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Home , Ciguatera fish poisoning, Ciguatoxin, Grayanotoxin, Snakebite, Toluene, Toluene toxicity

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

June 2017

CONTENTS General Toxicology 9 34 Management 17 Pesticides 35 Drugs 19 Chemical Warfare 36 Chemical Incidents & 28 Plants 36 Pollution Chemicals 29 Animals 37

CURRENT AWARENESS PAPERS OF THE MONTH

Is the treatment of choice for patients with ciguatera fish ? Mullins ME, Hoffman RS. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1327664: Context arises primarily from consumption of carnivorous reef fish caught in tropical and sub-tropical waters. , a class of tasteless, heat-stable, polycyclic produced by , accumulate through the and concentrate in various carnivorous fish, such as , barracudas, wrasses, amberjack, kingfishes, and eels. Characteristics of ciguatera fish poisoning include early , , and in the first one to two days post ingestion, followed by the appearance of sensory disturbances. The classic dysaesthesia is cold , often described as reversal of hot and cold sensation, but a more accurate description is burning pain on exposure to cold. Objective To discuss and appraise the evidence regarding the use of mannitol or other drugs in treating ciguatera framed in the historical context of the last four decades.

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

The NPIS is commissioned by Public Health England

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Methods We searched PubMed and Embase for all years from 1966 to March 31, 2017 with search terms "ciguatera", "mannitol", and "treatment". These searches identified 85 articles, of which 36 were relevant to the review question. We searched Google Scholar to supplement the primary search and reviewed the references of articles for sources overlooked in the original searches. These secondary searches identified another 23 references. We excluded six clinical reports (two case series and four case reports) which did not clearly describe ciguatera or which lacked information on treatment or outcome. Fifty-three clinical articles remained for review. We searched PubMed using "ciguatera" AND "treatment" NOT "mannitol" to better identify reports describing other treatments. The search identified 128 articles, of which nine described specific pharmacological treatments and their outcomes. We combined our findings into a consensus review of the evidence both for and against the use of mannitol or other for ciguatera fish poisoning. Early human evidence of effectiveness of mannitol A 1988 report described an unexpected discovery that intravenous mannitol could rapidly and effectively treat ciguatera fish poisoning. Several other uncontrolled case series and case reports appeared to support the use of mannitol. In 2002, a small randomized, controlled trial reported no significant difference between mannitol and normal saline. Subsequent case reports have cited this study as the reason for or to withhold mannitol. Thus, some controversy exists regarding whether mannitol is useful or not for treating ciguatera fish poisoning. Basic science and animal research on ciguatera and mannitol In vitro experiments of isolated demonstrate that ciguatoxins produce neuronal , open certain sodium channels, block potassium channels, cause uncontrolled and repetitive action potentials after a stimulus. Addition of mannitol decreases the edema and reduces the uncommanded action potentials. However, intraperitoneal of in rats increases neuronal refractory period and slows nerve conduction velocity. Treatment with mannitol fails to correct these effects. Comparative trials of mannitol Evidence supporting mannitol for ciguatera fish poisoning includes four uncontrolled case series, one prospective, unblinded comparative trial and several case reports. Evidence against mannitol consists of one RCT, which has a small sample size and several potential limitations. Empirical human experience with other treatments Evidence regarding other treatments consists only of ten case reports and three overlapping case series that describe using , , duloxetine, , , or . For each of these, a long duration of treatment appears to be necessary to maintain symptomatic improvement. None of these treatments has been shown to be superior to mannitol. Conclusions It is reasonable to consider using intravenous mannitol in cases of acute ciguatera fish poisoning. Medications used in other neuropathic syndromes appear to suppress the paresthesiae of persistent ciguatera cases. However, the human evidence is of low quality for all treatments. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1327664

