- Email: [email protected]
Fatal poisoning by vanadium
Forensic Science International 206 (2011) e79–e81
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case report
Fatal poisoning by vanadium Brahim Boulassel a, Nouredine Sadeg b,1, Olivier Roussel c, Martine Perrin c, Hafid Belhadj-Tahar d,* a
Service Me´decine Le´gale, CHU NEDIR Mohamed, Tizi-Ouzou, Algeria Laboratoire Claude Bernard, Centre Hospitalier Rene´ Dubos, 6 avenue Ile de France, 95300 Pontoise, France c IRCGN, 1 boulevard The´ophile SUEUR, 93111 Rosny-sous-bois, France d Groupe Recherche et Expertise Toxicologiques, AFPreMed, 9 rue Professeur Antoine Baisset, 31100 Toulouse, France b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 3 June 2010 Received in revised form 17 October 2010 Accepted 28 October 2010 Available online 3 December 2010
We report here a fatal intoxication case involving ammonium vanadate. A 24-year-old woman was admitted to the Emergency Department for abdominal pain, nausea, vomiting, multiple daily diarrheas, hypoglycaemia (0.2 g/L) and severe acute renal failure with glomerular filtration rate estimated at 21 ml/ min. This patient had taken an undetermined amount of ammonium vanadate 12 h after ingesting. She died next morning in the context of respiratory distress despite intensive care and oxygen therapy. The autopsy revealed widespread asphyxia syndrome and erosive gastritis. Determination of vanadium concentration in blood was carried out by means of mass spectrometer (ICP-MS) using rhodium (103Rh) as the internal standard. The vanadium concentration was 6.22 mg/L, corresponding to 6000 times higher than normal concentration in the general population. The latency and the brutality of clinical picture degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory process. ß 2010 Elsevier Ireland Ltd. All rights reserved.
Keywords: Vanadium ICP-MS Asphyxia syndrome
1. Introduction Ammonium vanadate (NH4VO3) is a salt of pentavalent vanadium that is used as a catalyst in reactions involving the oxidation of sulfur oxide, oxides of nitrogen and other compounds [1]. Although occupational toxicology inherent to vanadium salt has already been described, the acute toxicity of these compounds is not well documented in medical literature [2]. In general, the toxicity of vanadium salts depends mainly on the route of its administration and its oxidation degree (pentavalent is the most toxic). According to several authors, vanadium toxicity is high parenterally, low orally and intermediate via inhalation [1,2]. The purpose of this report is to describe a fatal poisoning case after massive ingestion of ammonium vanadate.
2. Case report A 24-year-old woman was admitted to the emergency department at 10:30 p.m. for diffuse abdominal pain, nausea, vomiting, and multiple daily diarrheas after she had taken an undetermined amount of ammonium vanadate at about 10 a.m.
* Corresponding author. Tel.: +33 646772224. E-mail addresses: [email protected] (H. Belhadj-Tahar), [email protected] (N. Sadeg). 1 Tel.: +33 1 30754254; fax: +33 1 30755369. 0379-0738/$ – see front matter ß 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.forsciint.2010.10.027
the same morning. Anamnesis revealed that ammonium vanadate came from the laboratory for water quality analysis where she works as a technician. The patient’s past medical history was negative for digestive and kidney diseases. Upon her admission to the Hospital University of Tizi-Ouzou (Algeria), she was conscious and presented blood pressure 110/60 mm Hg, heart rate 76 beats/ min, respiratory rate 16 breaths/min, an oxygen haemoglobin saturation (SpO2) below 99% under artificial breath (2 L of oxygen per minute) and body temperature 37.7 8C. The examination revealed an epigastralgia, a normal abdomen, a slight increase in echogenicity of the renal cortex and with a large aerocoly. Initial chemistry tests were normal except for glucose 0.2 g/L (1.1 mmol/ L), creatinine 265 mmol/L (normal 49–90 mmol/L), alanine amino transferase: 114 IU/L (normal 10–45 IU/L). The glomerular filtration