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

April 2016

CONTENTS General Toxicology 8 Metals 34 Management 18 Pesticides 36 Drugs 20 Chemical Warfare 38 Chemical Incidents & 30 Plants 38 Pollution Chemicals 30 Animals 39

CURRENT AWARENESS PAPERS OF THE MONTH

Systematic review of clinical adverse events reported after acute intravenous lipid emulsion administration Hayes BD, Gosselin S, Calello DP, Nacca N, Rollins CJ, Abourbih D, Morris M, Nesbitt-Miller A, Morais JA, Lavergne V, Lipid Emulsion Workgroup. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1151528: Background Intravenous lipid emulsions (ILEs) were initially developed to provide parenteral nutrition. In recent years, ILE has emerged as a treatment for poisoning by local anesthetics and various other drugs. The dosing regimen for the clinical toxicology indications differs significantly from those used for parenteral nutrition. The evidence on the efficacy of ILE to reverse acute toxicity of diverse substances consists mainly of case reports and animal experiments. Adverse events to ILE are important to consider when clinicians need to make a risk/benefit analysis for this therapy. Methods Multiple publication databases were searched to identify reports of adverse effects associated with acute ILE administration for either treatment of acute poisoning or parenteral nutrition. Articles were selected based on pre-defined criteria to reflect acute

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

use of ILE. Experimental studies and reports of adverse effects as a complication of long- term therapy exceeding 14 days were excluded. Results The search identified 789 full-text articles, of which 114 met the study criteria. 27 were animal studies, and 87 were human studies. The adverse effects associated with acute ILE administration included acute kidney injury, cardiac arrest, ventilation perfusion mismatch, acute lung injury, venous thromboembolism, hypersensitivity, fat embolism, fat overload syndrome, pancreatitis, extracorporeal circulation machine circuit obstruction, allergic reaction, and increased susceptibility to infection. Conclusion The emerging use of ILE administration in clinical toxicology warrants careful attention to its potential adverse effects. The dosing regimen and context of administration leading to the adverse events documented in this review are not generalizable to all clinical toxicology scenarios. Adverse effects seem to be proportional to the rate of infusion as well as total dose received. Further safety studies in humans and reporting of adverse events associated with ILE administration at the doses advocated in current clinical toxicology literature are needed. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1151528

Use of intravenous fat emulsion in the emergency department for the critically ill poisoned patient Lam SHF, Majlesi N, Vilke GM. J Emerg Med 2016; online early: doi: 10.1016/j.jemermed.2016.02.008: Abstract and full text available from: http://dx.doi.org/10.1016/j.jemermed.2016.02.008

Antipsychotic-related fatal poisoning, England and Wales, 1993–2013: impact of the withdrawal of thioridazine Handley S, Patel MX, Flanagan RJ. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1164861: Context Use of second generation antipsychotics in England and Wales has increased in recent years whilst prescription of first generation antipsychotics has decreased. Methods To evaluate the impact of this change and of the withdrawal of thioridazine in 2000 on antipsychotic-related fatal poisoning, we reviewed all such deaths in England and Wales 1993– 2013 recorded on the Office for National Statistics drug poisoning deaths database. We also reviewed antipsychotic prescribing in the community, England and Wales, 2001–2013. Use of routine mortality data When an antipsychotic was recorded with other drug(s), the death certificate does not normally say if the antipsychotic caused the death rather than the other substance(s). A second consideration concerns intent. A record of "undetermined intent" is likely to have been intentional self-poisoning, the evidence being insufficient to be certain that the individual intended to kill. A record of drug abuse/dependence, on the other hand, is likely to have been associated with an unintentional death. Accuracy of the diagnosis of poisoning When investigating a death in someone prescribed antipsychotics, toxicological analysis of

