Current Awareness in Clinical Toxicology Editors: Damian Ballam Msc and Allister Vale MD

Home , Bavel (restaurant), Haff disease, Hydroxytyrosol, Tear gas, Tolperisone

Current Awareness in Clinical Toxicology Editors: Damian Ballam MSc and Allister Vale MD

April 2015

CONTENTS General Toxicology 9 Metals 44 Management 22 Pesticides 49 Drugs 23 Chemical Warfare 51 Chemical Incidents & 36 Plants 52 Pollution Chemicals 37 Animals 52

CURRENT AWARENESS PAPERS OF THE MONTH

Acute toxicity profile of tolperisone in overdose: observational poison centre-based study Martos V, Hofer KE, Rauber-Lüthy C, Schenk-Jaeger KM, Kupferschmidt H, Ceschi A. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1022896: Introduction Tolperisone is a centrally acting muscle relaxant that acts by blocking voltage-gated sodium and calcium channels. There is a lack of information on the clinical features of tolperisone poisoning in the literature. The aim of this study was to investigate the demographics, circumstances and clinical features of acute overdoses with tolperisone. Methods An observational study of acute overdoses of tolperisone, either alone or in combination with one non-steroidal anti-inflammatory drug in a dose range not expected to cause central nervous system effects, in adults and children (< 16 years), reported to our poison centre between 1995 and 2013.

Current Awareness in Clinical Toxicology is produced monthly for the American Academy of Clinical Toxicology by the Birmingham Unit of the UK National Poisons Information Service, with contributions from the Cardiff, Edinburgh, and Newcastle Units.

The NPIS is commissioned by Public Health England

Results 75 cases were included: 51 females (68%) and 24 males (32%); 45 adults (60%) and 30 children (40%). Six adults (13%) and 17 children (57%) remained asymptomatic, and mild symptoms were seen in 25 adults (56%) and 10 children (33%). There were nine adults (20%) with moderate symptoms, and five adults (11%) and three children (10%) with severe symptoms. Signs and symptoms predominantly involved the central nervous system: somnolence, coma, seizures and agitation. Furthermore, some severe cardiovascular and respiratory signs and symptoms were reported. The minimal dose for seizures and severe symptoms in adults was 1500 mg. In 11 cases the latency between the ingestion and the onset of symptoms was known and was reported to be 0.5–1.5 h. Conclusions The acute overdose of tolperisone may be life-threatening, with a rapid onset of severe neurological, respiratory and cardiovascular symptoms. With alternative muscle relaxants available, indications for tolperisone should be rigorously evaluated. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1022896

Scorpion-related cardiomyopathy: clinical characteristics, pathophysiology, and treatment Abroug F, Souheil E, Ouanes I, Dachraoui F, Fekih-Hassen M, Ouanes Besbes L. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1030676: Context Scorpion envenomation is a threat to more than 2 billion people worldwide with an annual sting number exceeding one million. Acute heart failure presenting as cardiogenic shock or pulmonary edema, or both is the most severe presentation of scorpion envenomation accounting for 0.27% lethality rate. Objective The purpose of this review is to characterize the scorpion-related cardiomyopathy, clarify its pathophysiological mechanisms, and describe potentially useful treatments in this particular context. Methods We searched major databases on observational or interventional studies (whether clinical or experimental) on the cardiorespiratory consequences of scorpion envenomation and their treatment. No limit of age or language was imposed. A critical appraisal of the literature was conducted in order to provide a pathophysiological scheme that reconciles reported patterns of cardiovascular toxicity and hypotheses and assumptions made so far. Results Early cardiovascular dysfunction is related to the so-called "vascular phase" of scorpion envenomation, which is related to a profound catecholamine-related vasoconstriction leading to a sharp increase in left ventricular (LV) afterload, thereby impeding LV emptying, and increasing LV filling pressure. Following this vascular phase, a myocardial phase occurs, characterized by a striking alteration in LV contractility (myocardial stunning), low cardiac output, and hypotensive state. The right ventricle involvement is symmetric to that of LV with a profound and reversible alteration in right ventricular performance. This phase is unique in that it is reversible spontaneously or under inotropic treatment. Scorpion myocardiopathy combines the features of takotsubo myocardiopathy (or stress myocardiopathy) which is linked to a massive release in catecholamines leading to myocardial ischemia through coronary vasomotor abnormalities (epicardial coronary spasm

and/or increase in coronary microvascular resistance). Treatment of pulmonary edema due to scorpion envenomation follows the same principles as those applied for the treatment of cardiogenic pulmonary edema in general: this begins with oxygen supplementation targeting an oxygen saturation of 92% or more, by oxygen mask, continuous positive airway pressure, noninvasive ventilation, or conventional mechanical ventilation. Dobutamine effectively improves hemodynamic parameters and may reduce mortality in severe scorpion envenomation. Conclusion Scorpion cardiomyopathy is characterized by a marked and reversible alteration in biventricular performance. Supportive treatment relying on ventilatory support and dobutamine infusion is a bridge toward recovery in the majority of patients. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1030676

