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

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

June 2015

CONTENTS General Toxicology 8 Metals 33 Management 18 Pesticides 36 Drugs 20 Chemical Warfare 38 Chemical Incidents & 26 Plants 38 Pollution Chemicals 28 Animals 39

CURRENT AWARENESS PAPERS OF THE MONTH

CYP2D6 genetic polymorphisms and their relevance for poisoning due to amfetamines, opioid analgesics and antidepressants Haufroid V, Hantson P. Clin Toxicol 2015; 53: 501-10. Introduction Cytochrome P450 2D6 (CYP2D6) is a member of the cytochrome P450 (CYP) superfamily involved in the biotransformation of drugs and substances of abuse encountered in clinical toxicology. Among the CYP superfamily, the CYP2D6 gene is considered as the most polymorphic as more than 105 different alleles have been identified so far. CYP2D6 genetic polymorphisms have the potential to affect the toxicity of their substrates. Objective This review will focus specifically on CYP2D6 genetic polymorphisms and their relevance for poisoning due to amfetamines, opioid analgesics and antidepressants in humans. Methods PubMed (up to August 2013) was searched with the following selection criteria: ‘CYP2D6 AND (toxicology OR poisoning OR intoxication OR overdose)’. Of the 454 citations retrieved, only 46 papers dealt with the impact of CYP2D6 polymorphisms on poisoning due to amfetamines, opioid analgesics and antidepressants.

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

Amfetamines While some in vitro studies suggest that CYP2D6-mediated metabolites of 3,4-methylene- dioxymethamfetamine (MDMA) are substantially more cytotoxic compared with unchanged MDMA, it is not yet confirmed in human cases of MDMA intoxication that extensive/ultra- rapid CYP2D6 metabolisers could be at higher risk. This would also apply to methamfetamine exposure and the related cardiac and central nervous system toxicity. Opioid analgesics CYP2D6 ultra-rapid metabolisers are more likely to experience the adverse effects of codeine and tramadol. Opioid analgesics that do not rely on CYP2D6 for therapeutic activity, such as morphine and hydromorphone, may therefore be a better alternative to codeine and tramadol, with the limitation that these drugs have their own set of adverse reactions. Antidepressants CYP2D6 poor metabolisers are generally more prone to adverse effects. Among them, the four drugs with the highest level of evidence are amitriptyline, nortriptyline, venlafaxine and fluoxetine. Further data are needed, however, for doxepin and paroxetine, while citalopram adverse effects seem definitely less influenced by CYP2D6 genetic polymorphisms. Conclusions Either poor or extensive/ultra-rapid CYP2D6 metabolisers may be exposed to toxic effects of amfetamines, opioid analgesics and antidepressants. In these three categories, the level of evidence is substance dependent, with differences within the same pharmacological class.

Full text available from: http://dx.doi.org/10.3109/15563650.2015.1049355

NBOMe and 2C substitute phenylethylamine exposures reported to the National Poison Data System Srisuma S, Bronstein AC, Hoyte CO. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1054502: Background Hallucinogenic designer drugs, especially NBOMe and the 2C substitute phenylethylamine series, have been increasing ubiquitous in past years. The purpose of this study is to characterize and compare clinical features of NBOMe and 2C exposures in humans. Method This is a retrospective cohort study of all single agent exposures to NBOMe and 2C substitute phenylethlamine reported to the National Poison Data System (NPDS) from 1st September 2012 to 30th September 2014. Results Over the study period, there were a total 341 cases including 148 NBOMe exposures and 193 2C exposures. The majority cases involved men (73.9%); median age was 18 years (Interquartile-range, 16-21). Similar clinical effects were reported in both groups including tachycardia (45.2%), agitation/irritable (44.3%), hallucination/delusion (32.0%), confusion (19.1%) and hypertension (18.5%). There were higher incidences of hallucination/delusion, single episode seizure and benzodiazepine administration in NBOMe exposures (40.5%, 8.8% and 50.0% respectively) than those of 2C exposures (25.4%, 3.1%, and 32.6% respectively). There were 2.3% death; no difference between two groups. Discussion The higher rate of symptoms in NBOMe is consistent with the higher 5HT2A agonistic effects of NBOMe described in both molecular and animal studies.