biological samples collected post-mortem is usually performed. However, prolonged attempts at resuscitation, or diffusion from tissues into blood as autolysis proceeds, may serve to alter the composition of blood sampled after death from that circulating at death. With chlorpromazine and with olanzapine a further factor is that these compounds are notoriously unstable in post-mortem blood. Deaths from antipsychotics There were 1544 antipsychotic-related poisoning deaths. Deaths in males (N = 948) were almost twice those in females. For most antipsychotics, the proportion of deaths in which a specific antipsychotic featured either alone, or only with alcohol was 30–40%, but for clozapine (193 deaths) such mentions totalled 66%. For clozapine, the proportion of deaths attributed to either intentional self-harm, or undetermined intent was 44%, but for all other drugs except haloperidol (20 deaths) the proportion was 56% or more. The annual number of antipsychotic-related deaths increased from some 55 per year (1.0 per million population) between 1993 and 1998 to 74 (1.5 per million population) in 2000, and then after falling slightly in 2002 increased steadily to reach 109 (1.9 per million population) in 2013. Intent The annual number of intentional and unascertained intent poisoning deaths remained relatively constant throughout the study period (1993: 35 deaths, 2013: 38 deaths) hence the increase in antipsychotic-related deaths since 2002 was almost entirely in unintentional poisoning involving second generation antipsychotics. Clozapine, olanzapine, and quetiapine were the second generation antipsychotics mentioned most frequently in unintentional poisonings (99, 136, and 99 deaths, respectively). Mentions of diamorphine/morphine and methadone (67 and 99 deaths, respectively) together with an antipsychotic were mainly (84 and 90%, respectively) in either unintentional or drug abuse-related deaths. Deaths and community prescriptions Deaths involving antipsychotics (10 or more deaths) were in the range 11.3–17.1 deaths per million community prescriptions in England and Wales, 2001–2013. Almost all (96%) such deaths now involve second generation antipsychotics. This is keeping with the increase in annual numbers of prescriptions of these drugs overall (<1 million in 2000, 7 million in 2013), largely driven by increases in prescriptions for olanzapine and quetiapine. In contrast, deaths involving thioridazine declined markedly (from 40 in 2000 to 10 in 2003–2013) in line with the fall in prescriptions for thioridazine from 2001. Conclusions The removal of thioridazine has had no apparent effect on the incidence of antipsychotic- related fatal poisoning in England and Wales. That such deaths have increased steadily since 2001 is in large part attributable to an increase in unintentional deaths related to (i) clozapine, and (ii) co-exposure to opioids, principally diamorphine and methadone. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1164861

Missed opportunities?: an evaluation of potentially preventable poisoning deaths Srisuma S, Cao D, Kleinschmidt K, Heffner AC, Lavonas EJ. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1157721: Introduction Although most poisoning deaths are not preventable with current medical technology, in some cases different management decisions may have prevented fatal outcomes.

Objective This study aims to review reported poisoning-related deaths for preventability to provide insight to improve future care. Methods Fatality abstracts published in the US National Poison Data System (NPDS) Annual Reports (2008–2012) were analyzed. Preventability was graded using a Likert scale of 1 (definitely non-preventable) to 6 (definitely preventable). Two medical toxicologists screened all cases. Cases deemed definitely not preventable (score 1) by both reviewers were excluded from further review and considered to be "non-preventable". All cases considered at least possibly preventable by either screener were reviewed by a multidisciplinary panel of 5 physicians for preventability scoring. Differences were resolved by consensus. Cases determined to be "preventable" (scores 4–6) were characterized by type of improvement issue involved (diagnosis, treatment, monitoring, other) and recurring scenarios. Results Of 390 published abstracts, 78 (20.0%) deaths were considered at least possibly preventable by at least one screener. Of these, 34 (8.7%) deaths were determined to be "preventable" by the panel. Inter-observer agreement by weighted kappa analysis was 0.58 for screening, 0.24 for preventability, and 0.44 for specific aspects of care. The most common toxicants were salicylates (n = 9), opioids (n = 4), toxic alcohols (n = 3), fluoride containing product (n = 3), and bupropion (n = 3). The most common improvement opportunities involved treatment and monitoring. Discussion Most of the ingested substances in preventable deaths have delayed GI absorption or require metabolic activation to produce a delayed effect (such as salicylates, opioids, and toxic alcohols), and therefore provide an opportunity for early recognition and successful interventions. Most improvement opportunities are clearly described in the literature but may be not recognized. Conclusions Based on an analysis of published NPDS data, a considerable number of poisoning-related deaths reaching medical attention may be preventable. The most common scenarios involved in potentially preventable poisoning fatalities related to monitoring and treatment. Salicylates and opioids were the most common agents involved in preventable deaths. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1157721