Comparison of lisdexamfetamine and dextroamphetamine exposures reported to U.S. poison centers Kaland ME, Klein-Schwartz W. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1027903: Context Lisdexamfetamine is a pro-drug stimulant that requires the enzymatic hydrolysis of lysine from dexamphetamine for pharmacologic effects. There is limited information comparing non-therapeutic lisdexamfetamine and dextroamphetamine exposures. Objective The objective was to compare lisdexamfetamine exposures with dextroamphetamine/ amphetamine extended release and dextroamphetamine/amphetamine immediate release. Methods A retrospective observational case series of single-substance exposures to lisdexamfetamine, dextroamphetamine/amphetamine extended release, or dextroamphetamine/amphetamine immediate release reported to the National Poison Data System from 2007 to 2012 was performed. Data were analyzed for demographics, reason, clinical effects, management site, and outcomes. Results There were 23,553 exposures: lisdexamfetamine (7,113), dextroamphetamine/amphetamine extended release (6,245), and dextroamphetamine/amphetamine immediate release (10,195). The most frequent clinical effects observed for lisdexamfetamine, dextroamphetamine/amphetamine extended release, and dextroamphetamine/amphetamine immediate release were agitation (19.8%, 21.7%, and 25.1%, respectively) and tachycardia (19.2%, 22.8%, and 23.9%, respectively). The reason was most often exploratory (93.4%) in children < 6 years and therapeutic error (65.6%) in children aged 6-12 years. In adolescents and adults most common reasons were suicide attempts (28.4%) followed by abuse (19.5%) and therapeutic errors (18.8%). Overall, 61.6% of cases were managed in a health care facility, with the majority treated in the emergency department only. The majority of cases (76.0%) experienced no or minor effects. More serious outcomes (moderate/major/death) occurred in 21.2% of lisdexamfetamine, 24.7% of dextroamphetamine/amphetamine extended release, and 25.5% of dextroamphetamine/ amphetamine immediate release. There were 4 deaths (1 dextroamphetamine/amphetamine extended release and 3 dextroamphetamine/amphetamine immediate release). In patients aged 6 years and more, abuse/misuse was more frequently reported for dextro-

amphetamine/amphetamine immediate release (32.5%) and dextroamphetamine/ amphetamine extended release (23.0%) than that for lisdexamfetamine (13.5%). The odds of abuse/misuse was 2.3 (95% confidence interval [CI]: 2.0-2.4) times higher for dextroamphetamine/amphetamine immediate release than that for lisdexamfetamine and dextroamphetamine/amphetamine extended release combined; the odds of dextroamphetamine/amphetamine extended release abuse/misuse was 1.9 (95% CI: 1.7- 2.2) times higher than lisdexamfetamine. In 2011, the number of lisdexamfetamine abuse/misuse cases exceeded dextroamphetamine/amphetamine extended release by approximately 26% and plateaued in 2012, but was significantly lower (approximately 75%) than dextroamphetamine/amphetamine immediate release. Conclusions Toxic effects were similar for all three drugs. Although the majority of cases were treated at health care facilities, the majority of patients experienced no effects or minor toxicity. Serious outcomes occurred in approximately 21% of lisdexamfetamine and 25% of dextroamphetamine/amphetamine extended release and dextroamphetamine/amphetamine immediate release. Lisdexamfetamine may have less abuse potential, especially compared with the immediate-release dextroamphetamine/amphetamine formulation. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1027903

2-Methyl-4-chlorophenoxyacetic acid and bromoxynil herbicide death Berling I, Buckley NA, Mostafa A, Downes MA, Grice J, Medley G, Roberts MS, Isbister GK. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1030025: Case report We report a fatal case of a 37 year old gentleman who ingested a MCPA/bromoxynil co- formulation herbicide. Although clinically well on initial examination, our patient declined dramatically over his 18 h admission with increasing CO2 production, hyperthermia and metabolic derangement to eventually die from cardiac asystole 20 h post ingestion. Two hours after ingestion the MCPA concentration was 83.9 µg/mL and bromoxynil concentration was 137 µg/mL. Discussion The patients' mechanism of death appeared to be uncoupling of oxidative phosphorylation, excess CO2 production and hyperthermia. There is limited knowledge on the acute toxicity of these herbicides, in particular bromoxynil, and this case highlights the relentless progression of severe toxicity in humans. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1030025

Fab fragments of ovine antibody to colchicine enhance its clearance in the rat Peake PW, Pianta TJ, Succar L, Fernando M, Buckley NA, Endre ZH. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1030026: Context

Colchicine is an anti-inflammatory alkaloid used for the treatment of acute gout, but has a narrow therapeutic index. Colchicine overdoses are relatively rare, but have high mortality requiring rapid treatment. Objective To evaluate the ability of a newly available ovine fragment antigen-binding (Fab) antibody to colchicine (ColchiFab™) to protect rats against renal and other injury 24 h after colchicine ingestion. Materials and methods Rats were gavaged with colchicine (5 mg/kg), then 2 h later injected intraperitoneally with 5 ml of sterile saline, or Fab anti-colchicine, a newly available ovine antibody to colchicine. Samples of blood were taken at 1, 2, 5 and 24 h after gavage, and urine was collected from 5 to 24 h after gavage. Concentrations of colchicine in tissue, blood and urine were measured by liquid chromatography/mass spectrometry, concentrations of Fab anti- colchicine, urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 or KIM-1 by enzyme-linked immunosorbent assay or ELISA, while concentrations of creatine kinase and creatinine (Cr) were measured enzymatically. Results Colchicine equilibrated rapidly throughout the body and increased serum creatine kinase. Fab anti-colchicine also rapidly redistributed to the blood and remained at high concentrations over 24 h. Fab anti-colchicine caused a rapid 7.1-fold increase in serum colchicine level, followed by excretion of both colchicine and Fab anti-colchicine through the urine. This was associated with the accumulation of colchicine in the kidney, a reversal of colchicine-induced diarrhoea, and increasing urinary NGAL level; from 168 ± 48 to 477 ± 255 ng/mmol Cr [mean ± standard deviation or SD]. Discussion Fab anti-colchicine greatly increased the clearance of colchicine, although increasing NGAL level suggested the presence of mild kidney damage. Conclusion These data suggest clinical utility for Fab anti-colchicine in the treatment of colchicine overdose. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1030026