Conclusion Common clinical effects of NBOMe and 2C exposures were tachycardia, agitation/irritable, hallucination/delusion, confusion, and hypertension. There were higher incidences of hallucination/delusion, single episode seizure and benzodiazepine administration in NBOMe. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1054502

Prevalence of levamisole and aminorex in patients tested positive for cocaine in a French University Hospital Eiden C, Peyrière H, Diot C, Mathieu O. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1054499: Context The prevalence of levamisole in urine samples of subjects positive for cocaine in the US was estimated at 78% (95%confidence interval or CI: 73%–83%). However, levamisole was not quantified, and at the time of this report, aminorex was not known to be a possible metabolite of levamisole in human. Moreover no data are available in Europe. Objective The aim of this study was to determine the prevalence and concentration of levamisole and aminorex in positive cocaine urine toxicology tests, and in serum samples of cocaine-positive subjects driving under the influence of drugs or forensic autopsies. Materials and methods Consecutive urine toxicology samples tested positive for cocaine by immunoassay (EMIT, Siemens) from April to May 2014 at the toxicology laboratory of a French University Hospital, and blood samples of cocaine-positive subjects driving under the influence of drugs or forensic autopsies from April to December 2014 were analyzed by liquid chromatography– tandem mass spectrometry or LC–MS/MS (3200 QTrap, AB Sciex) to detect and quantify the presence of levamisole and aminorex. Results Forty-two urine samples tested positive for cocaine in 39 patients (79.5% males) with a median age of 43 [range: 20–51] years. Toxicological analyses were mainly required by addictions care centers (n = 17; 40%) in the context of the routine management of addict patients. Cocaine concentrations were above the limit of quantification for 33 patients, with a median value of 228 [0–645,000] ng/ml. Levamisole was detected in 32 urine samples (76%) (median concentration: 1,430 ng/ml, range: 30–258,000). Aminorex was never detected. During the study period, levamisole was detected in 87.5% of cocaine-positive blood samples of the subjects driving under the influence of drugs or forensic autopsies. Discussion In this prospective study, the prevalence of levamisole in cocaine-positive samples was 76%. Over this period, although clinical complications related to cocaine use were reported (agitation, road accident, and cardiac arrest), no complication specifically related to levamisole or aminorex was reported. Conclusion Our results show a high prevalence of levamisole in samples of subjects positive for cocaine, close to the prevalence found in the US. This high prevalence raises issues with respect to well-identified health risks associated with regular consumption of levamisole. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1054499

H2S induced coma and cardiogenic shock in the rat: effects of phenothiazinium chromophores Sonobe T, Haouzi P. Clin Toxicol 2015; 53: 525-39. Context

Hydrogen sulfide (H2S) intoxication produces an acute depression in cardiac contractility- induced circulatory failure, which has been shown to be one of the major contributors to the lethality of H2S intoxication or to the neurological sequelae in surviving animals. Methylene blue (MB), a phenothiazinium dye, can antagonize the effects of the inhibition of mitochondrial electron transport chain, a major effect of H2S toxicity. Objectives

We investigated whether MB could affect the immediate outcome of H2S-induced coma in un-anesthetized animals. Second, we sought to characterize the acute cardiovascular effects of MB and two of its demethylated metabolites-azure B and thionine-in anesthetized rats during lethal infusion of H2S. Materials and methods First, MB (4 mg/kg, intravenous [IV]) was administered in non-sedated rats during the phase of agonal breathing, following NaHS (20 mg/kg, IP)-induced coma. Second, in 4 groups of urethane-anesthetized rats, NaHS was infused at a rate lethal within 10 min (0.8 mg/min, IV). Whenever cardiac output (CO) reached 40% of its baseline volume, MB, azure B, thionine, or saline were injected, while sulfide infusion was maintained until cardiac arrest occurred. Results Seventy-five percent of the comatose rats that received saline (n = 8) died within 7 min, while all the 7 rats that were given MB survived (p = 0.007). In the anesthetized rats, arterial, left ventricular pressures and CO decreased during NaHS infusion, leading to a pulseless electrical activity within 530 s. MB produced a significant increase in CO and dP/dtmax for about 2 min. A similar effect was produced when MB was also injected in the pre-mortem phase of sulfide exposure, significantly increasing survival time. Azure B produced an even larger increase in blood pressure than MB, while thionine had no effect. Conclusion MB can counteract NaHS-induced acute cardiogenic shock; this effect is also produced by azure B, but not by thionine, suggesting that the presence of methyl groups is a prerequisite for producing this protective effect. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1043440