Could chest wall rigidity be a factor in rapid death from illicit fentanyl abuse? Burns G, DeRienz RT, Baker DD, Casavant M, Spiller HA. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1157722: Background There has been a significant spike in fentanyl-related deaths from illicit fentanyl supplied via the heroin trade. Past fentanyl access was primarily oral or dermal via prescription fentanyl patch diversion. One factor potentially driving this increase in fatalities is the change in route of administration. Rapid intravenous (IV) fentanyl can produce chest wall rigidity. We evaluated post-mortem fentanyl and norfentanyl concentrations in a recent surge of lethal fentanyl intoxications. Methods Fentanyl related deaths from the Franklin County coroner’s office from January to

September 2015 were identified. Presumptive positive fentanyl results were confirmed by quantitative analysis using liquid chromatography tandem mass spectrometry (LC/MS/MS) and were able to quantify fentanyl, norfentanyl, alfentanyl, and sufentanyl. Results 48 fentanyl deaths were identified. Mean fentanyl concentrations were 12.5 ng/ml, (range 0.5 ng/ml to >40 ng/ml). Mean norfentanyl concentrations were 1.9 ng/ml (range none detected to 8.3 ng/ml). No appreciable concentrations of norfentanyl could be detected in 20 of 48 cases (42%) and were less than 1 ng/ml in 25 cases (52%). Elevated fentanyl concentrations did not correlate with rises in norfentanyl levels. In several cases fentanyl concentrations were strikingly high (22 ng/ml and 20 ng/ml) with no norfentanyl detected. Discussion The lack of any measurable norfentanyl in half of our cases suggests a very rapid death, consistent with acute chest rigidity. An alternate explanation could be a dose-related rapid onset of respiratory arrest. Deaths occurred with low levels of fentanyl in the therapeutic range (1-2 ng/ml) in apparent non-naïve opiate abusers. Acute chest wall rigidity is a well- recognized complication in the medical community but unknown within the drug abuse community. The average abuser of illicit opioids may be unaware of the increasing fentanyl content of their illicit opioid purchase. Conclusion In summary we believe sudden onset chest wall rigidity may be a significant and previously unreported factor leading to an increased mortality, from illicit IV fentanyl use. Fentanyl and norfentanyl ratios and concentrations suggest a more rapid onset of death given the finding of fentanyl without norfentanyl in many of the fatalities. Chest wall rigidity may help explain the cause of death in these instances, in contrast to the typical opioid-related overdose deaths. Intravenous heroin users should be educated regarding this potentially fatal complication given the increasingly common substitution and combination with heroin of fentanyl. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1157722

Diglycolic acid, the toxic metabolite of diethylene glycol, chelates calcium and produces renal mitochondrial dysfunction in vitro Conrad T, Landry GM, Aw TY, Nichols R, McMartin KE. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1162312: Context Diethylene glycol (DEG) has caused many cases of acute kidney injury and deaths worldwide. Diglycolic acid (DGA) is the metabolite responsible for the renal toxicity, but its toxic mechanism remains unclear. Objective To characterize the mitochondrial dysfunction produced from DGA by examining several mitochondrial processes potentially contributing to renal cell toxicity. Materials and methods The effect of DGA on mitochondrial membrane potential was examined in normal human proximal tubule (HPT) cells. Isolated rat kidney mitochondria were used to assess the effects of DGA on mitochondrial function, including respiratory parameters (States 3 and 4), electron transport chain complex activities and calcium-induced opening of the mitochondrial permeability transition pore. DGA was compared with ethylene glycol tetraacetic acid (EGTA) to determine calcium chelating ability. DGA cytotoxicity was assessed using lactate dehydrogenase leakage from cultured proximal tubule cells.

Results DGA decreased the mitochondrial membrane potential in HPT cells. In rat kidney mitochondria, DGA decreased State 3 respiration, but did not affect State 4 respiration or the ADP/O ratio. DGA reduced glutamate/malate respiration at lower DGA concentrations (0.5 mmol/L) than succinate respiration (100 mmol/L). DGA inhibited Complex II activity without altering Complex I, III or IV activities. DGA blocked calcium-induced mitochondrial swelling, indicating inhibition of the calcium-dependent mitochondrial permeability transition. DGA and EGTA reduced the free calcium concentration in solution in an equimolar manner. DGA toxicity and mitochondrial dysfunction occurred as similar concentrations. Discussion DGA inhibited mitochondrial respiration, but without uncoupling oxidative phosphorylation. The more potent effect of DGA on glutamate/malate respiration and the inhibition of mitochondrial swelling was likely due to its chelation of calcium. Conclusion These results indicate that DGA produces mitochondrial dysfunction by chelating calcium to decrease the availability of substrates and of reducing equivalents to access Complex I and by inhibiting Complex II activity at higher concentrations. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1162312

