the cytoplasmic presence of histone H1b and H1d after 72 h oftungstate exposure. The addition of tungstate to cultures resulted in significant reductions in the quantity of interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), and IL-6 produced by stimulated [CD3/CD28, ConA, or lipopolysaccharide (LPS)] and tungstate-treated lymphocytes. Taken together, these data indicate that tungstate increases apoptosis of PBL, alters cell cycle progression, reduces cytokine production, and therefore warrants further investigation.

The use of tungsten as a replacement for lead and depleted uranium in munitions began in the mid 1990's. Recent reports demonstrate tungsten solubilizes in soil and can migrate into drinking water supplies and therefore is a potential health risk to humans. This study evaluated the reproductive and neurobehavioral effects of sodium tungstate in Sprague-Dawley rats following 70 days of daily pre- and postnatal exposure. Adult male and female rats were orally dosed with diH(2)O vehicle, 5 or 125 mg/kg/day of sodium tungstate through mating, gestation, and weaning (PND 0-20). Daily administration of sodium tungstate produced no overt evidence of toxicity and had no apparent effect on mating success or offspring physical development. Distress vocalizations were elevated in the highest dose group. There was no treatment related effect on righting reflex latencies, however, the males had significantly shorter latencies than the females. Locomotor activity was affected in both the low and high dose groups of F0 females. Those in the low dose group showed increased distance traveled, more time in ambulatory movements, and less time in stereotypic behavior than controls or high dose animals. The high dose group had more time in stereotypical movements than controls, and less time resting than controls and the lowest exposure group. Maternal retrieval was not affected by sodium tungstate exposure and there were no apparent effects of treatment on F1 acoustic startle response or water maze navigation. Overall, the results of this study suggest pre- and postnatal oral exposure to sodium tungstate may produce subtle neurobehavioral effects in offspring related to motor activity and emotionality. These findings warrant further investigation to characterize the neurotoxicity of sodium tungstate on dams and their developing pups.

 

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Decomposition of ammonium paratungstate under non-oxidizing atmosphere:

The first stage： 90~180℃，lose crystal water：
5(NH4)2O·12WO3·5H2O=5(NH4)2O·12WO3·H2O+4H2O↑

The second stage: 180 ~ 260 ℃, ammonia loss:
5(NH4)2O·12WO3·H2O=3(NH4)2O·12WO3·3H2O+4NH3↑
Ammonium metatungstate（AMT）

The third stage, 260 ~ 350 ℃, further of lose water and ammonia, ammonium tungsten bronze occurred (ATB):
3(NH4)2O·12WO3·3H2O＝(NH4)2O·12WO3+4NH3↑+5H2O↑

Fourth stage: 350 ~ 450 ℃, ammonia begins to decompose to generate hydrogen and nitrogen:
2NH3 =N2 ↑ + 3H2 ↑
This phase chemical reactions may be
(NH4)2O·12WO3 + H2＝12(NH4)xWO3+H2O+(2-x)NH3↑
(NH4)xWO2.8~3.0

Fifth stage: 450 ~ 550 ℃, ATB decomposition output WO3 and WO2.9

Sixth stage: 550 ~ 650 ℃, decomposition products in addition to small amounts of ATB, there are WO3, WO2.9 and tungsten oxide WO2.72 etc., even WO2.



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