Hospital outcomes and economic costs from poisoning cases in Illinois Krajewski AK, Friedman LS. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1030677: Context Since 2009, poisonings have been the leading cause of fatal injuries in the United States (US) and remain a continuing public health issue. Because of the varying definitions for what constitutes a poisoning case, there are inconsistencies in the annual number of cases reported among national health surveys. Objectives The main objective of this study was to describe poisonings treated in Illinois hospitals by type of exposure, as well as to detail demographic characteristics, acute outcomes, and general cost estimates for those exposed to poisoning. We also compared a broad definition for poisoning used in our analysis with the definitions used by four national health surveys in order to assess the adequacy of various definitions in capturing poisonings for surveillance.

Material and methods We conducted a comprehensive analysis of outpatients and inpatients treated in Illinois hospitals in 2010 using the Illinois hospital database. Age-adjusted incidence rates were calculated. Results In Illinois, 425,491 patients were treated in hospitals for poisoning in 2010, of whom 222,339 were inpatients. The age-adjusted incidence rate was 3,189 per 100,000 persons, with an average length of stay among inpatients of 5.5 days. The cumulative hospital charges were $7.9 billion. Discussion and conclusion The definitions used in national surveys miss 60–90% of poisoning cases. Poisoning is the leading cause of fatal injuries in the U.S., but as this study shows broadening the definition for poisoning may provide a more accurate representation of the direct and indirect effects of poisoning in the US. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1030677

Initiation of a medical toxicology consult service at a tertiary care children's hospital Wang GS, Monte A, Hatten B, Brent J, Buchanan J, Heard KJ. Clin Toxicol 2015; 53: 192-4. Currently, only 10% of board-certified medical toxicologists are pediatricians. Yet over half of poison center calls involve children < 6 years, poisoning continues to be a common pediatric diagnosis and bedside toxicology consultation is not common at children's hospitals. In collaboration with executive staff from Department of Pediatrics and Emergency Medicine, regional poison center, and our toxicology fellowship, we established a toxicology consulting service at our tertiary-care children's hospital. There were 139 consultations, and the service generated 13 consultations in the first month; median of 11 consultations per month thereafter (range 8–16). The service increased pediatric cases seen by the fellowship program from 30 to 94. The transition to a consult service required a culture change. Historically, call center advice was the mainstay of consulting practice and the medical staff was not accustomed to the availability of bedside medical toxicology consultations. However, after promotion of the service and full attending and fellowship coverage, consultations increased. In collaboration with toxicologists from different departments, a consultation service can be rapidly established. The service filled a clinical need that was disproportionately utilized for high acuity patients, immediately utilized by the medical staff and provided a robust pediatric population for the toxicology fellowship. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1013196

Global incidence of rhabdomyolysis after cooked seafood consumption (Haff disease) Diaz JH. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1016165: Context Haff disease is a syndrome of myalgia and rhabdomyolysis that occurs after consuming cooked seafood.

Objectives (1) To identify the most common seafood vectors of Haff disease worldwide. (2) To describe and to compare the most commonly recurring clinical and laboratory manifestations of Haff disease. (3) To compare the Haff disease toxidrome with other similar toxidromes. Methods Internet search engines were queried with the keywords, and selected articles were stratified by reporting Old World or New World nations. Continuous variables were reported as means with standard deviations; categorical values were reported as proportions. Results Over 1,000 cases of Haff disease were initially described in Eastern Europe and Sweden during and following the ingestion of several species of cooked freshwater fish including burbot, pike, freshwater eel, and whitefish. More recent case reports followed consumption of cooked freshwater pomfret and boiled crayfish in China, and cooked or raw boxfish in Japan. There were 29 case reports of Haff disease in the United States with most following consumption of buffalo fish, crayfish, or Atlantic salmon. Conclusion The consumption of several species of cooked fish has caused Haff disease outbreaks worldwide. The bioaccumulation of a new heat-stable, fresh, and/or brackish/ salt-water algal toxin in seafood, similar to palytoxin, but primarily myotoxic and not neurotoxic, is suspected for causing Haff disease. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1016165

Reducing the harm of opioid overdose with the safe use of naloxone: a pharmacologic review Kim HK, Nelson LS. Expert Opin Drug Saf 2015; online early: doi: 10.1517/14740338.2015.1037274: 1-10. Abstract and full text available from: http://dx.doi.org/10.1517/14740338.2015.1037274

Characterization of the toxicological hazards of hydrocarbon solvents McKee RH, Adenuga MD, Carrillo JC. Crit Rev Toxicol 2015; 45: 273-365. Abstract and full text available from: http://dx.doi.org/10.3109/10408444.2015.1016216