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A review of exposures with focus on syndrome effects Heise CW, Malashock H, Brooks DE. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1332369: Background Vilazodone is an with selective serotonin reuptake inhibition and partial 5HT1A agonism. is believed to be due to excessive stimulation of 5- HT2A and 5-HT1A receptors, resulting in the clinical triad of altered mentation, autonomic instability and neuromuscular abnormalities. The goal of this study is to define effects after vilazodone exposure. Methods A retrospective review of two databases: the American Association of Controls Centers' National Poison Data System (NPDS) and the American College of Medical Toxicology's Toxicology Investigators Consortium (ToxIC Registry). A case series of four patients from one medical toxicology service is also presented. Results During the 52-month study period, a total of 3192 vilazodone human exposures were reported to NPDS. Of these, 1734 (54%) were isolated vilazodone cases. The clinical effects of vilazodone included drowsiness (20%), vomiting (14%), (11%) and agitation (10%). Most patients (71%) had symptoms for between 2 and 24 h, though some (14%) remained symptomatic for more than 24 h. The most common treatment was intravenous fluids (15%) and the most serious intubation (2%). From the ToxIC Registry, a total of 23 cases of vilazodone exposures were identified. Of these, 17 (74%) had vilazodone listed as the first (primary) agent and 10 (43%) involved vilazodone-only ingestions. Nine (39%) cases documented serotonin syndrome; and most (8/9; 89%) listed vilazodone as the primary agent. All (n = 4) subjects in the case series with acute vilazodone toxicity had serotonin syndrome. Conclusions Vilazodone overdose, including vilazodone-only ingestions, are associated with serotonin syndrome. Serotonergic toxicity and appropriate treatments should be considered when caring for patients with vilazodone ingestions. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1332369

Hepatotoxicity evaluation of traditional Chinese medicines using a computational molecular model Zhao P, Liu B, Wang C, Acute Liver Failure Study Team (ALFST). Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1333123: Background Liver caused by traditional Chinese medicines (TCMs) is reported from many countries around the world. TCM hepatotoxicity has attracted worldwide concerns. Objective This study aims to develop a more applicable and optimal tool to evaluate TCM hepatotoxicity. Methods A quantitative structure-activity relationship (QSAR) analysis was performed based on published data and U.S. Food and Drug Administration's Liver Toxicity Knowledge Base (LTKB).

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Results Eleven herbal ingredients with proven liver toxicity in the literature were added into the dataset besides chemicals from LTKB. The finally generated QSAR model yielded a sensitivity of 83.8%, a specificity of 70.1%, and an accuracy of 80.2%. Among the externally tested 20 ingredients from TCMs, 14 hepatotoxic ingredients were all accurately identified by the QSAR model derived from the dataset containing natural hepatotoxins. Conclusions Adding natural hepatotoxins into the dataset makes the QSAR model more applicable for TCM hepatotoxicity assessment, which provides a right direction in the methodology study for TCM safety evaluation. The generated QSAR model has the practical value to prioritize the hepatotoxicity risk of TCM compounds. Furthermore, an open-access international specialized database on TCM hepatotoxicity should be quickly established. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1333123

Relationship between blood level and clinical features in patients with grayanotoxin poisoning – six clinical cases Choi HL, Park KH, Park JS, Choi HY, Kim H, Kim SM. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1331448: Background The purpose of this study was to investigate grayanotoxin (GTX) levels in the blood of patients with GTX intoxication and in the consumed liqueur, and to determine whether there was an association between blood GTX level and the patient's clinical status. Methods In September 2015, six patients were concurrently presented to the emergency department with various toxicity symptoms, which occurred after the consumption of Rhododendron liqueur at the same toxin concentration. Liquid chromatography-tandem analysis was conducted on blood samples obtained from six cases of GTX intoxication treated in our emergency department. Results At the initial evaluation in the emergency department, the mean arterial pressure of the patients ranged from 36.7 to 76.7 mm Hg. The concentrations of GTX-I and GTX-III in Rhododendron liqueur were 1.436 and 16.907 ng/mL, respectively. The initial blood GTX-III and GTX-I levels ranged from 2.9 to 58.0 ng/mL and the lower limit of quantification (LLOQ) to 8.33 ng/mL, respectively. After 20 h, the mean arterial pressure ranged from 76.7 to 93.3 mm Hg, while the blood GTX-III and GTX-I levels ranged from the LLOQ to 17.8 and 2.52 ng/mL, respectively. Discussion We estimated that the minimum blood GTX-III and GTX-I levels that caused were between 17.83 and 27.3 ng/mL, and 2.52 and 4.55 ng/mL, respectively. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1331448