rate was estimated at 21 mL/min. A rapid urine drug screening of abuse panel was negative. It was decided to hospitalize the patient and she was placed under medical supervision with a symptomatic treatment of rehydration, administration of antispasmodics and inhibitors of proton pump in order to do away with the gastric symptoms. Hypoglycemia was corrected by IV administration of glucose. Her clinical status suddenly worsened during the night by acute respiratory distress. The patient died the next morning, despite several resuscitation attempts. An autopsy has been ordered by the prosecution. A peripheral blood sample was obtained from the inferior vena cava, to perform toxicological analysis focusing on the vanadium determination by
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B. Boulassel et al. / Forensic Science International 206 (2011) e79–e81
ICP-MS. The sample was collected in a Becton–Dickinson vacuum tube with K3EDTA added as anticoagulant, and was stored for 2 months at 18 8C until analysis. 2.1. Analytical toxicology 2.1.1. Materials and methods Analysis of the vanadium in blood was performed using a mass spectrometer (ICP-MS), (ThermoOptek, X7/CCT model, Courtaboeuf, France) equipped with a quartz torch and a quartz nebulizer with a sample flow set at 0.81 mL/min and PlasmaLab 2.0. software. Instrumental parameters were as follow: 1200 W plasma, argon flows: 15 L/min in the plasma, 0.72 L/min in the nebulizer and 0.9 L/min as an auxiliary flow. The nebulizer was equipped with a Peltier effect cooler for regulating the temperature with 3 8C error. Rhodium (103Rh) is used as an internal standard for the ICP method. The autosampler consisted of a CETAC ASX-500 and an ID100 autodiluter. Reagents: Argon, 99.999% purity (Messer, France). Ultrapure water, purified on a Milli-Q device (Millipore, St Quentin en Yvelines, France), nitric acid suprapur 65% purity, 1butanol, Triton X-100 and the multielement standard solution (Cal I), containing 20 mineral elements at a concentration of 10 mg/L were purchased from VWR (Fontenay sous bois, France). 2.1.2. Sample preparation 100 mL of the sample was added to 10 mL of a mineralising solution prepared as follows: nitric acid 0.216 M, 0.5% (v/v) of 1butanol and 0.01% (v/v) of Triton X-100. The mix was left at room temperature for at least one night. The solution was then filtered on Millipore filters (0.45 mm) and injected into the ICP-MS. Blank samples, and calibrants (5 levels ranking from 0 to 107.14 mg/L), were prepared by spiking a negative whole blood matrix with the multi elemental solution and were injected with the same analytical conditions. The calculated lower LOQ is 0.4 mg/L, the chosen LLOQ is 1 mg/L. The accuracy is 89.9% and the bias is 1.49% at the 50 mg/L level. The limit of quantification (LOD) is calculated as of the blank signal average (blank spiked six times, n = 6) with 10 SD (standard deviation) of the calculated average. 3. Results: Post-mortem findings The examination of body revealed the absence of violence. However, a widespread asphyxia syndrome of the viscera and erosive gastritis were observed. In addition, Labial mucosa was a greenish colour. The vanadium concentration found is 6.22 mg/L. 4. Discussion To our knowledge no fatal poisoning with vanadium alone has been reported in the literature. We are facing a rare case of autolysis with an ammonium salt of vanadium. Schlake and collaborators [3] reported a case of a 22-year-old woman developing nausea, vomiting and diarrhea 2 h after ingesting 10–15 g of ammonium metavanadate. Endoscopy exploration revealed erosive gastritis. The digestive symptoms in our case were similar to those reported by Schlake and collaborators, the erosive gastritis could result from caustic effect of ammonium vanadate [4]. Serum concentration is normally less than 1 mg/L with values ranging from 0.07 to 1.1 mg/L [5–7]. In our case, the blood concentration of vanadium was 6.22 mg/L corresponding to 6000 times the upper range of the concentration of this metal in the general population.