Glyphosate-based herbicides potently affect cardiovascular system in mammals: review of the literature Gress S, Lemoine S, Séralini G-E, Puddu PE. Cardiovasc Toxicol 2015; 15: 117-26. Abstract and full text available from: http://dx.doi.org/10.1007/s12012-014-9282-y

Metabolism of classical cannabinoids and the synthetic cannabinoid JWH-018

Su M, Seely KA, Moran JH, Hoffman RS. Clin Pharmacol Ther 2015; online early: doi: 10.1002/cpt.114: Abstract and full text available from: http://dx.doi.org/10.1002/cpt.114

Metals in cosmetics: implications for human health Borowska S, Brzóska MM. J Appl Toxicol 2015; 35: 551-72. Abstract and full text available from: http://dx.doi.org/10.1002/jat.3129

Paralytic shellfish poisonings resulting from an algal bloom in Nicaragua Callejas L, Darce ACM, Amador JJ, Conklin L, Gaffga N, Rogers HS, DeGrasse S, Hall S, Earley M, Mei J, Rubin C, Aldighieri S, Backer LC, Azziz- Baumgartner E. BMC Res Notes 2015; 8: 74. Abstract and full text available from: http://dx.doi.org/10.1186/s13104-015-1012-4

Tetanus after envenomations caused by freshwater stingrays Torrez PPQ, Quiroga MM, Said R, Abati PAM, França FOS. Toxicon 2015; 97: 32-5. Abstract and full text available from: http://dx.doi.org/10.1016/j.toxicon.2014.12.001

Showering effectiveness for human hair decontamination of the nerve agent VX Josse D, Wartelle J, Cruz C. Chem Biol Interact 2015; 232: 94-100. Abstract and full text available from: http://dx.doi.org/10.1016/j.cbi.2015.03.010

First trimester exposure to topiramate and the risk of oral clefts in the offspring: a systematic review and meta-analysis Alsaad AMS, Chaudhry SA, Koren G. Reprod Toxicol 2015; 53: 45-50. Abstract and full text available from: http://dx.doi.org/10.1016/j.reprotox.2015.03.003

Exposure to nitrofurantoin during early pregnancy and congenital malformations: a systematic review and meta-analysis Goldberg O, Moretti M, Levy A, Koren G. J Obstet Gynaecol Can 2015; 37: 150-6. Abstract and full text available from: http://www.jogc.com/abstracts/full/201502_DrugsinPregnancy_1.pdf

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Chlordecone Kang X, Hu D-Y, Li C-B, Li X-H, Fan S-L, Liu Y, Tang G-Y, Cordier S, Bouquet E, Warembourg C, Massart C, Rouget Ai Z-S, Wu T, Mohan C, Zhou XJ, Liu J-Y, Peng A. F, Kadhel P, Bataille H, Monfort C, Boucher O, Muckle G, The volume ratio of ground glass opacity in early lung CT Multigner L. predicts mortality in acute paraquat poisoning. Perinatal exposure to chlordecone, thyroid hormone status PLoS ONE 2015; 10: e0121691. and neurodevelopment in infants: the Timoun cohort study in Guadeloupe (French West Indies). Li G, Yuzhen L, Yi C, Xiaoxiang C, Wei Z, Changqing Z, Environ Res 2015; 138: 271-8. Shuang Y. DNaseI protects against paraquat-induced acute lung injury and pulmonary fibrosis mediated by mitochondrial DDT DNA. Wong LIL, Labrecque MP, Ibuki N, Cox ME, Elliott JE, BioMed Res Int 2015; 2015: 386952. Beischlag TV. p,p'-dichlorodiphenyltrichloroethane ( p,p'-DDT) and p,p'- Yamada A, Aki T, Unuma K, Funakoshi T, Uemura K. dichlorodiphenyldichloroethylene (p,p'-DDE) repress Paraquat induces epithelial-mesenchymal transition-like prostate specific antigen levels in human prostate cancer cellular response resulting in fibrogenesis and the cell lines. prevention of apoptosis in human pulmonary epithelial Chem Biol Interact 2015; 230: 40-9. cells.

