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

February 2016

CONTENTS General Toxicology 9 Metals 38 Management 21 Pesticides 41 23 Chemical Warfare 42 Chemical Incidents & 32 Plants 43 Pollution Chemicals 33 Animals 43

CURRENT AWARENESS PAPERS OF THE MONTH

How toxic is ? Litjens RPW, Brunt TM. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1138226: Context Ibogaine is a psychoactive indole alkaloid found in the African rainforest shrub Tabernanthe Iboga. It is unlicensed but used in the treatment of and . However, reports of ibogaine's toxicity are cause for concern. Objectives To review ibogaine's and , mechanisms of action and reported toxicity. Methods A search of the literature available on PubMed was done, using the keywords "ibogaine" and "". The search criteria were "", "pharmacokinetics", "pharmacodynamics", "neurotransmitters", "toxicology", "toxicity", "cardiac", "neurotoxic", "human data", "animal data", "addiction", "anti-addictive", "withdrawal", "death" and "fatalities". The searches identified 382 unique references, of which 156 involved human data. Further research revealed 14 detailed toxicological case reports.

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

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

February 2016

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

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Pharmacokinetics and pharmacodynamics Ibogaine is metabolized mainly by CYP2D6 to the primary metabolite noribogaine (10- hydroxyibogamine). Noribogaine is present in clinically relevant concentrations for days, long after ibogaine has been cleared. Mechanisms of action Ibogaine and noribogaine interact with multiple neurotransmitter systems. They show micromolar affinity for N-methyl-D-aspartate (NMDA), κ- and µ- receptors and sigma-2 receptor sites. Furthermore, ibogaine has been shown to interact with the , and systems; it alters the expression of several proteins including , -derived neurotrophic factor (BDNF), c-fos and egr-1. Neurotoxicity Neurodegeneration was shown in , probably mediated by stimulation of the inferior olive, which has excitotoxic effects on Purkinje cells in the cerebellum. Neurotoxic effects of ibogaine may not be directly relevant to its anti-addictive properties, as no signs of neurotoxicity were found following doses lower than 25 mg/kg intra-peritoneal in rats. Noribogaine might be less neurotoxic than ibogaine. Cardiotoxicity -a-go-go-related gene (hERG) potassium channels in the heart might play a crucial role in ibogaine's cardiotoxicity, as hERG channels are vital in the repolarization phase of cardiac action potentials and blockade by ibogaine delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest. Twenty-seven fatalities have been reported following the ingestion of ibogaine, and pre- existing cardiovascular conditions have been implicated in the death of individuals for which post-mortem data were available. However, in this review, 8 case reports are presented which suggest that ibogaine caused ventricular tachyarrhythmias and prolongation of the QT interval in individuals without any pre-existing cardiovascular condition or family history. Noribogaine appears at least as harmful to cardiac functioning as ibogaine. Toxicity from drug-drug interaction Polymorphism in the CYP2D6 enzyme can influence blood concentrations of both ibogaine and its primary metabolite, which may have implications when a patient is taking other that is subject to significant CYP2D6 metabolism. Conclusions Alternative therapists and drug users are still using iboga extract, root scrapings, and ibogaine hydrochloride to treat drug addiction. With limited medical supervision, these are risky experiments and more ibogaine-related deaths are likely to occur, particularly in those with pre-existing cardiac conditions and those taking concurrent . Full text available from: http://dx.doi.org/10.3109/15563650.2016.1138226

Systematic review of the effect of intravenous lipid emulsion therapy for toxicity Hoegberg LCG, Bania TC, Lavergne V, Bailey B, Turgeon AF, Thomas SHL, Morris M, Miller-Nesbitt A, Mégarbane B, Magder S, Gosselin S, Lipid Emulsion Workgroup. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2015.1121270: Background Following national and regional recommendations, intravenous lipid emulsion (ILE) has

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become established in clinical practice as a treatment for acute local anesthetic (LA) toxicity, although evidence of efficacy is limited to animal studies and human case reports. A collaborative lipid emulsion workgroup was therefore established by the American Academy of Clinical Toxicology to review the evidence on the effect of ILE for LA toxicity. Methods We performed a systematic review of the literature published through 15 December 2014. Relevant articles were determined based on pre-defined inclusion and exclusion criteria. Pre- treatment experiments, pharmacokinetic studies not involving toxicity and studies that did not address antidotal use of ILE were excluded. Results We included 113 studies and reports. Of these, 76 were human and 38 animal studies. One publication included both a human case report and an animal study. Human studies included one randomized controlled crossover trial involving 16 healthy volunteers. The subclinical LA toxicity design did not show a difference in the effects of ILE versus saline. There was one case series and 73 case reports of ILE use in the context of toxicity (83 patients) including CNS depression or agitation (n = 45, 54%), (n = 49, 59%), hypotension, hypertension, EKG changes, arrhythmias (n = 39, 47%), cardiac arrest (n = 18, 22%), cardiopulmonary resuscitation, and/or requirement for endotracheal intubation and/or mechanical ventilation (n = 35, 42%). There were 81 (98%) survivors including 63 (76%) with no reported sequelae from the LA poisoning or ILE, although the presence or absence of sequelae was not reported in 15 (18%) cases. Animal studies included 29 randomized controlled studies, three observational studies, five case series, and one case report; bupivacaine was used in 29 of these reports (76%). Of 14 controlled experiments in animals, eight showed improved survival or time to return of spontaneous circulation and five no benefit of ILE versus saline or non-ILE treatments. Combining ILE with epinephrine improved survival in five of the six controlled animal experiments that studied this intervention. The studies were heterogeneous in the formulations and doses of ILE used as well as the doses of LA. The body of the literature identified by this systematic review yielded only a very low quality of evidence. Conclusion ILE appears to be effective for reversal of cardiovascular or neurological features in some cases of LA toxicity, but there is currently no convincing evidence showing that ILE is more effective than vasopressors or to indicate which treatment should be instituted as first line therapy in severe LA toxicity. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1121270