The toxicity of vanadium on the respiratory tract has been well described [8–11]. The following symptoms were frequently reported: cough with sputum, wheezing, sore throat, headache and rhinitis. It was observed that vanadyl sulfate causes pulmonary vasoconstriction that could be partly due to the inhibition of nitric oxide (NO) production [12]. In vitro studies have shown that vanadate acts directly on the smooth muscle of the bronchi. It promotes the release of Ca2+ in the cells by a mechanism involving the production of inositol triphosphate and inhibition of ATPase [13]. Vanadium has an ‘‘insulin-like’’ action [14,15]; this effect explains the observed hypoglycemia. The major toxic effects of vanadate involve the respiratory tract by its powerful effect on the enzyme systems including the production of NO, which leads to pulmonary vasoconstriction, and its inhibitory effect on membrane enzymes (Na+–K+) ATPase and (Ca2+–Mg2+) ATPase [16]. In the kidney, vanadium causes hypokalemic acidosis accentuating its pulmonary toxicity. In our case, the low glomerular filtration rate 21 mL/min indicates the severe acute renal failure. In addition, the elevation of blood alanine amino transferase level (2.5 times normal value) suggests a mild hepatic cytolysis. Otherwise, in vivo vanadium is concentrated in some subcellular structures, particularly in mitochondria [17]. Therefore, the oxidant vanadyl and vanadate ions interact (E8 vanadyl/vanadate: 1.0 V) on the respiratory chain and enzymes, namely, sulfhydryldependant succinic dehydrogenase implied in citric acid cycle leading to oxidative stress [1,17–19]. The latency observed could be linked to the time required for tissue distribution of vanadium and its accumulation in mitochondrial stroma leading to oxidative stress and inhibition of the mitochondrial respiratory chain. Inhibition of energetic mitochondrial process could explain the asphyxia effects observed on the viscera at the autopsy after this massive ammonium vanadate intoxication. 5. Conclusion This documented case is of great importance for understanding the mechanisms of vanadium toxicology. Symptoms of acute intoxication, namely digestive disorders, acute renal failure and hypoglycaemia, were observed with a latency estimated at 12 h. Despite intensive care and oxygen therapy, death occurred in the context of respiratory distress and widespread tissue asphyxia affecting all organs. The latency and the brutality of clinical degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory processes. The blockade of the oxygen cascade due to vanadium poisoning could be classified as follows: (a) cause, potential chemical asphyxiant, (b) mechanism, block of enzyme chain, and (c) effect, failure of oxidative metabolism leading to cell death. References [1] POISINDEX1 Editorial Staff, Vanadium, in: L.L. Toll, K.M. Hurlbut (Eds.), POISINDEX1 System, MICROMEDEX, Greenwood Village, Colorado, 2009. [2] D.G. Barceloux, Vanadium, Clin. Toxicol. 37 (1999) 265–278. [3] H.P. Schlake, H.P. Bertram, I.W. Husstedt, Acute systemic vanadate poisoning presenting as cerebrovascular ischemia with prolonged reversible neurological deficits (PRIND), Clin. Neurol Neurosurg. 96 (1994) 92–95. [4] F. Fieux, M. Chirica, A. Villa, M.R. Losser, P. Cattan, Corrosive ingestion in adults, Re´animation 18 (2009) 606–616. [5] C. Minoia, E. Sabbioni, P. Apostoli, R. Pietra, L. Pozzoli, M. Allorini, G. Nicolaou, L. Allessio, E. Capodaglio, Trace element reference values in tissues from inhabitants of the European Community. A study of 46 e´le´ments in urine, blood, and serum of Italian subjects, Sci. Total Environ. 95 (1990) 89–105. [6] O. Ishida, K. Kihira, Y. Tsukamoto, F. Marumo, Improved determination of vanadium in biological fluids by electrothermal atomic spectrometry, Clin. Chem. 35 (1989) 127–130.