PLoS ONE 2015; 10: e0120192. CHEMICAL WARFARE,

Zhang J, Zhao Y, Bai Y, Lv G, Wu J, Chen Y. BIOLOGICAL WARFARE AND The significance of serum uric acid level in humans with acute paraquat poisoning. RIOT CONTROL AGENTS Sci Rep 2015; 5: 9168. Chemical warfare General Piperonyl butoxide Steinritz D, Stenger B, Zehfuß F, Mückter H, Schmidt A, Yavuz O, Aksoy A, Das YK, Gulbahar MY, Guvenc D, Balszuweit F, Büch T, Breit A, Thiermann H, Gudermann T. Atmaca E, Yarim FG, Cenesiz M. Alkylating agent (sulfur mustard) induced calcium influx is Subacute oral toxicity of combinations of selected TRPA1 dependent. synthetic pyrethroids, piperonyl butoxide, and Naunyn Schmiedebergs Arch Pharmacol 2015; 388: S8- tetramethrin in rats. S9. Toxicol Ind Health 2015; 31: 289-97. Agent orange Pyrethroid insecticides Park W, Yang SH, Yang SY, Kim TG, Yoo WS, Kim DY, Lim TK. General Hepatitis C virus infection and risk of lymphoma whether Kim D, Moon J, Chun B. exposed to agent orange. The initial hyperglycemia in acute type II pyrethroid Hepatol Int 2015; 9 Suppl 1: S269. poisoning. J Korean Med Sci 2015; 30: 365-70. Yang SH, Park WH, Yang SY, Kim DY, Yoo WS, Kim TG, Kim SH. Romero A, Ares I, Ramos E, Castellano V, Martínez M, Association of hepatitis C virus infection with diabetes Martínez-Larrañaga MR, Anadón A, Martínez MA. mellitus focus on whether exposed to agent orange. Evidence for dose-additive effects of a type II pyrethroid Hepatol Int 2015; 9 Suppl 1: S266. mixture. In vitro assessment. Environ Res 2015; 138: 58-66. Riot control agents Steinritz D, Stenger B, Zehfuß F, Mückter H, Schmidt A, Yavuz O, Aksoy A, Das YK, Gulbahar MY, Guvenc D, Balszuweit F, Büch T, Breit A, Thiermann H, Gudermann T. Atmaca E, Yarim FG, Cenesiz M. Alkylating agent (sulfur mustard) induced calcium influx is Subacute oral toxicity of combinations of selected synthetic TRPA1 dependent. pyrethroids, piperonyl butoxide, and tetramethrin in rats. Naunyn Schmiedebergs Arch Pharmacol 2015; 388: S8-S9. Toxicol Ind Health 2015; 31: 289-97. Chlorobenzylidene malononitrile (Tear Cypermethrin gas) Mandarapu R, Prakhya BM. Brvar M. In vitro myelotoxic effects of cypermethrin and mancozeb Chlorobenzylidene malononitrile tear gas exposure: rinsing on human hematopoietic progenitor cells. with amphoteric, hypertonic, and chelating solution. J Immunotoxicol 2015; 12: 48-55. Hum Exp Toxicol 2015; online early: doi: 10.1177/0960327115578866:

Rodenticides Mustard gas (Sulphur mustard) Bhat S, Kenchetty KP. Pashandi Z, Saraygord-Afshari N, Naderi-Manesh H, Naderi M. N-acetyl cysteine in the management of rodenticide Comparative proteomic study reveals the molecular consumption – Life saving? aspects of delayed ocular symptoms induced by sulfur J Clin Diagn Res 2015; 9: OC10-OC13. mustard. Int J Proteomics 2015; 2015: 659241. Zeneli L, Sekovanic A, Daci N. Chronic exposure to aluminum, nickel, thallium and Steinritz D, Stenger B, Zehfuß F, Mückter H, Schmidt A, uranium and their relationship with essential elements in Balszuweit F, Büch T, Breit A, Thiermann H, Gudermann T. human whole blood and blood serum. Alkylating agent (sulfur mustard) induced calcium influx is J Environ Sci Health A 2015; 50: 540-6. TRPA1 dependent. Naunyn Schmiedebergs Arch Pharmacol 2015; 388: S8- Rotenone S9.

Worth AJ, Gillespie KP, Mesaros C, Guo L, Basu SS, Snyder NW, Blair IA. Nerve agents Rotenone stereospecifically increases (S)-2-hydroxyglutarate Housman KJ, Swift AT, Oyler JM. in SH-SY5Y neuronal cells. Fragmentation pathways and structural characterization of Chem Res Toxicol 2015; online early: 14 nerve agent compounds by electrospray ionization doi: 10.1021/tx500535c: tandem mass spectrometry. J Anal Toxicol 2015; 39: 96-105.

Thallium John H, Breyer F, Schmidt C, Mizaikoff B, Worek F, Zeneli L, Sekovanic A, Daci N. Thiermann H. Chronic exposure to aluminum, nickel, thallium and Small-scale purification of butyrylcholinesterase from uranium and their relationship with essential elements in human plasma and implementation of a muLC-UV/ESI human whole blood and blood serum. MS/MS method to detect its organophosphorus adducts. J Environ Sci Health A 2015; 50: 540-6. Drug Test Anal 2015; online early:

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Soman Ergot Kovarik Z, Hrvat NM, Katalinic M, Sit RK, Paradyse A, Craig AM, Klotz JL, Duringer JM. Zunec S, Musilek K, Fokin VV, Taylor P, Radic Z. Cases of ergotism in livestock and associated ergot Catalytic soman scavenging by Y337A/F338A alkaloid concentrations in feed. acetylcholinesterase mutant assisted with novel site- Front Chem 2015; 3: 8. directed aldoximes. Chem Res Toxicol 2015; online early: doi: 10.1021/acs.chemrestox.5b00060: Mycotoxin Peng X, Chen K, Chen J, Fang J, Cui H, Zuo Z, Deng J, Seeger T, Bierwisch A, Niessen KV, Worek F, Thiermann H. Chen Z, Geng Y, Lai W. Comparable recovery of soman-blocked respiratory muscle Aflatoxin B1 affects apoptosis and expression of Bax, Bcl- function by different tert-butyl-substituted bispyridinium 2, and Caspase-3 in thymus and bursa of fabricius in compounds. broiler chickens. Naunyn Schmiedebergs Arch Pharmacol 2015; 388: S80. Environ Toxicol 2015; online early: doi: 10.1002/tox.22120:

Tabun Kuca K, Hrabinova M, Jun D, Musilek K, Penhaker M, Myristica fragrans (Nutmeg) Krejcar O, Soukup O. Roeters Van Lennep JE, Schuit SCE, van Bruchem-Visser Universality of oxime k203 for reactivation of nerve agent- RL, Özcan B. inhibited AChE. Unintentional nutmeg autointoxication. Med Chem 2015; online early: Neth J Med 2015; 73: 46-8. doi: 10.2174/1573406411666150407154204: Salvia divinorum (Diviner's sage) VX Addy PH, Garcia-Romeu A, Metzger M, Wade J. Josse D, Wartelle J, Cruz C. The subjective experience of acute, experimentally- Showering effectiveness for human hair decontamination induced Salvia divinorum inebriation. of the nerve agent VX. J Psychopharmacol 2015; 29: 426-35. Chem Biol Interact 2015; 232: 94-100. ANIMALS PLANTS Birds General Ligabue-Braun R, Carlini CR. Yamani A, Bunel V, Antoine M-H, Husson C, Stévigny C, Poisonous birds: a timely review. Duez P, Elachouri M, Nortier J. Toxicon 2015; 99: 102-8. Substitution between Aristolochia and Bryonia genus in North-Eastern Morocco: toxicological implications. Varanus komodoensis (Komodo J Ethnopharmacol 2015; 166: 250-60. dragon)

Borek HA, Charlton NP. Abrus precatorius (Jequirity bean) How not to train your dragon: a case of a Komodo dragon Alhamdani M, Brown B, Narula P. bite. Abrin poisoning in an 18-month-old child. Wilderness Environ Med 2015; online early: Am J Case Rep 2015; 16: 146-8. doi: 10.1016/j.wem.2014.12.014:

Datura stramonium (Jimson weed) Microorganisms Disel NR, Yilmaz M, Kekec Z, Karanlik M. Botulism Poisoned after dinner: dolma with Datura stramonium. Kumar G, Swaminathan S. Turkiye Acil Tip Dergisi 2015; 15: 51-5. Recent developments with metalloprotease inhibitor class of drug candidates for botulinum neurotoxins. Litchi chinensis (Lychee) Curr Top Med Chem 2015; 15: 685-95. Pulla P. Toxicology. A child-killing toxin emerges from shadows. Sabatini D, Papetti L, Lonati D, Anniballi F, Auricchio B, Science 2015; 348: 15-6. Properzi E, Grassi MC.

A case of infant botulism in a 4-month old baby. Snake bite envenomation in Riyadh province of Saudi QJM 2015; online early: doi: 10.1093/qjmed/hcv061: Arabia over the period (2005–2010). Saudi J Biol Sci 2015; 22: 198-203. Fish/marine poisoning Callejas L, Darce ACM, Amador JJ, Conklin L, Gaffga N, Bush SP, Kinlaw SB. Rogers HS, DeGrasse S, Hall S, Earley M, Mei J, Rubin C, Management of a pediatric snake envenomation after Aldighieri S, Backer LC, Azziz-Baumgartner E. presentation with a tight tourniquet. Paralytic shellfish poisonings resulting from an algal bloom Wilderness Environ Med 2015; online early: in Nicaragua. doi: 10.1016/j.wem.2015.01.005: BMC Res Notes 2015; 8: 74. Sambo BT, Hodonou A, Youssouf M, Fatigba H, Allode A, Diaz JH. Mensah É, Chippaux J-P. Global incidence of rhabdomyolysis after cooked seafood Perineoscrotal gangrene after a snake bite: a case report. consumption (Haff disease). Med Sante Trop 2015; 25: 107-9. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1016165: Tin SS, Wiwanitkit V. Predictors of mortality in poisonous snake bite. Torrez PPQ, Quiroga MM, Said R, Abati PAM, França FOS. Int J Crit Illn Inj Sci 2015; 5: 62. Tetanus after envenomations caused by freshwater stingrays. Witham WR, McNeill C, Patel S. Toxicon 2015; 97: 32-5. Rebound coagulopathy in patients with snakebite presenting with marked initial coagulopathy. Turner AD, Higgins C, Davidson K, Veszelovszki A, Payne Wilderness Environ Med 2015; online early: D, Hungerford J, Higman W. doi: 10.1016/j.wem.2014.11.019: Potential threats posed by new or emerging marine biotoxins in UK waters and examination of detection Adders methodology used in their control: brevetoxins. Hønge BL, Hedegaard SK, Cederstrøm S, Nielsen H. Mar Drugs 2015; 13: 1224-54. Hospital contacts after bite by the European adder (Vipera berus). Ciguatera Dan Med J 2015; 61: A5022. Chan TY. Emergence and epidemiology of ciguatera in the coastal Rattlesnake cities of Southern China. Abdelmalek D, Arroyo-Plasencia A, Schwarz ES, Weber J, Mar Drugs 2015; 13: 1175-84. Sampson CS, Thornton SL, Mullins ME. Factitious snake envenomation and narcotic seeking behavior. Scorpions Am J Emerg Med 2015; online early: Abroug F, Souheil E, Ouanes I, Dachraoui F, Fekih-Hassen doi: 10.1016/j.ajem.2015.03.020: M, Ouanes Besbes L. Scorpion-related cardiomyopathy: clinical characteristics, Vipers pathophysiology, and treatment. Neki NS. Clin Toxicol 2015; online early: Acute myocardial infarction in snake bite envenomation - doi: 10.3109/15563650.2015.1030676: A case report. J Med (Bangladesh) 2015; 16: 46-7. Snake bites

Al-Sadoon MK.