Systematic review of the effect of intravenous lipid emulsion therapy for non-local anesthetics toxicity Levine M, Hoffman RS, Lavergne V, Stork CM, Graudins A, Chuang R, Stellpflug SJ, Morris M, Miller-Nesbitt A, Gosselin S, for the AACT Lipid Emulsion Workgroup. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2015.1126286: Background The use of intravenous lipid emulsion (ILE) therapy for the treatment of lipophilic drug toxicity is increasing. Despite this, the evidence for its effect in non-local anesthetic toxicity remains sparse. Furthermore, many case reports describe ILE use for substances in which no clear efficacy data exists. The American Academy of Clinical Toxicology established a lipid

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emulsion workgroup. The aim of this group is to review the available evidence regarding the effect of ILE in non-LA drug poisoning and develop consensus-based recommendations on the use of this therapy. Methods A systematic review of the literature was performed to capture articles through 15 December 2014. Relevant articles were determined based upon a predefined methodology. Articles involving pre-treatment experiments, pharmacokinetic studies not involving toxicity, and studies not addressing antidotal use of ILE met pre-defined exclusion criteria. Agreement of at least two members of the subgroup was required before an article could be excluded. Results The final analysis included 203 articles: 141 for humans and 62 for animals. These include 40 animal experiments and 22 case reports involving animal toxicity. There were three human randomized control trials (RCT): one RCT examined ILE in TCA overdose, one RCT examined ILE in various overdoses, and one study examined ILE in reversal of sedation after therapeutic administration of inhaled anesthesia. One observational study examined ILE in glyphosate overdose. In addition, 137 human case reports or case series were identified. Intravenous lipid emulsion therapy was used in the management of overdose with 65 unique substances. Conclusions Despite the use of ILE for multiple substances in the treatment of patients with poisoning and overdose, the effect of ILE in various non-local anesthetic poisonings is heterogenous, and the quality of evidence remains low to very low. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1126286

Extracorporeal treatment for digoxin poisoning: systematic review and recommendations from the EXTRIP Workgroup Mowry JB, Burdmann EA, Anseeuw K, Ayoub P, Ghannoum M, Hoffman RS, Lavergne V, Nolin TD, Gosselin S, on behalf of the EXTRIP workgroup. Clin Toxicol 2016; 54: 103-14. Background The Extracorporeal Treatments in Poisoning (EXTRIP) workgroup was formed to provide recommendations on the use of extracorporeal treatments (ECTR) in poisoning. Here, we present our results for digoxin. Methods After a systematic literature search, clinical and toxicokinetic data were extracted and summarized following a predetermined format. The entire workgroup voted through a two- round modified Delphi method to a consensus on voting statements. A RAND/UCLA Appropriateness Method was used to quantify disagreement, and anonymous votes were compiled and discussed in person. A second vote was conducted to determine the final workgroup recommendations. Results Out of 435 articles screened, 77 met inclusion criteria. Only in-vitro, animal studies, case reports and case series were identified yielding a very low quality of evidence for all recommendations. Based on data from 84 patients, including six fatalities, it was concluded that digoxin is slightly dialyzable (level of evidence = B), and that ECTR is unlikely to improve the outcome of digoxin-toxic patients whether or not (Fab) is

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administered. Despite the lack of robust clinical evidence, the workgroup recommended against the use of ECTR in cases of severe digoxin poisoning when Fab was available (1D) and also suggested against the use of ECTR when Fab was unavailable (2D). Conclusion ECTR, in any form, is not indicated for either suspected or proven , regardless of the clinical context, and is not indicated for removal of digoxin-Fab complex. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1118488

Intoxications involving the analogs , 4- methoxybutyrfentanyl and : results from the Swedish STRIDA project Helander A, Bäckberg M, Beck O. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1139715: Background Potent and potentially harmful new psychoactive substances (NPS) are continuously introduced on the recreational drugs market. This report from the Swedish STRIDA project describes analytically confirmed cases of intoxication involving the fentanyl analogs acetylfentanyl, 4-methoxybutyrfentanyl, and furanylfentanyl. Methods Patients with suspected NPS exposure presenting in emergency departments and intensive care units in Sweden and requiring hospital care are invited to the STRIDA project. Toxicological analysis of serum and urine samples was performed by multi-component liquid chromatographic-mass spectrometric methods. Data on clinical features were retrieved from telephone consultations with the Swedish Poisons Information Centre and from medical records. Results Between April and November 2015, 14 analytically confirmed intoxications involving acetylfentanyl (nine cases), 4-methoxybutyrfentanyl (3), furanylfentanyl (1), and 4- methoxybutyrfentanyl together with furanylfentanyl (1) were identified. The patients were aged 20-40 (mean 28.5) years and 86% were men. Twelve patients (86%) were admitted to intensive care, where two required intubation and mechanical ventilation. Typical clinical features were decreased consciousness, respiratory depression, and miosis. In eight cases, the was administered to counter the effects. The serum acetylfentanyl concentration (N = 7) was 0.6-51.6 (mean 18.3 and median 14.8) ng/mL, and in urine (N = 8) 0.1-686 (mean 155 and median 66.6) ng/mmol creatinine. The serum 4-methoxy- concentration (N = 2) was 1.3 and 3.1 ng/mL, and 5.1-51.3 ng/mmol creatinine in urine (N = 3). For furanylfentanyl, the serum concentrations were 4.4 and 148 ng/mL and in urine 9.2 and 85 ng/mmol creatinine, respectively. In 13 cases (93%), other NPS and/or classical drugs were also detected. Drug products brought to hospital by patients contained acetylfentanyl (nasal spray and pink ), 4-methoxybutyrfentanyl (green tablet), furanylfentanyl/traces of 4-methoxybutyrfentanyl (nasal spray), and 4- fluorobutyrfentanyl (purple tablet). Conclusion Potentially life-threatening opioid toxicity was seen in acute intoxications involving acetylfentanyl, 4-methoxybutyrfentanyl, and furanylfentanyl. Intensive care treatment for one month was necessary in one acetylfentanyl case and one acetylfentanyl patient died from cerebral hemorrhage. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1139715