B. Boulassel et al. / Forensic Science International 206 (2011) e79–e81 [7] J. Kucera, J. Lener, J. Mnukova, Vanadium, levels in urine and cystine levels in fingernails and hair of exposed and normal persons, Biol. Trace Elem. Res. 43–45 (1994) 327–334. [8] A.W. Musk, J.G. Tees, Asthma caused by occupational exposure to vanadium compounds, Med. J. Aust. 1 (1982) 183–184. [9] C. Zenz, B.A. Berg, Human responses to controlled vanadium pentoxide exposure, Arch. Environ. Health 4 (1967) 709–712. [10] A.J. Ghio, R. Silbajoris, J.L. Carson, J.M. Samet, Biological effects of oil fly ash, Environ. Health Perspect. 110 (2002) 89–94. [11] R. Hauser, S. Elreedy, P.B. Ryan, D.C. Christiani, Urine vanadium concentrations in workers overhauling an oil-fired boiler, Am. J. Ind. Med. 33 (1998) 55–60. [12] Z. Li, J.D. Cartier, L.A. Dailey, Y.C. Huang, Vanadyl sulfate inhibits NO production via threonine phosphorylation of eNOS, Environ. Health Perspect. 112 (2004) 201–206. [13] J. Cortijo, V. Villagrasa, M. Marti-cabrera, V. Villar, J. Moreau, C. Advenier, E.J. Morcillo, R.C. Small, The spasmogenic effects of vanadate in human isolated bronchus, Br. J. Pharmacol. 121 (1997) 1339–1349.
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[14] M.Z. Mehdi, S.K. Pandey, J.F. Thberge, A.K. Srivastava, Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium, Cell Biochem. Biophys. 44 (2006) 73–81. [15] S.M. Brichard, J.C. Henquin, The role of vanadium in the management of diabetes, Trends Pharmacol. Sci. 16 (1995) 65–70. [16] J.D. Robinson, Vanadate inhibition of brain (Ca + Mg)-ATPase, Neurochem. Res. 6 (1981) 225–232. [17] S.S. Soares, H. Martins, R.O. Duarte, J.J.G. Moura, J. Coucelo, C. Gutie´rrez-Merino, M. Aureliano, Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration, J. Inorg. Biochem. 101 (1) (2007) 80–88. [18] S.J. Stohs, D. Bagchi, Oxidative mechanisms in the toxicity of metal ions, Free Radic. Biol. Med. 18 (1995) 321–336. [19] Y. Zhao, L. Ye, H. Liu, Q. Xia, Y. Zhang, X. Yang, K. Wang, Vanadium compounds induced mitochondria permeability transition pore (PTP) opening related to oxidative stress, J. Inorg. Biochem. 104 (4) (2010) 371–378.
Contents lists available at ScienceDirect
Forensic Science International journal homepage: www.elsevier.com/locate/forsciint
Case report
Fatal poisoning by vanadium Brahim Boulassel a, Nouredine Sadeg b,1, Olivier Roussel c, Martine Perrin c, Hafid Belhadj-Tahar d,* a
Service Me´decine Le´gale, CHU NEDIR Mohamed, Tizi-Ouzou, Algeria Laboratoire Claude Bernard, Centre Hospitalier Rene´ Dubos, 6 avenue Ile de France, 95300 Pontoise, France c IRCGN, 1 boulevard The´ophile SUEUR, 93111 Rosny-sous-bois, France d Groupe Recherche et Expertise Toxicologiques, AFPreMed, 9 rue Professeur Antoine Baisset, 31100 Toulouse, France b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 3 June 2010 Received in revised form 17 October 2010 Accepted 28 October 2010 Available online 3 December 2010
We report here a fatal intoxication case involving ammonium vanadate. A 24-year-old woman was admitted to the Emergency Department for abdominal pain, nausea, vomiting, multiple daily diarrheas, hypoglycaemia (0.2 g/L) and severe acute renal failure with glomerular filtration rate estimated at 21 ml/ min. This patient had taken an undetermined amount of ammonium vanadate 12 h after ingesting. She died next morning in the context of respiratory distress despite intensive care and oxygen therapy. The autopsy revealed widespread asphyxia syndrome and erosive gastritis. Determination of vanadium concentration in blood was carried out by means of mass spectrometer (ICP-MS) using rhodium (103Rh) as the internal standard. The vanadium concentration was 6.22 mg/L, corresponding to 6000 times higher than normal concentration in the general population. The latency and the brutality of clinical picture degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory process. ß 2010 Elsevier Ireland Ltd. All rights reserved.