Estimation of monocrotophos renal elimination half-life in humans Jose A, Selvakumar R, Peter JV, Karthik G, Fleming DH, Fleming JJ. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1054500: Introduction Monocrotophos, implicated in about 1/4th of organophosphate poisonings in our centre, is associated with the highest mortality (24%). Yet data on its pharmacokinetics in humans is limited. We estimated the renal elimination half-life of monocrotophos. Patients and Methods Consecutive patients presenting with monocrotophos overdose over a 2-month period who had normal renal function were recruited. Monocrotophos in plasma and urine were quantitated by high-performance liquid chromatography. Urine was obtained from

catheterised samples at 0–2, 2–4, 4–6, 6–8, 8–12 and 12–24 h. Plasma specimens were collected at the time of admission, and at the midpoint of the urine sample collections at 1, 3, 5, 7, 10, 15 and 21 h. Renal elimination half-life was calculated from the cumulative amount excreted in the urine. Results The cohort of 5 male patients, aged 35.8 ± 2.94 years, presented with typical organophosphate (cholinergic) toxidrome following intentional monocrotophos overdose. All patients required mechanical ventilation; one patient died. Plasma data was available from 5 patients and urine data from 3 patients. The median renal elimination half-life was 3.3 (range: 1.9–5.0 h). Plasma monocrotophos values, as natural log, fell in a linear fashion up to around 10 h after admission. After the 10-hour period, there was a secondary rise in values in all the 3 patients in whom sampling was continued after 10 h. Conclusion A renal elimination half-life of 3.3 h for monocrotophos is consistent with a water-soluble compound which is rapidly cleared from the plasma. The secondary rise in plasma monocrotophos values suggests possible re-distribution. Determining the elimination profile of this compound will help develop better strategies for treatment. Full text available from: http://dx.doi.org/10.3109/15563650.2015.1054500

Comparison of abdominal computed tomography with and without oral contrast in diagnosis of body packers and body stuffers Shahnazi M, Hassanian-Moghaddam H, Gachkar L, Ahmadi N, Zamani N, Bahrami-Motlagh H, Langroudi TF, Shabestari AA, Alizadeh AM. Clin Toxicol 2015; online early: doi: 10.3109/15563650.2015.1054501: Context Toxicity due to body packing/pushing/stuffing is a major concern in many countries. Of different imaging techniques, computed tomography (CT) scan is described as the method of choice in detecting body couriers, but there is no study to concomitantly compare with- and without-contrast abdominopelvic CTs to determine the more accurate one for this purpose. Objective We aimed to evaluate the efficacy of abdominopelvic CT "with" and "without" oral contrast in diagnosis of existence, number, and type of packets in body packers/pushers and stuffers. Materials and methods In a prospective observational case series, all suspected cases of body packing/stuffing were included and underwent abdominopelvic CT with and without oral contrast in a one-year period. CT scans were reported by three independent attending radiologists blind to the demographic and clinical results and compared to our defined "gold standard" which was surgery or expulsion of packets. The existence and number of packets detected by each method were compared to define the better method of diagnosis. Results Of 11 suspect body packers/pushers, 10 carried packs. Abdominopelvic CT with and without oral contrast detected six and seven of them, respectively. In 24 body stuffers, CT without oral contrast was more accurate in diagnosis of existence (9/24 vs. 7/24, p = 0.003) and number (sensitivity and positive predictive values of 29.2% vs. 37.5% and 100% vs. 100% for CTs with and without oral contrast, respectively, p = 0.021).

Discussion and conclusions There is a remarkable gap between detection of existence and number of packets/baggies reported by the radiologists and the real condition of the patients. A close teamwork between radiologists and toxicologists is needed to manage these problematic cases.