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Human bromethalin exposures reported to a U.S. Statewide Poison Control System Huntington S, Fenik Y, Vohra R, Geller RJ. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1139713: Background Bromethalin is an increasingly used alternative to long-acting and cholecalciferol rodenticides. There are few reports of human exposures, and no existing professional society guidelines on medical management of bromethalin ingestions. The aim of this retrospective data review is to characterize bromethalin exposures reported to the California Poison Control System (CPCS) between 1997 and 2014. Methods This is an observational retrospective case review of our statewide poison control system’s electronic medical records. Following Institutional Board Review and Research Committee approvals, poison center exposures related to bromethalin were extracted using substance code and free text search strategies. Case notes of bromethalin exposures were reviewed for demographic, clinical, laboratory, and outcome information; inclusion criteria for the study was single-substance, human exposure to bromethalin. Results There were 129 calls related to human bromethalin exposures (three cases met exclusion criteria). The age range of cases was 7 months–90 years old, with the majority of exposures (89 cases; 70.6%), occurring in children younger than 5 years of age (median age of 2 years). Most exposures occurred in the pediatric population as a result of exploratory oral exposure. One hundred and thirteen patients (89.7%) had no effects post exposure, while 10 patients (7.9%) had a minor outcome. Adverse effects were minor, self-limited, and mostly gastrointestinal upset. There were no moderate, major, or fatal effects in our study population. The approximate ingested dose, available in six cases, ranged from 0.067 mg/kg to 0.3 mg/kg (milligrams of bromethalin ingested per kilogram of body weight), and no dose-symptom threshold could be established from this series. Exposures were not confirmed through urine or serum laboratory testing. Discussion The prognosis for most accidental ingestions appears to be excellent. However, bromethalin exposures may result in a higher number of symptomatic patients than long-acting anticoagulant agents. Parents, physicians and poison control specialists are encouraged to maintain a high index of suspicion for bromethalin-related complications in all cases of rodenticide exposures. Conclusions Accidental bromethalin exposures in children appear to be self-limited in toxicity. Additional studies are warranted to determine whether more severe effects are precipitated when larger amounts are involved, particularly in suicidal ingestion. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1139713

Non-targeted screening for novel psychoactive substances among agitated emergency department patients Lung D, Wilson N, Chatenet F-T, LaCroix C, Gerona R. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1139714: Context Novel psychoactive substances (NPS) are being created and introduced at an unprecedented

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rate, causing frequent, large-scale epidemics. Current identification of NPS in clinical settings in the USA is limited to the retrospective case or small cluster analysis. Objective The purpose of this study was to assess the utility of non-targeted comprehensive drug screening in the agitated patients in an emergency department (ED) setting. Materials and methods This is a prospective, observational case series that was conducted in the ED of an urban Level I Trauma Center with an annual census of approximately 65,000 patients per year. Since it is common clinical practice at this facility for to be used as a second-line chemical restraint when initial dose(s) of are deemed insufficient, we surmised that the subset of ED patients with psychomotor agitation severe enough to receive both these pharmaceuticals would be likely users of NPS. For 1 month, biweekly pharmacy medication audits identified 49 of these patients. There were sufficient, remaining blood samples from 23 of these patients for analysis. Serum from stored blood samples was analyzed using liquid chromatography-time-of-flight mass spectrometry (LC-TOF/MS; LC 1260, TOF/MS 6230, Agilent). Retrospective chart review was done to identify patient clinical information. Results Six patient samples yielded seven different NPS: JWH-073, JWH-081, JWH-200, methylenedioxybenzylpiperazine, , , and . Conclusion This study demonstrates that prospective, non-targeted NPS screening in a selected ED patient population is feasible and effective in identifying NPS. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1139714

Quantitative analysis of powdered caffeine products purchased from the Internet using liquid chromatography–quadrupole time-of-flight mass spectrometry Beauchamp GA, Lin T, Zeng WZD, Hendrickson RG, Gerona R. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1138225: Context Powdered caffeine is sold on the Internet as a supplement. Severe toxicity and fatalities have been reported with use, but it is unclear if this toxicity was due to excessive dosing, mislabeled products, or adulterant . Our objective was to analyze the contents of commercially available powdered caffeine products in order to assess product purity and presence of additional ingredients, contaminants, or adulterants which may contribute to toxicity. Methods A sample of nine powdered caffeine products was purchased from the Internet. Two sample replicates of each caffeine product were analyzed. Liquid chromatography–quadrupole time- of-flight mass spectrometry (LC-QTOF/MS) was used to identify and quantify substances in the purchased products and purity of the compounds were calculated. Results Comparison of actual mass versus labeled mass of caffeine demonstrated a mean purity of 88.25% (SD 13.41%) and median purity of 90.1%. The products studied contained 1.6–5.3 g per teaspoon. Labeling on these products had limited instructions regarding how to measure the recommended dose.