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Do rapid comprehensive urine drug screens change clinical management in children? Christian MR, Lowry JA, Algren DA, Thornton SL, Deng S, Garg U. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1329537: Context Multiple studies have concluded that urine drug screens rarely change clinical management. The rapid comprehensive urine drug screen (RCUDS) at our institution detects over 300 substances using a combination of EIA and GC/MS and typically takes 2–5 h for completion. Objective We sought to determine whether this RCUDS altered management in the pediatric population. Methods All patients >1 month and <18 years of age in which a RCUDS was completed from 1 January 2012 to 31 December 2012 were eligible for the study. Assuming that clinical management would not be altered in at least 90% of cases with a confidence interval of 95%, an error of 5%, we calculated a sample size of 122 cases to ensure adequate study power. Four board-certified medical toxicologists reviewed 160 cases. Cases were assigned to the toxicologists based on a random-number generator. In addition, each toxicologist reviewed 12 random cases from the other three toxicologist's cases to determine inter-rater reliability. All four toxicologists reviewed any case in which a RCUDS was believed to have changed management. Results A total of 908 RCUDS were performed during the study period, and 160 were selected for study. Mean age was 10.5 years; male = 83, female = 77. Most were ordered from the ED (101/160 = 63%), followed by the inpatient unit (36/160 = 23%), outpatient (14/160 = 9%), and ICU (9/160 = 6%). 111/160 (69%) had a history of ingestion. Of the 160 randomly chosen cases, only three cases were found in which overall clinical management was altered based on the results of the RCUDS. All three cases were children <3 years old with a RCUDS positive for amfetamines. In all the three cases, police, Division of Family Services (DFS), and social work were involved. In no case did the acute clinical management change occurred due to the results of the RCUDS. Conclusions The RCUDS rarely changed management in patients at our institution. Further study is warranted. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1329537

Serum creatinine and cystatin C provide conflicting evidence of following acute ingestion of and oxalic acid Wijerathna TM, Gawarammana IB, Dissanayaka DM, Palanagasinghe C, Shihana F, Dassanayaka G, Shahmy S, Endre ZH, Mohamed F, Buckley NA. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1326607: Aim Acute kidney injury (AKI) is common following deliberate self-poisoning with a combination washing powder containing oxalic acid (H2C2O4) and potassium permanganate (KMnO4). Early and rapid increases in serum creatinine (sCr) follow severe poisoning. We investigated the relationship of these increases with direct nephrotoxicity in an ongoing multicenter

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prospective cohort study in Sri Lanka exploring AKI following poisoning. Methods Multiple measures of change in kidney function were evaluated in 48 consenting patients who had serial sCr and serum cystatin C (sCysC) data available. Results Thirty-eight (38/48, 79%) patients developed AKI (AKIN criteria). Twenty-eight (58%) had AKIN stage 2 or 3. Initial increases in urine creatinine (uCr) excretion were followed by a substantial loss of renal function. The AKIN stage 2 and 3 (AKIN2/3) group had very rapid rises in sCr (a median of 118% at 24 h and by 400% at 72 h post ingestion). We excluded the possibility that the rapid rise resulted from the assay used or muscle damage. In contrast, the average sCysC increase was 65% by 72 h. Conclusions In most AKI, sCysC increases to the same extent but more rapidly than sCr, as sCysC has a shorter half-life. This suggests either a reduction in Cystatin C production or, conversely, that the rapid early rise of sCr results from increased production of creatine and creatinine to meet energy demands following severe oxidative stress mediated by H2C2O4 and KMnO4. Increased early creatinine excretion supports the latter explanation, since creatinine excretion usually decreases transiently in AKIN2/3 from other causes. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1326607