Full text available from: http://dx.doi.org/10.3109/15563650.2015.1054501

Management of body stuffers presenting to the emergency department Yamamoto T, Malavasi E, Archer JRH, Dargan PI, Wood DM. Eur J Emerg Med 2015; online early: doi: 10.1097/MEJ.0000000000000277: Abstract and full text available from: http://dx.doi.org/10.1097/MEJ.0000000000000277

Extracorporeal treatment for salicylate poisoning: systematic review and recommendations from the EXTRIP workgroup Juurlink DN, Gosselin S, Kielstein JT, Ghannoum M, Lavergne V, Nolin TD, Hoffman RS. Ann Emerg Med 2015; online early: doi: 10.1016/j.annemergmed.2015.03.031:

Abstract and full text available from: http://dx.doi.org/10.1016/j.annemergmed.2015.03.031

Soft tissue sarcoma, non-Hodgkin's lymphoma and chronic lymphocytic leukaemia in workers exposed to phenoxy herbicides: extended follow-up of a UK cohort Coggon D, Ntani G, Harris EC, Jayakody N, Palmer KT. Occup Environ Med 2015; 72: 435-41.

Abstract and full text available from: http://dx.doi.org/10.1136/oemed-2014-102654

Phenoxy herbicides, soft-tissue sarcoma and non-Hodgkin lymphoma: a systematic review of evidence from cohort and case– control studies Jayakody N, Harris EC, Coggon D. Br Med Bull 2015; 114: 75-94.

Abstract and full text available from: http://dx.doi.org/10.1093/bmb/ldv008

Extracorporeal membrane oxygenation (ECMO) for severe toxicological exposures: review of the toxicology investigators consortium (ToxIC) Wang GS, Levitan R, Wiegand TJ, Lowry J, Schult RF, Yin S, on Behalf of the Toxicology Investigators Consortium. J Med Toxicol 2015; online early: doi: 10.1007/s13181-015-0486-8:

Abstract and full text available from: http://dx.doi.org/10.1007/s13181-015-0486-8

Intracranial haemorrhages associated with venom induced consumption coagulopathy in Australian snakebites (ASP-21) Berling I, Brown SGA, Miteff F, Levi C, Isbister GK. Toxicon 2015; 102: 8-13.

Abstract and full text available from: http://dx.doi.org/10.1016/j.toxicon.2015.05.012

Hepatotoxicity of green tea: an update Mazzanti G, Di Sotto A, Vitalone A. Arch Toxicol 2015; online early: doi: 10.1007/s00204-015-1521-x:

Abstract and full text available from: http://dx.doi.org/10.1007/s00204-015-1521-x

Efficacy and safety of pulse immunosuppressive therapy with glucocorticoid and cyclophosphamide in patients with paraquat poisoning: a meta-analysis He F, Xu P, Zhang J, Zhang Q, Gu S, Liu Y, Wang J. Int Immunopharmacol 2015; 27: 1-7.

Abstract and full text available from: http://dx.doi.org/10.1016/j.intimp.2015.04.030

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Traditional chinese medicine Xuebijing treatment is associated with decreased mortality risk of patients with CHEMICAL WARFARE, moderate paraquat poisoning. BIOLOGICAL WARFARE AND PLoS ONE 2015; 10: e0123504. RIOT CONTROL AGENTS

He F, Xu P, Zhang J, Zhang Q, Gu S, Liu Y, Wang J. Biological warfare Efficacy and safety of pulse immunosuppressive therapy Ricin with glucocorticoid and cyclophosphamide in patients with Chen GM, Yu ZH, Nie XJ, Li Z, Sun ZW, Weng ZF, Yang paraquat poisoning: a meta-analysis. YY, Chen SL, Wang CF, Zheng SR, Luo YY, Lu YT, Cao HQ, Int Immunopharmacol 2015; 27: 1-7. Zhan HX. Plasma exchange parameter selection and safety

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Textile/metal-organic-framework composites as self- Kim DS, Kang C, Kim DH, Kim SC, Lee SH, Jeong JH, Kang detoxifying filters for chemical-warfare agents. TS, Jung SM, Lee SB, Lee KW, Kim RB. Angew Chem (Engl) 2015; online early: External validation of the prognostic index in acute doi: 10.1002/anie.201502094: paraquat poisoning. Hum Exp Toxicol 2015; online early: Nerve agents doi: 10.1177/0960327115586821: Lavon O, Eisenkraft A, Blanca M, Raveh L, Ramaty E, Krivoy A, Atsmon J, Grauer E, Brandeis R. Yao R, Cao Y, He Y, Lau WB, Zeng Z, Liang Z. Is rivastigmine safe as pretreatment against nerve agents Adiponectin attenuates lung fibroblasts activation and poisoning? A pharmacological, physiological and cognitive pulmonary fibrosis induced by paraquat. assessment in healthy young adult volunteers. Neurotoxicology 2015; online early: PLoS ONE 2015; 10: e0125169. doi: 10.1016/j.neuro.2015.05.003:

Zhou C-Y, Kang X, Li C-B, Li X-H, Liu Y, Wang Z, Wang L, Sarin Wu T, Mohan C, Hu D-Y, Peng A. Brewer KL, Tran T, Meggs WJ. Pneumomediastinum predicts early mortality in acute Chronic treatment with naltrexone prevents memory paraquat poisoning. retention deficits in rats poisoned with the sarin analog Clin Toxicol 2015; 53: 551-6. diisopropylfluorophosphate (DFP) and treated with atropine and pralidoxime. J Med Toxicol 2015; online early: doi: 10.1007/s13181- Pyrethroid insecticides 015-0480-1: General Kim B, Jung A, Yun D, Lee M, Lee M-R, Choi Y-H, Kim Y, Gore A, Brandeis R, Egoz I, Turetz J, Nili U, Grauer E, Park C, Hong Y-C, Kim S. Bloch-Shilderman E. Synergism between anticholinergic and oxime treatments Association of urinary 3-phenoxybenzoic acid levels with against sarin- induced ocular insult in rats. self-reported depression symptoms in a rural elderly Toxicol Sci 2015; online early: population in Asan, South Korea. doi: 10.1093/toxsci/kfv092: Environ Health Toxicol 2015; 30: e2015002. Soman Toshima H, Yoshinaga J, Shiraishi H, Ito Y, Kamijima M, Bennion BJ, Essiz SG, Lau EY, Fattebert J-L, Emigh A, Ueyama J. Lightstone FC. Comparison of different urine pretreatments for biological A wrench in the works of human acetylcholinesterase: monitoring of pyrethroid insecticides. soman induced conformational changes revealed by J Anal Toxicol 2015; 39: 133-6. molecular dynamics simulations. PLoS ONE 2015; 10: e0121092.

Wagner-Schuman M, Richardson JR, Auinger P, Braun JM, Lanphear BP, Epstein JN, Yolton K, Froehlich TE. Guo H, Liu J, Van Shura K, Chen H, Flora MN, Myers TM, McDonough JH, McCabe JT. Association of pyrethroid pesticide exposure with N-acetyl-aspartyl-glutamate and inhibition of glutamate attention-deficit/hyperactivity disorder in a nationally carboxypeptidases protects against soman-induced representative sample of U.S. children. neuropathology. Environ Health 2015; 14: 44. Neurotoxicology 2015; 48: 180-91.

Transfluthrin PLANTS Shringi KL, Dulara SC, Aseri RK, Daria U. Aconitum spp. Uncontrolled seizures and unusual rise in leucocyte counts: Chan TYK. transfluthrin, liquid mosquito repellent suicidal poisoning. Incidence and causes of Aconitum alkaloid poisoning in Indian J Anaesth 2015; 59: 47-9. Hong Kong from 1989 to 2010.

Phytother Res 2015; online early: doi: 10.1002/ptr.5370: Trainer VL, Hardy FJ. Integrative monitoring of marine and freshwater harmful Camellia sinensis (Tea) algae in Washington State for public health protection. Toxins (Basel) 2015; 7: 1206-34. Mazzanti G, Di Sotto A, Vitalone A.

Hepatotoxicity of green tea: an update. Arch Toxicol 2015; online early: doi: 10.1007/s00204- Ciguatera 015-1521-x: Brett J, Murnion B. Pregabalin to treat ciguatera fish poisoning. Cinnamon Clin Toxicol 2015; 53: 588.

Brancheau D, Patel B, Zughaib M. Do cinnamon supplements cause acute hepatitis? Ornithorhynchus anatinus (Platypus) Am J Case Rep 2015; 16: 250-4. Hobbins P. A spur to atavism: placing platypus poison. J Hist Biol 2015; online early: doi: 10.1007/s10739-015- Dysosma pleiantha 9409-4: Karuppaiya P, Tsay HS. Therapeutic values, chemical constituents and toxicity of Taiwanese Dysosma pleiantha - A review. Scorpions Toxicol Lett 2015; 236: 90-7. Abroug F, Ouanes-Besbes L, Elatrous S. Should dobutamine be used in severe scorpion envenomation. Mushrooms Clin Toxicol 2015; 53: 584. Rahmani F, Bakhtavar HE, Ghavidel A. Acute hepatorenal failure in a patient following consumption Ananda PM, Krishnamurthy S, Srinivasaraghavan R, of mushrooms: a case report. Mahadevan S, Harichandrakumar KT. Iran Red Crescent Med J 2015; 17: e17973. Predictors of myocardial dysfunction in children with Indian red scorpion (Mesobuthus tamulus) sting envenomation. ANIMALS Indian Pediatr 2015; 52: 297-301.