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Conclusions Powdered caffeine products that are readily available on the Internet contained relatively pure caffeine with no additional detected stimulants. High purity, small serving size, and lack of clear dosing instructions may place users at risk of toxicity. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1138225

Who gets ? Choosing the chosen few Buckley NA, Dawson AH, Juurlink DN, Isbister GK. Br J Clin Pharmacol 2016; online early: doi: 10.1111/bcp.12894: Abstract and full text available from: http://dx.doi.org/10.1111/bcp.12894

Lead contamination in Flint – An abject failure to protect public health Bellinger DC. N Engl J Med 2016; online early: doi: 10.1056/NEJMp1601013: Abstract and full text available from: http://dx.doi.org/10.1056/NEJMp1601013

Superwarfarin ingestion treated successfully with prothrombin complex concentrate Haesloop O, Tillick A, Nichol G, Strote J. Am J Emerg Med 2016; 34: 116.e1-116.e2. Abstract and full text available from: http://dx.doi.org/10.1016/j.ajem.2015.05.033

Association between use of oral fluconazole during and risk of spontaneous abortion and stillbirth Mølgaard-Nielsen D, Svanström H, Melbye M, Hviid A, Pasternak B. JAMA 2016; 315: 58-67.

Abstract and full text available from: http://dx.doi.org/10.1001/jama.2015.17844

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TOXICOLOGY Inoue H, Negishi S, Nakazono Y, Iwata YT, Tsujikawa K, Ohtsuru O, Miyamoto K, Yamashita T, Kasuya F. Analytical toxicology Differentiation of ring-substituted bromoamphetamine Bartolomé M, Gallego-Picó A, Huetos O, Lucena MÁ, analogs by gas chromatography-tandem mass spectrometry. Castaño A. Forensic Toxicol 2016; 34: 125-32. A fast method for analysing six perfluoroalkyl substances in human serum by solid-phase extraction on-line coupled Jafari-Nodoushan M, Barzin J, Mobedi H. to liquid chromatography tandem mass spectrometry. A stability-indicating HPLC method for simultaneous Anal Bioanal Chem 2016; online early: determination of and . doi: 10.1007/s00216-016-9319-0: J Chromatogr B Biomed Sci Appl 2016; 1011: 163-70.

Burrai L, Nieddu M, Carta A, Trignano C, Sanna R, Boatto G. Kerrigan S, Savage M, Cavazos C, Bella P. Validated LCMS-MS method for multiresidual analysis of Thermal degradation of synthetic cathinones: implications 13 illicit in amniotic fluid. for forensic toxicology. J Anal Toxicol 2016; online early: J Anal Toxicol 2016; 40: 1-11. doi: 10.1093/jat/bkv143: Klotz K, Angerer J. Criado-García L, Ruszkiewicz DM, Eiceman GA, Thomas CLP. Quantification of naphthoquinone mercapturic acids in A rapid and non-invasive method to determine toxic levels urine as biomarkers of naphthalene exposure. of and gamma-hydroxybutyric acid in saliva J Chromatogr B Biomed Sci Appl 2016; 1012-1013: 89-96. samples by gas chromatography-differential mobility spectrometry. Knittel JL, Holler JM, Chmiel JD, Vorce SP, Magluilo J, Jr., J Breath Res 2016; 10: 017101. Levine B, Ramos G, Bosy TZ.

Analysis of parent synthetic in blood and D'Avila FB, Ferreira PCL, Salazar FR, Pereira AG, dos urinary metabolites by liquid chromatography tandem Santos MK, Pechansky F, Limberger RP, Fröehlich PE. mass spectrometry. Analysis of /crack biomarkers in meconium by J Anal Toxicol 2016; online early: doi: 10.1093/jat/bkv137: LCMS.

J Chromatogr B Biomed Sci Appl 2016; 1012-1013: 113-7. Lanzarotta A, Kelley CM.