Sticky situations: cyanoacrylate exposures reported to a poison control system Carstairs SD, Koh C, Qian L, Qozi M, Seivard G, Cantrell FL. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1327067: Introduction Cyanoacrylate (Super Glue®) exposures are commonly reported to poison control centers, but little has been published in the medical literature regarding these exposures. We sought to characterize cyanoacrylate exposures reported to a poison control system. Methods We performed a retrospective review of a poison system's database for all cases of single- substance human exposure to cyanoacrylate-containing products from 2005 to 2015. Data collected included age, gender, route of exposure, clinical effects, treatments recommended and medical outcome. Results There were a total of 893 patients, 505 (56.6%) of which were female. Patient ages ranged from 6 months to 88 years with a median of 11 years. The vast majority of exposures (n = 871, 97.5%) were unintentional, but a small number of exposures (n = 22, 2.5%) were due to intentional misuse (such as trying to stop a cut) or malicious intent (such as purposefully gluing a person's eyes shut as a prank). Routes of exposure included: ingestion, n = 337 (37.7%); ocular, n = 322 (36.1%); dermatologic, n = 285 (31.9%); inhalation, n = 16 (1.8%); nasal, n = 1 (0.1%); and otic, n = 1 (0.1%); some patients had multiple routes of exposure. Treatments recommended by the poison center included irrigation (n = 411), (n = 143), oil (n = 131), topical ointment (n = 82), peanut butter (n = 6), (n = 4) and WD-40® (n = 2). A total of 657 patients (73.6%) were managed on-site, while 236 (26.4%) were seen in a health care facility. Among all exposures, effects were classified as none (n = 287), minor (n = 529) and moderate (n = 77). No major effects or deaths were reported.

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Conclusions In this case series, the majority of cases occurred in children and most exposures did not result in significant morbidity. Notably, there was wide variation in terms of recommended treatments; further study is needed to determine the optimal treatment method and to standardize poison center recommendations for treating patients with cyanoacrylate exposures. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1327067

Should we treat very large paracetamol overdose differently? Bateman DN, Dear JW. Br J Clin Pharmacol 2017; 83: 1163-5. Full text available from: http://dx.doi.org/10.1111/bcp.13279

Pharmacokinetic modelling of modified infusion regimens used in the treatment of Wong A, Landersdorfer C, Graudins A. Eur J Clin Pharmacol 2017; online early: doi: 10.1007/s00228-017-2277-4: Abstract and full text available from: http://dx.doi.org/10.1007/s00228-017-2277-4

The blood of my veins – mercury, Minamata and the soul of Japan O'Malley GF. Clin Toxicol 2017; online early: doi: 10.1080/15563650.2017.1326606: The methylmercury contamination of Minamata Bay during the WWII postwar period resulted in thousands of Japanese citizens suffering horrific neurological injury. and miscommunication destroyed and changed family and social structure. In addition, the Minamata poisoning caused momentous changes in the civic discourse in Japan and was an instrumental event in the democratization of the country. This manuscript describes the effects that the environmental contamination and human poising had in the transition of Japan from a feudal society to a democratic one. Full text available from: http://dx.doi.org/10.1080/15563650.2017.1326606

QT interval prolongation in agonist treatment: analysis of continuous 12-lead electrocardiogram recordings Isbister GK, Brown AL, Gill A, Scott AJ, Calver L, Dunlop AJ. Br J Clin Pharmacol 2017; online early: doi: 10.1111/bcp.13326: Abstract and full text available from: http://dx.doi.org/10.1111/bcp.13326

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A critical note on treatment of a severe intoxication; high-dose calcium and glucagon infusions Van Veggel NM, Van der Veen GJ, Jansen TC, Westerman EM. Basic Clin Pharmacol Toxicol 2017; online early: doi: 10.1111/bcpt.12809: Abstract and full text available from: http://dx.doi.org/10.1111/bcpt.12809