Keywords: Vanadium ICP-MS Asphyxia syndrome
1. Introduction Ammonium vanadate (NH4VO3) is a salt of pentavalent vanadium that is used as a catalyst in reactions involving the oxidation of sulfur oxide, oxides of nitrogen and other compounds [1]. Although occupational toxicology inherent to vanadium salt has already been described, the acute toxicity of these compounds is not well documented in medical literature [2]. In general, the toxicity of vanadium salts depends mainly on the route of its administration and its oxidation degree (pentavalent is the most toxic). According to several authors, vanadium toxicity is high parenterally, low orally and intermediate via inhalation [1,2]. The purpose of this report is to describe a fatal poisoning case after massive ingestion of ammonium vanadate.
2. Case report A 24-year-old woman was admitted to the emergency department at 10:30 p.m. for diffuse abdominal pain, nausea, vomiting, and multiple daily diarrheas after she had taken an undetermined amount of ammonium vanadate at about 10 a.m.
* Corresponding author. Tel.: +33 646772224. E-mail addresses: [email protected] (H. Belhadj-Tahar), [email protected] (N. Sadeg). 1 Tel.: +33 1 30754254; fax: +33 1 30755369. 0379-0738/$ – see front matter ß 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.forsciint.2010.10.027
the same morning. Anamnesis revealed that ammonium vanadate came from the laboratory for water quality analysis where she works as a technician. The patient’s past medical history was negative for digestive and kidney diseases. Upon her admission to the Hospital University of Tizi-Ouzou (Algeria), she was conscious and presented blood pressure 110/60 mm Hg, heart rate 76 beats/ min, respiratory rate 16 breaths/min, an oxygen haemoglobin saturation (SpO2) below 99% under artificial breath (2 L of oxygen per minute) and body temperature 37.7 8C. The examination revealed an epigastralgia, a normal abdomen, a slight increase in echogenicity of the renal cortex and with a large aerocoly. Initial chemistry tests were normal except for glucose 0.2 g/L (1.1 mmol/ L), creatinine 265 mmol/L (normal 49–90 mmol/L), alanine amino transferase: 114 IU/L (normal 10–45 IU/L). The glomerular filtration rate was estimated at 21 mL/min. A rapid urine drug screening of abuse panel was negative. It was decided to hospitalize the patient and she was placed under medical supervision with a symptomatic treatment of rehydration, administration of antispasmodics and inhibitors of proton pump in order to do away with the gastric symptoms. Hypoglycemia was corrected by IV administration of glucose. Her clinical status suddenly worsened during the night by acute respiratory distress. The patient died the next morning, despite several resuscitation attempts. An autopsy has been ordered by the prosecution. A peripheral blood sample was obtained from the inferior vena cava, to perform toxicological analysis focusing on the vanadium determination by
e80
B. Boulassel et al. / Forensic Science International 206 (2011) e79–e81
ICP-MS. The sample was collected in a Becton–Dickinson vacuum tube with K3EDTA added as anticoagulant, and was stored for 2 months at 18 8C until analysis. 2.1. Analytical toxicology 2.1.1. Materials and methods Analysis of the vanadium in blood was performed using a mass spectrometer (ICP-MS), (ThermoOptek, X7/CCT model, Courtaboeuf, France) equipped with a quartz torch and a quartz nebulizer with a sample flow set at 0.81 mL/min and PlasmaLab 2.0. software. Instrumental parameters were as follow: 1200 W plasma, argon flows: 15 L/min in the plasma, 0.72 L/min in the nebulizer and 0.9 L/min as an auxiliary flow. The nebulizer was equipped with a Peltier effect cooler for regulating the temperature with 3 8C error. Rhodium (103Rh) is used as an internal standard for the ICP method. The autosampler consisted of a CETAC ASX-500 and an ID100 autodiluter. Reagents: Argon, 99.999% purity (Messer, France). Ultrapure water, purified on a Milli-Q device (Millipore, St Quentin en Yvelines, France), nitric acid suprapur 65% purity, 1butanol, Triton X-100 and the multielement standard solution (Cal I), containing 20 mineral elements at a concentration of 10 mg/L were purchased from VWR (Fontenay sous bois, France). 