Incidence and patterns of cardiomyopathy in carbon monoxide- poisoned patients with myocardial injury Cha YS, Kim H, Hwang SO, Kim JY, Yun KK, Choi EH, Kim OH, Kim HI, Cha KC, Lee KH. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1162310: Objectives Sustained myocardial injury is a significant predictor of mortality in carbon monoxide (CO) poisoning. There are few reports in the literature regarding the presence of CO-induced cardiomyopathy from early stages in the emergency department (ED). We prospectively investigated the early incidence of CO-induced cardiomyopathy and its patterns in patients with cardiomyopathy. Materials and methods During a 10-month period, transthoracic echocardiography (TTE) was performed in 43 consecutive patients with CO poisoning and myocardial injury, which was defined as elevated high-sensitive troponin I within 24 h after ED arrival. Measurements of left ventricular ejection fraction and wall motion abnormalities were performed to evaluate cardiac function. If a patient had CO-induced cardiomyopathy, we measured cardiac function at the time of patient admission, day 1, day 2, and once within seven days of hospitalization. Results The incidence of cardiomyopathy was as high as 74.4% (32 of 43 patients) in CO-poisoned patients with myocardial injury based on initial ED results. Echocardiographic patterns included non-cardiomyopathy (25.6%), global dysfunction (51.2%), and Takotsubo-like cardiomyopathy (23.2%). Patients in the global dysfunction group had significantly more normalized cardiac dysfunction within 72 h than did those in the Takotsubo-like cardiomyopathy group (81.8% vs. 22.2%, p = 0.001). Discussion and conclusion Patients with CO poisoning and myocardial injury experienced cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern. Investigation of cardiomyopathy

needs to be considered in patients with CO poisoning and myocardial injury. Full text available from: http://dx.doi.org/10.3109/15563650.2016.1162310

Management of cocaine-induced myocardial infarction: 4–year experience at an urban medical center Chibungu A, Gundareddy V, Wright SM, Nwabuo C, Bollampally P, Landis R, Eid SM. South Med J 2016; 109: 185-90. Abstract and full text available from: http://dx.doi.org/10.14423/SMJ.0000000000000430

Acute animal and human poisonings from cyanotoxin exposure – A review of the literature Wood R. Environ Int 2016; 91: 276-82. Abstract and full text available from: http://dx.doi.org/10.1016/j.envint.2016.02.026

Irritant gases Meulenbelt J. Medicine 2016; 44: 175-8. Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.12.004

Drugs of abuse Hill SL, Thomas SHL. Medicine 2016; 44: 160-9. Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.12.030

Corrosives Dargan PI. Medicine 2016; 44: 153-6. Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.12.007

Plants Bradberry S, Vale A. Medicine 2016; 44: 113-5. Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.11.017

Metabolic effects of poisoning Jones AF. Medicine 2016; 44: 87-90. Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.11.013

Venomous animals Warrell DA. Medicine 2016; 44: 120-4.

Abstract and full text available from: http://dx.doi.org/10.1016/j.mpmed.2015.11.001

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Phytother Res 2016; online early: doi: 10.1002/ptr.5604: Nerve agents Kirkpatrick MG, diTargiani RC, Sweeney RE, Otto TC. Abrus Precatorius (Jequirity bean) Use of V agents and V-analogue compounds to probe the active site of atypical butyrylcholinesterase from Oryzias Bradberry S. latipes. Ricin and abrin. Chem Biol Interact 2016; online early: Medicine 2016; 44: 109-10. doi: 10.1016/j.cbi.2016.03.016: Patil MM, Patil SV, Akki A, Lakhkar B, Badiger S. Scheffel C, Rappenglück S, Niessen K, Worek F, An arrow poison (abrus precatorius) causing fatal Thiermann H, Wanner K, Seeger T. poisoning in a child. Electrophysiological drug-screening of bispyridinium-non- J Clin Diagn Res 2016; 10: SD03-SD04. oxime-compounds on human nicotinic 7 acetylcholine receptors - an alternative approach for the treatment of Aloe vera nerve agent poisoning -. Guo X, Mei N.