INDEX

25C-NBOMe ...... 30 Analytical toxicology ...... 9 Abrus precatorius ...... 52 Animals, general ...... 52 Acetaminophen ...... 35 Antiarrhythmic drugs ...... 25 Acetylcysteine ...... 22 Antibiotics ...... 25 Acrolein ...... 37 Anticoagulants ...... 26 Acyclovir ...... 28 Anticonvulsants ...... 26 Adders ...... 53 Antidepressants ...... 26 Agent orange ...... 51 Antidotes ...... 22 Air pollution ...... 36 Antiemetics ...... 27 Alcohol ...... 37 Antifungal drugs ...... 27 Aldehydes ...... 38 Antimalarial drugs ...... 27 Alprazolam ...... 28 Antineoplastics ...... 27 Aluminium ...... 44 Antipsychotics ...... 27 Aluminium phosphide ...... 49 Antithyroid drugs ...... 27 Amanita mushrooms ...... 52 Antituberculous drugs ...... 27 Amfetamines ...... 24 Antivenom ...... 22 Aminoglycosides ...... 25 Antiviral drugs ...... 28 Amiodarone ...... 25 Aripiprazole ...... 27 Anabolic steroids ...... 25 Arsenic ...... 44 Anaesthetics ...... 25 Atorvastatin ...... 35

Baclofen ...... 22 Diviner's sage ...... 35, 52 Benzene ...... 42 Driving under the influence ...... 11 Benzodiazepines ...... 28 Dronedarone ...... 25 Benzyl alcohol ...... 22 Drugs, general ...... 23 Beta-blockers ...... 22 Dyes ...... 40 Biological warfare...... 51 E-cigarettes ...... 30, 40 Biomarkers ...... 9 Ecstasy ...... 24 Birds ...... 52 Endocrine disrupting chemicals ...... 40 Bisphenol A ...... 38 Ephedrone ...... 30 Bisphosphonates ...... 28 Epidemiology ...... 11 Bleomycin ...... 27 Ergot ...... 52 Body packers ...... 9 Essential oils ...... 41 Botulism ...... 52 Ethanol ...... 37 Brominated diphenyl ethers ...... 38 Ethnic remedies ...... 31 Bronopol ...... 39 Ethyl carbamate ...... 41 Bufotenine ...... 31 Ethylene glycol ...... 41 Buprenorphine ...... 34 Etizolam ...... 28 Butanediols ...... 28 Eucalyptus oil ...... 41 Cadmium ...... 45 Exhaust fumes ...... 36 Caffeine...... 28 Extracorporeal treatments ...... 22 Cannabis ...... 28 Fentanyl ...... 34 Carbamate insecticides ...... 49 Fipronil ...... 49 Carbamazepine ...... 26 Fish/marine poisoning ...... 53 Carbofuran ...... 49 Fluoride ...... 41 Carbon ...... 39 Forensic toxicology ...... 12 Carbon black ...... 39 Fungicides ...... 49 Carbon monoxide ...... 39 Gabapentin ...... 26 Carbon-based fuels ...... 39 Gamma hydroxybutyrate ...... 30 Carcinogenicity ...... 10 Gamma-butyrolactone ...... 30 Cardiotoxicity ...... 10 Ganciclovir ...... 28 Cement ...... 39 Gasoline ...... 42 Ceramics ...... 39 GBH ...... 30 Chemical warfare, general ...... 51 Genotoxicity ...... 13 Chemicals, general ...... 37 GHB ...... 30 Chlordecone ...... 50 Glyburide ...... 31 Chlorine...... 39 Glyphosate ...... 49 Chlorobenzylidene malononitrile ...... 51 Gold ...... 46 Chloroquine ...... 27 Granisetron ...... 27 Chromium ...... 45 Haemodialysis ...... 22 Ciguatera ...... 53 Hallucinogens ...... 31 Clay ...... 39 Haloperidol ...... 27 Clopidogrel ...... 32 Hazardous waste ...... 37 Closantel ...... 36 Hepatotoxicity ...... 13 Coal dust ...... 39 Herbal medicines ...... 31 Cobalt ...... 45 Herbicides ...... 49 Cocaine ...... 29 Heroin ...... 31 Codeine ...... 34 Household products ...... 41 Colchicine ...... 29 Hydrocarbons ...... 41 Colistin ...... 25 Hydrochloric acid ...... 41 Contrast media ...... 39 Hydrofluoric acid ...... 41 Copper ...... 46 Hydrogen sulphide ...... 41 Corrosives ...... 40 Hypoglycaemics ...... 31 Cosmetics ...... 40 Imidacloprid ...... 50 Crotonaldehyde ...... 40 Immunosuppressants ...... 31 Cyanide ...... 40 Indium ...... 46 Cypermethrin ...... 51 Inhalation toxicity ...... 14 Cypraconazole ...... 49 Ink ...... 41 Cytotoxic drugs ...... 29 Insecticides ...... 49 Dabigatran ...... 26 Insulin ...... 31 Datura stramonium ...... 52 Iron ...... 46 DDT ...... 50 Isoniazid ...... 28 Dermal toxicity ...... 10 Isopropyl alcohol ...... 41 Designer drugs ...... 29 Isotretinoin ...... 31 Detergents ...... 40 Jequirity bean ...... 52 Developmental toxicology ...... 11 Jimson weed ...... 52 Dexmedetomidine ...... 40 Ketamine ...... 31 Diacetylmorphine ...... 31 Kinetics ...... 14 Dichloroethane ...... 40 Komodo dragon ...... 52 Dietary supplements ...... 31 Lead ...... 46 Diethylhexyl phthalate ...... 40 L-ergothioneine ...... 41 Dioxin ...... 40 Lipid emulsion therapy ...... 22 Diquat ...... 50 Litchi chinensis ...... 52