2.1.2. Sample preparation 100 mL of the sample was added to 10 mL of a mineralising solution prepared as follows: nitric acid 0.216 M, 0.5% (v/v) of 1butanol and 0.01% (v/v) of Triton X-100. The mix was left at room temperature for at least one night. The solution was then filtered on Millipore filters (0.45 mm) and injected into the ICP-MS. Blank samples, and calibrants (5 levels ranking from 0 to 107.14 mg/L), were prepared by spiking a negative whole blood matrix with the multi elemental solution and were injected with the same analytical conditions. The calculated lower LOQ is 0.4 mg/L, the chosen LLOQ is 1 mg/L. The accuracy is 89.9% and the bias is 1.49% at the 50 mg/L level. The limit of quantification (LOD) is calculated as of the blank signal average (blank spiked six times, n = 6) with 10 SD (standard deviation) of the calculated average. 3. Results: Post-mortem findings The examination of body revealed the absence of violence. However, a widespread asphyxia syndrome of the viscera and erosive gastritis were observed. In addition, Labial mucosa was a greenish colour. The vanadium concentration found is 6.22 mg/L. 4. Discussion To our knowledge no fatal poisoning with vanadium alone has been reported in the literature. We are facing a rare case of autolysis with an ammonium salt of vanadium. Schlake and collaborators [3] reported a case of a 22-year-old woman developing nausea, vomiting and diarrhea 2 h after ingesting 10–15 g of ammonium metavanadate. Endoscopy exploration revealed erosive gastritis. The digestive symptoms in our case were similar to those reported by Schlake and collaborators, the erosive gastritis could result from caustic effect of ammonium vanadate [4]. Serum concentration is normally less than 1 mg/L with values ranging from 0.07 to 1.1 mg/L [5–7]. In our case, the blood concentration of vanadium was 6.22 mg/L corresponding to 6000 times the upper range of the concentration of this metal in the general population.
The toxicity of vanadium on the respiratory tract has been well described [8–11]. The following symptoms were frequently reported: cough with sputum, wheezing, sore throat, headache and rhinitis. It was observed that vanadyl sulfate causes pulmonary vasoconstriction that could be partly due to the inhibition of nitric oxide (NO) production [12]. In vitro studies have shown that vanadate acts directly on the smooth muscle of the bronchi. It promotes the release of Ca2+ in the cells by a mechanism involving the production of inositol triphosphate and inhibition of ATPase [13]. Vanadium has an ‘‘insulin-like’’ action [14,15]; this effect explains the observed hypoglycemia. The major toxic effects of vanadate involve the respiratory tract by its powerful effect on the enzyme systems including the production of NO, which leads to pulmonary vasoconstriction, and its inhibitory effect on membrane enzymes (Na+–K+) ATPase and (Ca2+–Mg2+) ATPase [16]. In the kidney, vanadium causes hypokalemic acidosis accentuating its pulmonary toxicity. In our case, the low glomerular filtration rate 21 mL/min indicates the severe acute renal failure. In addition, the elevation of blood alanine amino transferase level (2.5 times normal value) suggests a mild hepatic cytolysis. Otherwise, in vivo vanadium is concentrated in some subcellular structures, particularly in mitochondria [17]. Therefore, the oxidant vanadyl and vanadate ions interact (E8 vanadyl/vanadate: 1.0 V) on the respiratory chain and enzymes, namely, sulfhydryldependant succinic dehydrogenase implied in citric acid cycle leading to oxidative stress [1,17–19]. The latency observed could be linked to the time required for tissue distribution of vanadium and its accumulation in mitochondrial stroma leading to oxidative stress and inhibition of the mitochondrial respiratory chain. Inhibition of energetic mitochondrial process could explain the asphyxia effects observed on the viscera at the autopsy after this massive ammonium vanadate intoxication. 