Dose of for the treatment of with neurotoxic envenoming: Evidence from a randomised controlled trial in Nepal Alirol E, Sharma SK, Ghimire A, Poncet A, Combescure C, Thapa C, Paudel VP, Adhikary K, Taylor WR, Warrell D, Kuch U, Chappuis F. PLoS Negl Trop Dis 2017; 11: e0005612. Abstract and full text available from: http://dx.doi.org/10.1371/journal.pntd.0005612

Are Dutch hospitals prepared for chemical, biological, or radionuclear incidents? A survey study Mortelmans LJM, Gaakeer MI, Dieltiens G, Anseeuw K, Sabbe MB. Prehosp Disaster Med 2017; online early: doi: 10.1017/S1049023X17006513: Abstract and full text available from: http://dx.doi.org/10.1017/S1049023X17006513

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Sharma R. Mattioli AV, Pennella S, Farinetti A, Manenti A. Editorial: sorafenib toxicity, a biomarker of effect? Authors' Energy drinks and atrial fibrillation in young adults. reply. Clin Nutr 2017; online early: Aliment Pharmacol Ther 2017; 45: 1470-1. doi: 10.1016/j.clnu.2017.05.002:

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Mehrpour O, Gurjar M. Risk factors of allopurinol-induced severe cutaneous Cardiogenic shock: the main cause of mortality in acute adverse reactions in a Thai population. aluminum phosphide poisoning. Pharmacogenet Genomics 2017; online early: Indian J Crit Care Med 2017; 21: 246-7. doi: 10.1097/FPC.0000000000000285:

Osadchii OE. Sartori R, Colombo S. Assessments of the QT/QRS restitution in perfused guinea- Stevens-Johnson syndrome/toxic epidermal necrolysis pig heart can discriminate safe and arrhythmogenic drugs. caused by cefadroxil in a cat. J Pharmacol Toxicol Methods 2017; online early: doi: J Feline Med Surg 2016; 2: 10.1016/j.vascn.2017.04.010: doi: 10.1177/2055116916653616.

Piano MR. Sue GR, Karanas YL, Davis DJ, Press B. smoking and cardiovascular health: it's complicated. The unusual presentation of a from methyl Clin Pharmacol Ther 2017; online early: exposure: a case report and review of the literature. doi: 10.1002/cpt.721: 2017; 43: e43-e46.

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Toxicon 2017; 133: 63-7. Lowland copperhead (Austrelaps superbus) envenomation causing severe neuromuscular paralysis in a dog. Sartim MA, Cezarette GN, Jacob-Ferreira AL, Frantz FG, Aust Vet J 2017; 95: 207-10. Faccioli LH, Sampaio SV. Disseminated intravascular coagulation caused by Spiders moojenactivase, a procoagulant metallo- Varl T, Grenc D, Kostanjšek R, Brvar M. protease. Yellow sac spider (Cheiracanthium punctorium) bites in Int J Biol Macromol 2017; online early: Slovenia: case series and review. doi: 10.1016/j.ijbiomac.2017.05.146: Wien Klin Wochenschr 2017; online early: doi: 10.1007/s00508-017-1217-8: Wright LV, Indrawirawan YH.