Forensic analysis of human autopsy tissue for the de Oliveira Silveira G, Belitsky ÍT, Loddi S, Rodrigues de presence of polydimethylsiloxane (silicone) and volatile Oliveira CD, Zucoloto AD, Fruchtengarten LVG, Yonamine M. cyclic siloxanes using macro FT-IR, FT-IR spectroscopic Development of a method for the determination of cocaine, imaging and headspace GC-MS. cocaethylene and nococaine in human breast milk using J Forensic Sci 2016; online early: liquid phase microextraction and gas chromatography-mass doi: 10.1111/1556-4029.13018: spectrometry. Forensic Sci Int 2016; 265: 22-8. Lesiak AD, Cody RB, Ubukata M, Musah RA. dos Santos MF, Yamada A, Seulin SC, Leyton V, Pasqualucci Direct analysis in real time high resolution mass CAG, Muñoz DR, Yonamine M. spectrometry as a tool for rapid characterization of mind- Liquid-phase microextraction and gas chromatographic- altering plant materials and revelation of supplement mass spectrometric analysis of in vitreous adulteration–the case of Kanna. humor: study of matrix effect of human and bovine vitreous Forensic Sci Int 2016; 260: 66-73. and saline solution. J Anal Toxicol 2016; online early: doi: 10.1093/jat/bkv141: Lessmann F, Schütze A, Weiss T, Brüning T, Koch HM. Determination of metabolites of di(2-ethylhexyl) tere- Ellefsen KN, Wohlfarth A, Swortwood MJ, Diao X, Concheiro phthalate (DEHTP) in human urine by HPLC-MS/MS with M, Huestis MA. on-line clean-up. 4-Methoxy--PVP: in silico prediction, metabolic stability, J Chromatogr B Analyt Technol Biomed Life Sci 2015; and metabolite identification by human hepatocyte 1011: 196-203. incubation and high-resolution mass spectrometry. Forensic Toxicol 2016; 34: 61-75. Liu Y, Li X, Xu A, Nasser AF, Heidbreder C. Simultaneous determination of , Ford LT, Berg JD. and naloxone in human plasma by 1-adamantylamine a simple urine marker for screening for liquid chromatography/tandem mass spectrometry. third generation adamantyl-type by J Pharm Biomed Anal 2015; 120: 142-52. UPLC-MS/MS. Ann Clin Biochem 2016; online early: Mardal M, Gracia-Lor E, Leibnitz S, Castiglioni S, Meyer MR. doi: 10.1177/0004563216628892: Toxicokinetics of new psychoactive substances: , metabolic stability, and human phase I Gervais JR, Hobbs GA. metabolism of the synthetic WIN 55,212-2 Use of an acetyl derivative to improve GC-MS determination studied using in vitro tools and LC-HR-MS/MS. of norbuprenorphine in the presence of high concentrations Anal 2016; online early: of buprenorphine in urine. doi: 10.1002/dta.1938: J Anal Toxicol 2016; online early: doi: 10.1093/jat/bkw001: Monteiro C, Proença P, Tavares C, Castañera A, Real FC. Heikman P, Sundström M, Pelander A, Ojanperä I. Interference of anesthetics in blood alcohol analysis by New psychoactive substances as part of polydrug abuse HS-GC-FID: a case report. within opioid maintenance treatment revealed by Forensic Sci Int 2016; 265: 65-9. comprehensive high-resolution mass spectrometric urine drug screening. Parnmen S, Sikaphan S, Leudang S, Boonpratuang T, Hum Psychopharmacol 2016; 31: 44-52. Rangsiruji A, Naksuwankul K.

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Molecular identification of poisonous mushrooms using Simultaneous determination of gefitinib and its major nuclear ITS region and peptide toxins: a retrospective metabolites in mouse plasma by HPLC-MS/MS and its study on fatal cases in Thailand. application to a pharmacokinetics study. J Toxicol Sci 2016; 41: 65-76. J Chromatogr B Biomed Sci Appl 2016; 1011: 215-22.

Perez ER, Knapp JA, Horn CK, Stillman SL, Evans JE, Biomarkers Arfsten DP. Carbonari D, Chiarella P, Mansi A, Pigini D, Iavicoli S, Comparison of LCMS-MS and GC-MS analysis of Tranfo G. compounds included in the drug demand Biomarkers of susceptibility following exposure: reduction urinalysis program. influence of genetic polymorphisms on benzene metabolism J Anal Toxicol 2016; online early: and health effects. doi: 10.1093/jat/bkv140: Biomark Med 2016; 10: 145-63.

Poklis JL, Wolf CE, Poklis A. Chaguri JL, Godinho AF, Horta DF, Gonçalves-Rizzi VH, 4-fluoroamphetamine in serum and urine from an Possomato-Vieira JS, Nascimento RA, Dias-Junior CA. intoxicated patient with life-threatening hyperpyrexia. Exposure to fipronil elevates systolic blood pressure and J Anal Toxicol 2016; online early: disturbs related biomarkers in plasma of rats. doi: 10.1093/jat/bkv139: Environ Toxicol Pharmacol 2015; 42: 63-8.

Roche L, Pinguet J, Herviou P, Libert F, Chenaf C, Eschalier Jacobo-Estrada T, Cardenas-Gonzalez M, Santoyo-Sánchez A, Authier N, Richard D. M, Parada-Cruz B, Uria-Galicia E, Arreola-Mendoza L, Fully automated semi-quantitative toxicological screening Barbier O. in three biological matrices using turbulent flow chro- Evaluation of injury biomarkers in amniotic fluid matography/high resolution mass spectrometry. after gestational exposure to cadmium. Clin Chim Acta 2016; online early: J Appl Toxicol 2016; online early: doi: 10.1002/jat.3286: doi: 10.1016/j.cca.2016.01.017: Karabacak M, Turkdogan KA, Coskun A, Akpinar O, Duman Severino P, Silveira EF, Vazzana M, Chaud MV, Santana A, Kapci M, Eren SH, Karabacak P. MH, Souto EB. Detection of neutrophil-lymphocyte ratio as a serum Validation of an UV spectrophotometric assay for the marker associated with inflammations by acute carbon quantification of polymyxin B in solid lipid nanoparticles. monoxide poisoning. Pharmazie 2015; 70: 693-7. J Acute Dis 2015; 4: 305-8.

Shanks KG, Clark W, Behonick G. Klotz K, Angerer J. Death associated with the use of the synthetic cannabinoid Quantification of naphthoquinone mercapturic acids in ADB-FUBINACA. urine as biomarkers of naphthalene exposure. J Anal Toxicol 2016; online early: doi: 10.1093/jat/bkv142: J Chromatogr B Biomed Sci Appl 2016; 1012-1013: 89-96.