5. Conclusion This documented case is of great importance for understanding the mechanisms of vanadium toxicology. Symptoms of acute intoxication, namely digestive disorders, acute renal failure and hypoglycaemia, were observed with a latency estimated at 12 h. Despite intensive care and oxygen therapy, death occurred in the context of respiratory distress and widespread tissue asphyxia affecting all organs. The latency and the brutality of clinical degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory processes. The blockade of the oxygen cascade due to vanadium poisoning could be classified as follows: (a) cause, potential chemical asphyxiant, (b) mechanism, block of enzyme chain, and (c) effect, failure of oxidative metabolism leading to cell death. References [1] POISINDEX1 Editorial Staff, Vanadium, in: L.L. Toll, K.M. Hurlbut (Eds.), POISINDEX1 System, MICROMEDEX, Greenwood Village, Colorado, 2009. [2] D.G. Barceloux, Vanadium, Clin. Toxicol. 37 (1999) 265–278. [3] H.P. Schlake, H.P. Bertram, I.W. Husstedt, Acute systemic vanadate poisoning presenting as cerebrovascular ischemia with prolonged reversible neurological deficits (PRIND), Clin. Neurol Neurosurg. 96 (1994) 92–95. [4] F. Fieux, M. Chirica, A. Villa, M.R. Losser, P. Cattan, Corrosive ingestion in adults, Re´animation 18 (2009) 606–616. [5] C. Minoia, E. Sabbioni, P. Apostoli, R. Pietra, L. Pozzoli, M. Allorini, G. Nicolaou, L. Allessio, E. Capodaglio, Trace element reference values in tissues from inhabitants of the European Community. A study of 46 e´le´ments in urine, blood, and serum of Italian subjects, Sci. Total Environ. 95 (1990) 89–105. [6] O. Ishida, K. Kihira, Y. Tsukamoto, F. Marumo, Improved determination of vanadium in biological fluids by electrothermal atomic spectrometry, Clin. Chem. 35 (1989) 127–130.
B. Boulassel et al. / Forensic Science International 206 (2011) e79–e81 [7] J. Kucera, J. Lener, J. Mnukova, Vanadium, levels in urine and cystine levels in fingernails and hair of exposed and normal persons, Biol. Trace Elem. Res. 43–45 (1994) 327–334. [8] A.W. Musk, J.G. Tees, Asthma caused by occupational exposure to vanadium compounds, Med. J. Aust. 1 (1982) 183–184. [9] C. Zenz, B.A. Berg, Human responses to controlled vanadium pentoxide exposure, Arch. Environ. Health 4 (1967) 709–712. [10] A.J. Ghio, R. Silbajoris, J.L. Carson, J.M. Samet, Biological effects of oil fly ash, Environ. Health Perspect. 110 (2002) 89–94. [11] R. Hauser, S. Elreedy, P.B. Ryan, D.C. Christiani, Urine vanadium concentrations in workers overhauling an oil-fired boiler, Am. J. Ind. Med. 33 (1998) 55–60. [12] Z. Li, J.D. Cartier, L.A. Dailey, Y.C. Huang, Vanadyl sulfate inhibits NO production via threonine phosphorylation of eNOS, Environ. Health Perspect. 112 (2004) 201–206. [13] J. Cortijo, V. Villagrasa, M. Marti-cabrera, V. Villar, J. Moreau, C. Advenier, E.J. Morcillo, R.C. Small, The spasmogenic effects of vanadate in human isolated bronchus, Br. J. Pharmacol. 121 (1997) 1339–1349.
e81
[14] M.Z. Mehdi, S.K. Pandey, J.F. Thberge, A.K. Srivastava, Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium, Cell Biochem. Biophys. 44 (2006) 73–81. [15] S.M. Brichard, J.C. Henquin, The role of vanadium in the management of diabetes, Trends Pharmacol. Sci. 16 (1995) 65–70. [16] J.D. Robinson, Vanadate inhibition of brain (Ca + Mg)-ATPase, Neurochem. Res. 6 (1981) 225–232. [17] S.S. Soares, H. Martins, R.O. Duarte, J.J.G. Moura, J. Coucelo, C. Gutie´rrez-Merino, M. Aureliano, Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration, J. Inorg. Biochem. 101 (1) (2007) 80–88. [18] S.J. Stohs, D. Bagchi, Oxidative mechanisms in the toxicity of metal ions, Free Radic. Biol. Med. 18 (1995) 321–336. [19] Y. Zhao, L. Ye, H. Liu, Q. Xia, Y. Zhang, X. Yang, K. Wang, Vanadium compounds induced mitochondria permeability transition pore (PTP) opening related to oxidative stress, J. Inorg. Biochem. 104 (4) (2010) 371–378.