General Snake bites Hobbins P. Berling I, Brown SGA, Miteff F, Levi C, Isbister GK. A spur to atavism: placing platypus poison. Intracranial haemorrhages associated with venom induced J Hist Biol 2015; online early: doi: 10.1007/s10739-015- consumption coagulopathy in Australian snakebites (ASP-21). 9409-4: Toxicon 2015; 102: 8-13.

Fish/marine poisoning Darracq MA, Cantrell FL, Klauk B, Thornton SL. Burrell S, Clion V, Auroy V, Foley B, Turner AD. A chance to cut is not always a chance to cure- Heat treatment and the use of additives to improve the Fasciotomy in the treatment of rattlesnake envenomation: stability of paralytic shellfish poisoning toxins in shellfish a retrospective poison center study. tissue reference materials for internal quality control and Toxicon 2015; 101: 23-6. proficiency testing. Toxicon 2015; 99: 80-8. Mohankumar P, Sivagurunathan C, Umadevi R. Study on the clinico-epidemiological profile and the Ferreiro SF, Carrera C, Vilariño N, Louzao MC, outcome of snake bite victims in a rural health centre in Santamarina G, Cantalapiedra AG, Botana LM. Kancheepuram district, Tamil Nadu. Acute cardiotoxicity evaluation of the marine biotoxins OA, Int J Pharma Bio Sci 2015; 6: B544-B550. DTX-1 and YTX. Toxins (Basel) 2015; 7: 1030-47. Vásquez J, Alarcón JC, Jiménez SL, Jaramillo GI, Gómez- Betancur IC, Rey-Suárez JP, Jaramillo KM, Muñoz DC, Haddad V, Stolf HO, Risk JY, Franca FOS, Cardoso JLC. Marín DM, Romero JO. Report of 15 injuries caused by lionfish (pterois volitans) Main plants used in traditional medicine for the treatment in aquarists in Brazil: a critical assessment of the severity of snake bites in the regions of the department of of envenomations. Antioquia, Colombia. J Venom Anim Toxins Incl Trop Dis 2015; 21: 8. J Ethnopharmacol 2015; online early: doi: 10.1016/j.jep.2015.04.059: Rodríguez LP, González V, Martinez A, Paz B, Lago J, Cordeiro V, Blanco L, Vieites JM, Cabado AG. Crotalinae (Pit vipers) Occurrence of lipophilic marine toxins in shellfish from Lavonas EJ, Gerardo CJ, for the Copperhead Snakebite Galicia (NW of Spain) and synergies among them. Recovery Outcome Group. Mar Drugs 2015; 13: 1666-87. Prospective study of recovery from copperhead snake envenomation: an observational study. Turner AD, Tarnovius S, Johnson S, Higman WA, Algoet M. BMC Emerg Med 2015; 15: 9. Testing and application of a refined rapid detection method for paralytic shellfish poisoning toxins in UK shellfish. Viperinae (True vipers) Toxicon 2015; 100: 32-41. Palangasinghe DR, Weerakkody RM, Dalpatadu CG, Gnanathasan CA. Algae A fatal outcome due to pulmonary hemorrhage following Silva M, Pratheepa VK, Botana LM, Vasconcelos V. Russell's viper bite. Emergent toxins in North Atlantic temperate waters: a Saudi Med J 2015; 36: 634-7. challenge for monitoring programs and legislation. Toxins (Basel) 2015; 7: 859-85. Saraiva RM, Caldas AS, Rodriguez TT, Casais-e-Silva LL.

Influence of thyroid states on the local effects induced by Therapeutic plasma exchange for refractory hemolysis after Bothrops envenoming. brown recluse spider (Loxosceles reclusa) envenomation. Toxicon 2015; 102: 25-31. J Med Toxicol 2015; online early: doi: 10.1007/s13181- 015-0485-9: Spiders Abraham M, Tilzer L, Hoehn KS, Thornton SL.