Shi Y, Cui X, Shen M, Xiang P. Maule AL, Proctor SP, Blount BC, Chambers DM, McClean MD. Quantitative analysis of the endogenous GHB level in the Volatile organic compounds in blood as biomarkers of hair of the Chinese population using GC/MS/MS. exposure to JP-8 jet fuel among US Air Force personnel. J Forensic Leg Med 2016; 39: 10-5. J Occup Environ Med 2016; 58: 24-9.

Singh SP, Dwivedi N, Raju KSR, Taneja I, Wahajuddin M. Robinson JF, Gormley MJ, Fisher SJ. Validation of a rapid and sensitive UPLC-MS-MS method A genomics-based framework for identifying biomarkers of coupled with protein precipitation for the simultaneous human neurodevelopmental toxicity. determination of seven pyrethroids in 100 L of rat Reprod Toxicol 2016; online early: plasma by using ammonium adduct as precursor ion. doi: 10.1016/j.reprotox.2016.01.007: J Anal Toxicol 2016; online early: doi: 10.1093/jat/bkw002: Severin MJ, Trebucobich MS, Buszniez P, Brandoni A, Torres AM. Stice S, Liu G, Matulis S, Boise LH, Cai Y. The urinary of an organic anion transporter as Determination of multiple human arsenic metabolites an early biomarker of methotrexate-induced kidney injury. employing high performance liquid chromatography Toxicol Res (Camb) 2016; online early: inductively coupled plasma mass spectrometry. doi: 10.1039/C5TX00436E: J Chromatogr B Biomed Sci Appl 2016; 1009-1010: 55-65. Stachel N, Skopp G. Sun B, Chen Y. Formation and inhibition of ethyl glucoronide and ethyl A simple and rapid method for detection of paraquat in sulfate. human plasma by high-performance liquid chromatography. Forensic Sci Int 2016; 265: 61-4. Int J Clin Exp Med 2015; 8: 17067-71. Tedesco G, Cadossi M, Savarino L, Mazzotti A, Sambri A, Viaene J, Lanckmans K, Dejaegher B, Mangelings D, Baldini N, Giannini S. Vander Heyden Y. Potential markers of systemic toxicity induced by metal Comparison of a triple-quadrupole and a quadrupole time- ions in patients with hip resurfacing. of-flight mass analyzer to quantify 16 in human HIP Int 2015; 25: S61. plasma. J Pharm Biomed Anal 2016; online early: Weldon BA, Shubin SP, Smith MN, Workman T, Artemenko doi: 10.1016/j.jpba.2015.12.055: A, Griffith WC, Thompson B, Faustman EM. Urinary microRNAs as potential biomarkers of pesticide Zheng N, Zhao C, He X-R, Jiang S-T, Han S-Y, Xu G-B, Li P-P. exposure.

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Efficacy of tiotropium bromide and rehabilitation treatment on pulmonary function of patients with sulfur mustard ANIMALS lung injury. Fish/marine poisoning Iran Red Crescent Med J 2015; 17: e20026. Blanco J, Arévalo F, Correa J, Porro MC, Cabado AG, Vieites JM, Moroño A. Nerve agents Effect of the industrial canning on the toxicity of mussels contaminated with diarrhetic shellfish poisoning (DSP) Soman toxins. Wei Z, Liu Y-Q, Wang Y, Li W-H, Zhou X-B, Zhao J, Huang Toxicon 2016; 112: 1-7. C, Li X, Liu J, Zheng Z, Li S. Novel nonquaternary reactivators showing reactivation Pterois volitans (Lionfish) efficiency for soman-inhibited human acetylcholinesterase. Resiere D, Cerland L, de Haro L, Valentino R, Criquet- Toxicol Lett 2016; online early: Hayot A, Chabartier C, Kaidomar S, Brouste Y, Mégarbane doi: 10.1016/j.toxlet.2016.01.015: B, Mehdaoui H. Envenomation by the invasive Pterois volitans species PLANTS (lionfish) in the French West Indies – a two-year prospective study in Martinique. Aconitum spp. Clin Toxicol 2016; online early: doi: Chan TYK. 10.3109/15563650.2016.1143100: Aconitum alkaloid poisoning because of contamination of herbs by aconite roots. Seaweed Phytother Res 2016; 30: 3-8. Desideri D, Cantaluppi C, Ceccotto F, Meli MA, Roselli C, Feduzi L. Guayusa (Ilex guayusa) Essential and toxic elements in seaweeds for human con- Kapp RW, Jr., Mendes O, Roy S, McQuate RS, Kraska R. sumption. General and genetic toxicology of guayusa concentrate J Toxicol Environ Health A 2016; online early: (Ilex guayusa ). doi: 10.1080/15287394.2015.1113598: Int J Toxicol 2016; online early: doi: 10.1177/1091581815625594: Micro-organisms Botulism Mushrooms and other fungi Mottate K, Yokote H, Mori S, Horita A, Miyatsu Y, Torii Y, Park JS, Min JH, Kim H, Lee SW, Kang JH, An JY. Kozaki S, Iwaki M, Takahashi M, Ginnaga A. Four cases of successful treatment after Podostroma Retrospective survey to evaluate the safety and efficacy of cornu-damae intoxication. Japanese botulinum antitoxin therapy in Japan. Hong Kong J Emerg Med 2016; 23: 55-9. Toxicon 2016; 110: 12-8.