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Prospective, consecutive case series of 158 snakebite Answers to comments about 'Hyperglycemia is a risk patients treated at Savannakhet provincial hospital, Lao factor for high-grade envenomations after European viper People's Democratic Republic with high incidence of bites (Vipera spp.) in children'. anaphylactic shock to horse derived F(ab')2 antivenom. Clin Toxicol 2016; online early: Toxicon 2016; 117: 13-21. doi: 10.3109/15563650.2016.1166231:

Crotalinae (Pit vipers) Mamede CCN, de Sousa BB, Pereira DFC, Matias MS, Dijkman MA, Damhuis DE, Meulenbelt J, De Vries I. Queiroz MR, Morais NCG, Vieira SAPB, Stanziola L, de Clinical presentation and management of an Aruban Oliveira F. rattlesnake bite in the Netherlands. Comparative analysis of local effects caused by Bothrops Clin Toxicol 2016; online early: alternatus and Bothrops moojeni snake venoms: enzymatic doi: 10.3109/15563650.2016.1156688: contributions and inflammatory modulations. Toxicon 2016; online early: doi: 10.1016/j.toxicon.2016.03.006: Elapidae Padula AM, Winkel KD. Marano M, Lonati D, Locatelli CA, Pisani M. Fatal presumed tiger snake (Notechis scutatus) en- Letter in response to: "Hyperglycemia is a risk factor for venomation in a cat with measurement of venom and high-grade envenomations after European viper bites antivenom concentration. (Vipera spp.) in children". Toxicon 2016; 113: 7-10. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1166374: Lamprophiidae Razafimahatratra B, Wang C, Mori A, Glaw F. Valenta J, Stach Z, Michálek P. Potential envenomation by the aglyphous pseudoxyrhophiine Snakebite envenoming by Sochurek's saw-scaled viper snake Leioheterodon madagascariensis and description of its Echis carinatus Sochureki. dentition. Prague Med Rep 2016; 117: 61-7. J Venom Anim Toxins Incl Trop Dis 2015; 21: 47.

Viperinae (True vipers) Claudet I, Grouteau E, Cordier L, Franchitto N, Bréhin C.

INDEX

Abrus Precatorius ...... 38 Azacitidine ...... 23 Acetaminophen ...... 28 Azathioprine ...... 26 Acetone ...... 30 Benzene ...... 31 Acetylcysteine ...... 18 Benzodiazepines ...... 23 Air pollution ...... 30 Beta2 Agonists ...... 24 Alcohol ...... 30 Beta-blockers ...... 20 Algae ...... 39 Beta-Blockers ...... 24 Alkyl Nitrites ...... 21 Biological warfare ...... 38 Aloe vera ...... 38 Biomarkers ...... 8 Alpha-chloralose ...... 37 Bisphenol A ...... 31 Aluminium ...... 35 Bispyridinium-non-oxime-compounds ...... 19 Amfetamines ...... 21 Bleomycin ...... 23 Amiodarone ...... 22 Body packers ...... 9 Amitriptyline ...... 29 Buprenorphine ...... 20 Amoxicillin ...... 22 Cadmium ...... 35 Anaesthetics ...... 22 Caffeine ...... 24 Analytical toxicology ...... 8 Calciferol ...... 29 Animals, general ...... 39 Calcium Channel Blockers ...... 24 Anisomorpha buprestoides...... 39 Cannabis ...... 24 Antiarrhythmic drugs ...... 22 Capsaicin ...... 31 Antibiotics ...... 22 Carbamazepine ...... 22 Antibodies ...... 20 Carbon ...... 31 Anticoagulants ...... 22 Carbon black ...... 31 Anticonvulsants ...... 22 Carbon monoxide ...... 31 Antidepressants ...... 23 Carbon tetrachloride ...... 31 Antidotes ...... 18 Carcinogenicity ...... 9 Antihistamines ...... 23 Cardiotoxicity ...... 9 Antimalarial Drugs ...... 23 Cement ...... 31 Antineoplastic Drugs ...... 23 Chemical warfare, general ...... 38 Antipsychotics ...... 23 Chemicals, general ...... 30 Antituberculous Drugs ...... 23 Chlorine ...... 31 Antivenom ...... 19 Chloroquine...... 24 Antiviral Drugs ...... 23 Cholinesterase Inhibitors ...... 24 Arsenic ...... 35 Ciclosporin ...... 26 Asbestos...... 31 Cisplatin ...... 23