INDEX

1,3-dimethylamylamine ...... 20 Cardiotoxicity ...... 9 4-methyl-1-cyclohexanemethanol ...... 28 Chelating agents ...... 18 Acetaminophen ...... 25 Chemical incidents ...... 27 Aconitum spp...... 38 Chemical warfare, general ...... 38 Acrylamide ...... 28 Chemicals, general ...... 28 Adrenaline ...... 20 Chlordecone ...... 37 Air pollution ...... 26 Chromium ...... 34 Alcohol ...... 28 Ciguatera ...... 39 Aldicarb ...... 36 Cinnamon ...... 39 Algae ...... 39 Clonidine ...... 18 Alkali ...... 28 Cobalt ...... 35 Aluminium phosphide ...... 36 Cocaine...... 23 Amfetamines ...... 20 Colistin ...... 21 Amitriptyline ...... 26 Contrast media ...... 29 Amlodipine ...... 22 Copper ...... 35 Anabolic steroids ...... 21 Cosmetics ...... 29 Anaesthetics ...... 21 Creatine ...... 18 Analytical toxicology ...... 8 Crotalinae ...... 39 Angiotensin receptor blockers ...... 21 DDT ...... 37 Animals, general ...... 39 Dermal toxicity ...... 9 Antibiotics ...... 21 Designer drugs ...... 23 Anticoagulants ...... 21 Developmental toxicology ...... 10 Anticonvulsants ...... 21 Diacetylmorphine...... 24 Antidepressants ...... 21 Diazinon ...... 37 Antidotes ...... 18 Dichlorvos ...... 37 Antifungal drugs ...... 21 Dietary supplements ...... 23 Antineoplastics ...... 21 Digoxin ...... 23 Antipsychotics ...... 22 Dioxin ...... 29 Antiviral drugs ...... 22 Dioxins ...... 30 Arsenic ...... 34 Diquat ...... 37 Arsenic trioxide ...... 22 Disinfectants ...... 30 Asbestos...... 29 Dithiocarbamates ...... 36 Asphalt ...... 29 Driving under the influence ...... 10 Ayahuasca ...... 22 Drugs, general ...... 20 Baclofen ...... 22 Dust ...... 30 Barbiturates ...... 22 Dysosma pleiantha ...... 39 Barium sulphate ...... 29 E-cigarettes ...... 30 Benzene ...... 29 Ecstasy ...... 20 Benzodiazepines ...... 22 Endocrine disrupting chemicals ...... 30 Berberine ...... 22 Epidemiology...... 10 Biological warfare...... 38 Ethanol ...... 28 Biomarkers ...... 8 Ethnic remedies ...... 23 Bisphenol A ...... 29 Ethylbenzene ...... 30 Bittern solution ...... 29 Ethylone ...... 23 Body packers ...... 8 Everolimus ...... 22 Bortezomib ...... 22 Exhaust fumes ...... 27 Buprenorphine ...... 19, 25 Extracorporeal membrane oxygenation ...... 19 Cadmium ...... 34 Extracorporeal treatments ...... 18 Caffeine...... 22 Fenarimol ...... 36 Calciferol ...... 22 Fentanyl...... 25 Calcium channel blockers...... 22 Ferric oxide ...... 30 Camellia sinensis ...... 39 Fipronil ...... 36 Cannabis ...... 22 Fish/marine poisoning ...... 39 Carbamate insecticides ...... 36 Flame retardants ...... 30 Carbamazepine ...... 21 Fluoride ...... 30 Carbon black ...... 29 Fluoxetine ...... 26 Carbon monoxide ...... 29 Folic acid ...... 19 Carcinogenicity ...... 8 Food additives ...... 30