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snake venoms on rodent blood coagulation. Rhododendron spp. Toxicon 2016; 110: 19-26. Erenler AK. Cardiac effects of mad honey poisoning and its management Karabuva S, Vrkic I, Brizic I, Ivic I, Lukžic B. in emergency department: a review from Turkey. Venomous snakebites in children in southern Croatia. Cardiovasc Toxicol 2016; 16: 1-4. Toxicon 2016; 112: 8-15.

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Moon JM, Chun BJ. Roth B, Sharma K, Onisko N, Chen T. Severe coagulopathy after ingestion of "Snake Wine". Prospective evaluation of pain, swelling, and disability J Emerg Med 2016; online early: from copperhead envenomation. doi: 10.1016/j.jemermed.2015.11.037: Clin Toxicol 2016; online early: doi: 10.3109/15563650.2015.1130227: Colubridae Keyler DE, Richards DP, Warrell DA, Weinstein SA. Zhang XC, Kearney A, Gibbs FJ, Hack JB. Local envenomation from the bite of a juvenile false water Snakebite! Crotalinae envenomation of a man in Rhode cobra (Hydrodynastes gigas; Dipsadidae). Island. Toxicon 2016; 111: 58-61. R I Med J (2013) 2016; 99: 25-7.

Coral snake Elapidae Bucaretchi F, de Capitani EM, Vieira RJ, Rodrigues CK, Isbister GK, Gault A, Tasoulis T, O'Leary MA. Zannin M, Da Silva NJ, Jr., Casais-e-Silva LL, Hyslop S. A definite bite by the Ornamental Snake (Denisonia Coral snake bites (Micrurus spp.) in Brazil: a review of maculata) causing mild envenoming. literature reports. Clin Toxicol 2016; online early: Clin Toxicol 2016; online early: doi: 10.3109/15563650.2015.1128545: doi: 10.3109/15563650.2015.1135337: Viperinae (True vipers) Crotalinae (Pit vipers) Fahmi L, Makran B, Boussadda L, Lkhider M, Ghalim N. Olives TD, Topeff JM, Willhite LA, Kubic VL, Keyler DE, Haemostasis disorders caused by envenomation by Cole JB. Cerastes cerastes and Macrovipera mauritanica vipers. Complete clinical course of envenomation by Protobothrops Toxicon 2015; online early: mangshanensis: delayed coagulopathy and response to doi: 10.1016/j.toxicon.2015.12.012: Trimeresurus albolabris antivenom. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1138227:

INDEX

4-aminopyridine ...... 23 Beta blockers ...... 25 Acetaminophen ...... 31 Beta2 agonists ...... 26 Acetylcysteine ...... 21 Biological warfare ...... 42 Aconitine ...... 23 Biomarkers ...... 10 Aconitum spp...... 43 Bisphenol A ...... 34 Acrylamide ...... 33 Body packers ...... 11 Agent Orange ...... 42 Botulism ...... 43 Air pollution ...... 32 Bromethalin ...... 42 Alcohol ...... 33 Buprenorphine ...... 30 Aluminium ...... 38 Cadmium ...... 39 Aluminium phosphate ...... 34 Caffeine ...... 26 Aluminium phosphide ...... 41 Calcium channel blockers ...... 26 Amanita mushrooms ...... 43 Cannabis ...... 26 Amfetamines ...... 23 Capecitabine ...... 25 Amiodarone ...... 24 Carbamazepine ...... 24 Anaesthetics ...... 24 Carbon monoxide ...... 34 Analytical toxicology ...... 9 Carcinogenicity ...... 11 Animals, general ...... 43 Cardiotoxicity ...... 11 Antiarrhythmic drugs ...... 24 Ceftriaxone ...... 24 Antibiotics ...... 24 Chemical warfare, general ...... 42 Anticoagulants ...... 24 Chemicals, general ...... 33 Anticonvulsants ...... 24 Chenodeoxycholic acid ...... 26 Antidepressants ...... 25 Chlorpyrifos ...... 41 Antidotes ...... 21 Chrome ...... 39 Antifungal drugs ...... 25 Chromium ...... 39 Antineoplastic drugs ...... 25 Citalopram ...... 32 Antipsychotics ...... 25 Clarithromycin ...... 24 Antituberculous drugs ...... 25 Clenbuterol ...... 26 Antivenom ...... 21 Clonazepam ...... 25 Antiviral drugs ...... 25 Clozapine ...... 25 Arsenic ...... 38 Cobalt ...... 39 Asbestos...... 34 Cocaine...... 26 Aspartate...... 22 Colchicine ...... 27 Atropine ...... 25 Colubridae ...... 44 Bactrim ...... 24 Coral snake ...... 44 Batteries ...... 34 Corrosives ...... 35 Benzene ...... 34 Crocin ...... 35 Benzodiazepines ...... 22, 25 Crotalinae ...... 44