INDEX

Abacavir ...... 23 Cardiotoxicity ...... 10 Acetaminophen ...... 27 Catha edulis F...... 37 Acetic acid ...... 29 Cefadroxil ...... 21 Acetonitrile ...... 29 Chemical warfare, general ...... 36 Acetylcysteine ...... 17 Chemicals, general ...... 29 Aconitum spp...... 36 Chlorhexidine ...... 30 Acrolein ...... 29 Chlorine ...... 30 Acrylamide ...... 29 Chloroquine...... 22 Activated charcoal ...... 18 Chlorpyrifos ...... 36 Adrenaline ...... 20 Chromium ...... 34 Air pollution ...... 28 Ciguatera ...... 37 Alcohol ...... 29 Clenbuterol ...... 23 Allopurinol ...... 20 Clozapine ...... 22 Aluminium phosphide ...... 35 Cocaine...... 23 Amfetamines ...... 21 Codeine ...... 26 Amino acid alkyl amides ...... 30 Contrast media ...... 30 Amiodarone ...... 21 Copper sulfate ...... 30 Amitriptyline ...... 28 Cosmetics ...... 30 Anaesthetics ...... 21 Cyanide ...... 30 Analytical toxicology ...... 9 Cyanoacrylates ...... 30 Animals, general ...... 37 Cyclophosphamide ...... 22 Anthemis nobilis ...... 36 Dabigatran ...... 21 Antiarrhythmic drugs ...... 21 DDT ...... 36 Antibiotics ...... 21 Deferasirox ...... 23 Anticoagulants ...... 21 Delphinium spp...... 37 Anticonvulsants ...... 21 Dermal toxicity ...... 11 Antidepressants ...... 22 Detergents ...... 30 Antidotes ...... 17 Developmental toxicology ...... 11 Antifungal drugs ...... 22 Diacetylmorphine...... 24 Antihistamines ...... 22 Dichlorvos ...... 36 Antimalarial drugs ...... 22 Dietary supplements ...... 23 Antineoplastic drugs ...... 22 Diethylene glycol ...... 30 Antipsychotic drugs ...... 22 Diketones ...... 31 Antivenom ...... 18 Diltiazem ...... 23 Antiviral drugs ...... 23 Diospyros rhodocalyx ...... 37 Arsenic ...... 34 Dioxins ...... 31 Asbestos...... 30 Disinfectants ...... 31 Ascorbic acid ...... 18 Doxazosin ...... 18 Beta blockers ...... 23 Doxorubicin ...... 22 Betamethasone ...... 28 Driving under the influence ...... 12 Biological warfare...... 36 Drugs, general ...... 19 Biomarkers ...... 10 E-cigarettes and e-liquids ...... 31 Bipyridyl herbicides ...... 35 Ecstasy ...... 21 Borax ...... 18 Efavirenz ...... 23 Bupivacaine ...... 21 Elapidae ...... 38 ...... 23 Endocrine disrupting chemicals ...... 31 Calciferol ...... 28 Epidemiology...... 12 Calcium channel blockers...... 23 Epinephrine ...... 18, 20 Camphor ...... 30 Ethanol ...... 29 Cannabis ...... 23 Ethnic remedies ...... 23 Carbamate insecticides ...... 35 Ethylene glycol ...... 31 Carbamazepine ...... 21 Extracorporeal membrane oxygenation ...... 19 Carbon monoxide ...... 30 Extracorporeal treatments ...... 19