Forensic toxicology ...... 10 Paraquat ...... 37 Formaldehyde ...... 30 Pazopanib ...... 22 Fungicides ...... 36 Penehyclidine hydrochloride ...... 20 Gamma hydroxybutyrate ...... 23 Perchloroethylene ...... 31 Gasoline ...... 31 Perfluorinated compounds ...... 31 Genotoxicity ...... 11 Pesticides and cancer...... 36 Haemodialysis ...... 19 Pesticides, general ...... 36 Haemoperfusion...... 19 Petrol...... 31 Hair dye ...... 30 Petroleum gas ...... 31 Hazardous waste ...... 27 Phenethylamines ...... 23 Hepatotoxicity ...... 11 Phenobarbital ...... 22 Herbal medicines ...... 19, 23 Phenoxyacetate herbicides ...... 37 Herbicides ...... 36 Phenytoin...... 21 Heroin ...... 24 Phosphine ...... 32 Hydrogen sulphide ...... 31 Phthalate esters ...... 32 Hydroxychloroquine ...... 24 Piperazines...... 23 Hyperbaric oxygen therapy ...... 19 Pit vipers ...... 39 Ifosfamide ...... 22 Plants, general ...... 38 Immunosuppressants ...... 24 Plasma exchange ...... 19 Inhalation toxicity ...... 12 Plasmapheresis ...... 19 Iodine ...... 31 Platypus ...... 39 Kinetics ...... 12 Pollution ...... 27 Lamotrigine ...... 21 Polybrominated diphenyl ether ...... 32 Lead...... 35 Polychlorinated biphenyls ...... 32 Levetiracetam ...... 21 Polychlorinated dibenzofurans ...... 32 Lignocaine ...... 21 Polycyclic aromatic hydrocarbons ...... 32 Lipid emulsion therapy ...... 18 Polymorphisms ...... 16 Liquefied petroleum gas ...... 31 Polystyrene ...... 32 Lithium ...... 24, 35 Polytetrafluoroethylene ...... 32 Lorazepam ...... 22 Propofol ...... 21 Management, general ...... 18 Psychiatric aspects ...... 16 Maneb ...... 36 Psychotropic drugs ...... 26 Manganese ...... 35 Pyrethroid insecticides, general ...... 38 Marijuana ...... 22 Quetiapine ...... 22 MARS ...... 19 Radon ...... 33 MDMA ...... 20 Reprotoxicity ...... 17 Mechanisms ...... 12 Ricin ...... 38 Medication errors ...... 12 Risk assessment ...... 17 Mercury ...... 35 Salicylate ...... 26 Metabolism ...... 12 Sarin ...... 38 Metals, general ...... 33 Scorpions ...... 39 Methadone ...... 19, 25 Selenium ...... 18 Methanol ...... 31 Silibinin ...... 18 Methiozolin ...... 36 Sirolimus ...... 24 Methotrexate ...... 24 Site enhancement oil ...... 33 Methyl bromide ...... 37 Smoke ...... 33 Minoxidil ...... 24 Sodium bicarbonate ...... 18 Monoclonal antibodies ...... 19 Sodium ferrocyanide ...... 33 Mushrooms ...... 39 Solvents ...... 33 Naloxone ...... 19 Soman ...... 38 Naltrexone ...... 20 Spiders ...... 40 Nanoparticles ...... 31 SSRIs and SNRIs ...... 26 Naproxen ...... 24 Steroids ...... 26 Nephrotoxicity ...... 12 Substance abuse ...... 26 Nerve agents ...... 38 Suicide ...... 17 Neurotoxicity ...... 13 Sulindac ...... 24 Nicotine ...... 24 Surfactants ...... 33 Nitrous oxide ...... 31 Synthetic cannabinoids ...... 23 NSAIDs ...... 24 Synthetic cathinones ...... 23 Occupational toxicology ...... 13 Tea ...... 39 Ocular toxicity ...... 14 Telaprevir ...... 22 Opioid maintenance therapy ...... 19 Temozolomide ...... 22 Opioids ...... 24 Thallium...... 36 Organic solvents ...... 31 Tobacco ...... 33 Organochlorine pesticides, general ...... 37 Toluene ...... 33 Organophosphorus insecticides, general ...... 37 Toxicology, general ...... 8 Ornithorhynchus anatinus ...... 39 Transfluthrin ...... 38 Oximes ...... 18 Trazodone ...... 21 Ozone ...... 31 Trichloramines...... 33 Paediatric toxicology ...... 15 Triclosan ...... 33 Pamidronate ...... 20 Tricyclic antidepressants ...... 26 Paracetamol ...... 25 Trihalomethane ...... 33

True vipers ...... 39 Viperinae ...... 39 Tryptamines ...... 26 Volatile organic compounds ...... 33 Uranium ...... 36 Voriconazole ...... 21 Valproate ...... 21 Water pollution ...... 27 Valsartan ...... 21 Wood smoke ...... 33 Vancomycin ...... 21

The NPIS is commissioned by Public Health England