46

Curcumin ...... 22 Lead ...... 39 Cyanide ...... 35 Levamisole ...... 29 DDT ...... 41 Lionfish ...... 43 Dermal toxicity...... 11 Lipid emulsion therapy ...... 21 Designer drugs ...... 27 Lithium ...... 29, 40 Developmental toxicology ...... 11 Loperamide ...... 30 Dexamethasone ...... 22 Management, general ...... 21 Diacetylmorphine ...... 29 Manganese ...... 40 Dietary supplements ...... 28 Marijuana ...... 26 Digoxin ...... 28 MDMA ...... 23 Dimethyl sulfoxide...... 35 Mechanisms ...... 16 Dinitrobenzene ...... 35 Mephedrone ...... 27 Dioxins ...... 35 Mercury ...... 40 Diquat ...... 42 Metabolism ...... 16 Disulfiram ...... 22 Metals, general ...... 38 Driving under the influence ...... 12 Metformin ...... 29 Dronedarone ...... 24 Methadone ...... 22, 31 Drugs, general ...... 23 Methanol...... 36 Dusts ...... 35 Methotrexate ...... 30 E-cigarettes ...... 35 Methyl tertiary butyl ether ...... 36 Ecstasy ...... 23 Micro-organisms ...... 43 Embutramide ...... 31 Mineral oils...... 36 Epidemiology ...... 12 Mirtazapine ...... 25 Epoxy resins ...... 36 Morphine ...... 31 Essential oils ...... 36 Mushrooms ...... 43 Ethanol...... 33 Mustard gas ...... 42 Ethnic remedies ...... 28 Mycotoxins ...... 43 Ethylene glycol ...... 36 Nalmefene ...... 22 Ethylphenidate ...... 28 Naloxone ...... 23 Exhaust fumes ...... 32 Naltrexone ...... 31 Extracorporeal membrane oxygenation...... 22 Nanoparticles ...... 37 Extracorporeal treatments ...... 22 Naphthalene ...... 37 Fentanyl ...... 31 Neonicotinoids ...... 41 Fipronil ...... 41 Nephrotoxicity ...... 16 Fish/marine poisoning ...... 43 Nerve agents ...... 43 Flame retardants ...... 36 Neurotoxicity ...... 16 Fluconazole ...... 25 Nicotinamide ...... 32 Fluoride ...... 36 Nicotine ...... 30 Fluorocarbons ...... 36 Nitrofurantoin ...... 24 Fluorouracil ...... 25 NSAIDs ...... 30 Forensic toxicology ...... 13 Obidoxime ...... 22 Formaldehyde ...... 36 Occupational toxicology ...... 17 Gabapentin ...... 25 Ocular toxicity ...... 18 Gamma hydroxybutyrate ...... 28 Opioid maintenance therapy ...... 22 Gasoline ...... 37 Opioids ...... 30 Gefitinib ...... 25 Organochlorine pesticides, general ...... 41 Genotoxicity ...... 15 Organophosphorus insecticides, general ...... 41 Glucocorticoids ...... 28 Organosilicon compounds ...... 37 Glyphosate ...... 41 Oximes ...... 22 Guayusa ...... 43 Paediatric toxicology ...... 18 Hazardous waste ...... 33 Palladium ...... 40 Helium ...... 36 Paracetamol ...... 31 Hepatotoxicity ...... 15 Paraquat ...... 42 Herbal medicines ...... 22, 28 Perfluorinated compounds ...... 37 Herbicides ...... 41 Perfluoroalkyl derivatives ...... 37 Heroin ...... 29 Permethrin ...... 42 Honey ...... 36 Pesticides, general ...... 41 Hydrocarbons ...... 36 Petrol...... 37 Hydrogen sulphide ...... 36 Phenethylamines ...... 27 Hydroxychloroquine ...... 29 Phenobarbital ...... 23 Hyperbaric oxygen therapy ...... 21 Phosphate enema ...... 31 Hypoglycaemic drugs ...... 29 Phthalate esters ...... 37 Ibogaine ...... 29 Pit vipers ...... 44 Ibrutinib ...... 25 Plants, general ...... 43 Ibuprofen ...... 30 Plasma exchange ...... 22 Icatibant ...... 22 Poison information centres ...... 19 Ilex guayusa ...... 43 Poisons information ...... 19 Immunosuppressants ...... 29 Pollution ...... 33 Inhalation toxicity ...... 15 Polybrominated diphenyl ethers ...... 37 Insulin ...... 22, 29 Polychlorinated biphenyls ...... 37 Isoniazid...... 25 Polycyclic aromatic hydrocarbons ...... 37 Kinetics ...... 15 Polymyxin B ...... 24

47

Pregabalin ...... 25 Superwarfarin ...... 42 Prothrombin complex concentrate ...... 23, 31 Synthetic cannabinoids ...... 27 Psychiatric aspects ...... 19 Synthetic cathinones ...... 28 Psychotropic drugs ...... 31 Tapentadol ...... 31 Pterois volitans ...... 43 Thallium...... 41 Pyrethroid insecticides, general ...... 42 Theophylline ...... 32 Reprotoxicity ...... 20 Thujone ...... 38 Rhododendron spp...... 43 Thyroxine...... 32 Risk assessment...... 20 Tiotropium bromide ...... 23 Rodenticides ...... 42 Tobacco ...... 38 Ropivacaine ...... 24 Tocilizumab ...... 29 Safranal...... 37 Toluene ...... 38 Salicylate ...... 31 Toxicology, general ...... 9 Scorpions ...... 43 Tramadol ...... 31 Seaweed ...... 43 Trichloroethylene ...... 38 Selenium ...... 40 True vipers...... 44 Silver...... 40 Vaccines ...... 32 Smoke ...... 37 Vegetable oils ...... 38 Snake bites ...... 43 Verapamil ...... 26 Soman ...... 43 Veterinary products ...... 32 SSRIs ...... 32 Viperinae ...... 44 Substance abuse ...... 32 Vitamins...... 32 Suicide ...... 20 Warfarin ...... 24, 42 Super coumadin ...... 42 Yellow phosphorus ...... 38

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