39

Fentanyl ...... 26 Mothballs ...... 32 Fish/marine poisoning ...... 37 Mushrooms ...... 37 Flame lily ...... 37 Naloxone ...... 18 Flame retardants ...... 31 Nanomedicines ...... 24 Flecainide ...... 21 Nanoparticles ...... 32 Fluconazole ...... 22 Nephrotoxicity ...... 14 Fluorouracil ...... 22 Neurotoxicity ...... 14 Forensic toxicology ...... 12 n-Hexane ...... 32 Formaldehyde ...... 31 Nicotine ...... 24 Fragrance chemicals ...... 31 Nimodipine ...... 19 Gale of the wind ...... 37 Novel psychoactive substances ...... 25 Gamma hydroxybutyrate ...... 23 NSAIDs ...... 25 Gemcitabine ...... 22 Occupational toxicology ...... 15 Genotoxicity ...... 13 Ocular toxicity ...... 15 Gloria superba ...... 37 Olanzapine ...... 23 Glyphosate ...... 36 Opioid maintenance therapy ...... 19 Haemodialysis ...... 19 Opioids ...... 26 Haemofiltration ...... 19 Opium ...... 27 Haemoperfusion...... 19 Organochlorine pesticides, general ...... 36 Hazardous waste ...... 29 Organophosphorus insecticides, general ...... 36 Hepatotoxicity ...... 13 Oxalic acid ...... 32 Herbal medicines ...... 23 Oxycodone ...... 27 Heroin ...... 24 Oxygen ...... 19 Hydrogen sulphide ...... 32 Oxytetracycline...... 21 Hydroxyzine ...... 22 Paediatric toxicology ...... 15 Hyperbaric oxygen therapy ...... 18 Parabens...... 32 Ibuprofen ...... 25 Paracetamol ...... 27 Infliximab ...... 24 Pemetrexed ...... 22 Inhalation toxicity ...... 13 Pesticides, general ...... 35 Insecticides ...... 36 Phenethylamines ...... 25 Insulin glargine ...... 24 Phenytoin...... 22 Isethionate salts ...... 32 Phyllanthus niruri...... 37 Ketamine ...... 24 Plants, general ...... 36 Khat ...... 24, 37 Plasmapheresis ...... 19 Kinetics ...... 13 Plastics ...... 33 Kratom ...... 24, 37 Pollution ...... 29 Lambda-cyhalothrin ...... 36 Polonium...... 35 Larkspur ...... 37 Polyaminopropyl biguanide...... 33 Lead...... 34 Polychlorinated biphenyls ...... 33 Lidocaine ...... 21 Polycyclic aromatic hydrocarbons ...... 33 Lipid emulsion therapy ...... 18 Potassium permanganate ...... 33 Liquefied petroleum gas ...... 32 Pramipexole ...... 27 Lithium ...... 24, 34 Propafenone ...... 21 Loperamide ...... 24 Propranolol ...... 23 LSD ...... 24 Psilocybin ...... 27 Management, general ...... 17 Psychotropic drugs ...... 27 Mannitol ...... 19 Pyrethroid insecticides, general ...... 36 Marijuana ...... 23 Quetiapine ...... 23 MDMA ...... 21 Radiation ...... 33 Mechanisms ...... 14 Reprotoxicity ...... 16 Medication errors ...... 14 Risk assessment ...... 17 Mefenamic acid ...... 26 Rivastigmine ...... 27 Melatonin ...... 19 Rodenticides ...... 36 Meloxicam ...... 26 Roman chamomile ...... 36 Mephedrone ...... 24 Rotenone ...... 36 Mercury ...... 34 Salicylates ...... 27 Metabolism ...... 14 Scopolamine ...... 27 Metals, general ...... 34 Scorpions ...... 37 Methadone ...... 27 Sertraline ...... 28 Methanol ...... 32 Silica ...... 33 Methiocarb ...... 35 Smoke ...... 33 Methomyl ...... 36 Snake bites ...... 37 Methotrexate ...... 22 Solvents ...... 33 Methoxetamine ...... 25 Sorafenib ...... 27 Methyl bromide ...... 36 Spiders ...... 38 Methylphenidate ...... 24 SSRIs and SNRIs ...... 28 Mirtazapine ...... 22 Statins ...... 28 Mitragyna speciosa...... 37 Steroids ...... 28 Monensin ...... 21 Substance abuse ...... 28 Monkshood ...... 36 Sucralfate ...... 19 Monoclonal antibodies ...... 24 Suicide ...... 17 Morphine ...... 27 Synthetic cannabinoids ...... 25

40

Synthetic cathinones ...... 25 Tricyclic antidepressants ...... 28 Synthetic opioids ...... 25 Uranium ...... 35 Tafenoquine ...... 22 Valproate ...... 22 Tako-Na ...... 37 Verapamil ...... 21 Tapentadol ...... 27 Vilazodone ...... 28 Tartrazine ...... 33 Vincristine ...... 22 Taxus baccata...... 37 Vitamins...... 28 Theophylline ...... 28 Water ...... 34 Tin ...... 35 Water pollution ...... 29 Tobacco ...... 33 Yew ...... 37 Toluene ...... 34 Zinc oxide ...... 34 Toxicology, general ...... 9 Zinc phosphide ...... 36 Tramadol ...... 27

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