Lithium ...... 32, 47 Phosphine ...... 42 Loperamide ...... 32 Phosphorus ...... 42 Lormetazepam ...... 28 Phthalate esters ...... 42 LSD ...... 31 Piperonyl butoxide ...... 51 Lychee ...... 52 Plants, general ...... 52 Management, general ...... 22 Plasma exchange ...... 22 Mancozeb ...... 49 PM10 ...... 36 Manganese ...... 47 Poison information centres ...... 21 Marijuana ...... 28 Poisons information ...... 21 MDMA ...... 24 Pollution ...... 37 Mechanisms ...... 15 Polybrominated diphenyl ethers ...... 43 Memantine ...... 32 Polychlorinated biphenyls ...... 43 Mephedrone ...... 30 Polyurethane ...... 43 Mepronizine ...... 32 Ponatinib ...... 27 Mercury ...... 47 Procainamide ...... 25 Metabolism ...... 15 Prochloraz ...... 49 Metal working fluids ...... 41 Propylthiouracil ...... 27 Metals, general ...... 44 Psilocin ...... 31 Methacrylate ...... 41 Psychiatric aspects ...... 21 Methadone ...... 34 Pyrethroid insecticides, general ...... 51 Methanol ...... 41 Pyridostigmine ...... 22 Methcathinone ...... 32 Quetiapine ...... 27 Methotrexate ...... 27 Radiation ...... 43 Methylenecyclopropylglycine ...... 41 Rattlesnake ...... 53 Methylone ...... 30 Reprotoxicity ...... 21 Methylphenidate ...... 23, 32 Resin cements ...... 43 Metronidazole ...... 26 Riot control agents ...... 51 Microorganisms ...... 52 Risk assessment ...... 21 Monoclonal antibodies ...... 23 Rodenticides ...... 51 Morphine ...... 34 Rotenone ...... 51 Moxifloxacin ...... 26 Salicylate ...... 35 Muscle relaxants ...... 32 Salvia divinorum ...... 35, 52 Mushrooms ...... 52 Sarin ...... 52 Mustard gas ...... 51 Scorpions ...... 53 Mycotoxin ...... 52 Selenium ...... 48 Myristica fragrans ...... 52 Sertraline ...... 35 Naloxone ...... 23, 34 Sevoflurane ...... 25 Naltrexone ...... 23 Silica ...... 43 Neonicotinoids ...... 50 Silver ...... 48 Nephrotoxicity ...... 15 Smoke ...... 43 Nerve agents ...... 51 Snake bites ...... 53 Neurotoxicity ...... 15 Sodium nitroprusside ...... 35, 43 Nickel ...... 48 Solvents ...... 43 Nicotine ...... 32 Soman ...... 52 Nilotinib ...... 27 SSRIs ...... 35 Nitrofurantoin ...... 26 Statins ...... 35 Nitrogen dioxide ...... 42 Substance abuse ...... 35 Nitrosamines...... 42 Suicide ...... 21 N-nitrosamines ...... 42 Sulphur dioxide ...... 43 NSAIDs ...... 32 Sulphur mustard ...... 51 Nutmeg ...... 52 Sunitinib ...... 27 Occupational toxicology ...... 16 Synthetic cannabinoids ...... 30 Ocular toxicity ...... 18 Synthetic cathinones ...... 30 Opioid maintenance therapy ...... 23 Tabun ...... 52 Opioids ...... 33 Tacrolimus ...... 31 Organochlorine pesticides, general ...... 50 Talc ...... 43 Organophosphorus esters ...... 42 Tear gas ...... 51 Organophosphorus insecticides, general ...... 50 Tetrachlorobenzoquinone ...... 43 Oximes ...... 22 Thallium ...... 48, 51 Ozone ...... 42 Theophylline ...... 36 Paediatric toxicology ...... 18 Tiagabine ...... 26 Parabens ...... 42 Titanium dioxide ...... 43 Paracetamol ...... 35 Tizanidine ...... 32 Paraoxon ...... 50 Tobacco ...... 36, 44 Paraquat ...... 50 Tolperisone ...... 32 Pentachlorophenol ...... 50 Toluene ...... 44 Perfluorinated compounds ...... 42 Topiramate ...... 26 Pesticides and cancer ...... 49 Toxicology, general ...... 9 Pesticides, general ...... 49 Tramadol ...... 34 Petrol ...... 42 Tricresyl phosphate ...... 44 Phenylpyrazole...... 50 Uranium ...... 48 Phosphate ...... 42 Valproate ...... 26

Vancomycin ...... 26 VX ...... 52 Varanus komodoensis ...... 52 Warfarin ...... 26 Veterinary products ...... 36 Water pollution ...... 37 Vincristine ...... 27 Welding fumes ...... 44 Vipers ...... 53 Zinc ...... 49 Voriconazole ...... 27

The NPIS is commissioned by Public Health England