Clarithromycin ...... 22 Jellyfish...... 39 Clonazepam ...... 24 Jequirity bean ...... 38 Coal dust ...... 32 Ketamine ...... 26 Cobalt ...... 35 Kinetics ...... 13 Cocaine ...... 24 Lactulose ...... 20 Codeine ...... 28 Lambda-cyhalothrin ...... 37 Colchicine ...... 25 Lamprophiidae ...... 40 Corrosives ...... 32 Lead ...... 35 Cosmetics ...... 32 Lewisite ...... 38 Cow dung powder ...... 32 Lidocaine ...... 22 Crotalinae ...... 40 Lionfish ...... 39 Cryogenic agents ...... 32 Lipid emulsion therapy ...... 19 Curcumin ...... 32 Lithium ...... 26, 36 Cyanide ...... 32 Loperamide ...... 26 Cyanobacteria ...... 39 LSD ...... 26 Dabigatran ...... 22 Management, general ...... 18 DDT ...... 37 Marijuana ...... 24 Dermal toxicity...... 10 MDMA ...... 21 Designer Drugs ...... 25 Mechanisms ...... 13 Developmental toxicology ...... 10 Medication errors ...... 13 Dietary supplements ...... 25 Mephedrone ...... 27 Diethylene glycol ...... 32 Mercury ...... 36 Digoxin ...... 25 Metabolism ...... 14 Dimethyl trisulfide ...... 20 Metals, general ...... 34 Dioxin ...... 32 Methadone ...... 20, 28 Diquat ...... 37 Methanol...... 33 Dosulepin ...... 29 Methoxphenidine ...... 25 Driving under the influence ...... 10 Methyl tertiary butyl ether ...... 33 Drugs, general ...... 20 Methylphenidate ...... 27 E-cigarettes and e-liquids ...... 32 Microorganisms ...... 39 Ecstasy ...... 21 Mushrooms ...... 39 Elapidae ...... 40 Mustard gas ...... 38 Epidemiology ...... 11 Naloxone ...... 19 Essential oils ...... 32 Nanoparticles ...... 33 Ethanol...... 30 Nephrotoxicity ...... 14 Ethnic remedies ...... 25 Nerve agents ...... 38 Ethylene glycol ...... 32 Neurotoxicity ...... 14 Exhaust fumes ...... 30 Nicotine ...... 27 Extracorporeal treatments ...... 20 Nitrites ...... 27 Eye Drops ...... 25 NSAIDs ...... 27 Fentanyl ...... 28 Occupational toxicology ...... 14 Fipronil ...... 37 Ocular toxicity ...... 15 Fish/marine poisoning ...... 39 Oligonucleotides ...... 27 Flame retardants ...... 32 Opioid maintenance therapy ...... 20 Flunitrazepam ...... 24 Opioids ...... 27 Fluoride ...... 32 Oral Contraceptives ...... 28 Forensic toxicology ...... 11 Organochlorine pesticides, general ...... 37 Fungicides ...... 37 Organophosphorus insecticides, general ...... 37 Gabapentin ...... 22 Oximes ...... 19 Gases ...... 32 Oxygen ...... 33 Gasoline ...... 33 Paediatric toxicology ...... 16 Genotoxicity ...... 12 Paliperidone ...... 23 Glycyrrhizin ...... 20 Paracetamol ...... 28 Glyphosate ...... 37 Paraphenylenediamine ...... 33 Haemofiltration ...... 20 Paraquat ...... 37 Haemoperfusion...... 20 Perfluorinated compounds ...... 33 Hazardous waste ...... 30 Pesticides, general ...... 36 Helium ...... 32 Petrol...... 33 Hepatotoxicity ...... 12 Phencyclidine ...... 28 Herbal medicines ...... 25 Phenytoin...... 23 Herbicides ...... 37 Phosphine ...... 33 Household products ...... 33 Phthalate esters ...... 33 Hydrazine ...... 33 Pit vipers ...... 40 Hydrogen sulphide ...... 33 Plants, general ...... 38 Hydroxychloroquine ...... 26 Plasticizers ...... 34 Hymenoptera ...... 39 Poison information centres ...... 17 Hyperbaric oxygen therapy ...... 19 Poisons information ...... 17 Hypericum spp ...... 39 Pollution ...... 30 Hypoglycaemics ...... 26 Polybrominated diphenyl ethers ...... 34 Immunosuppressants ...... 26 Polychlorinated biphenyls ...... 34 Inhalation toxicity ...... 13 Polycyclic aromatic hydrocarbons ...... 34 Iron ...... 26, 35 Polymethoxyflavones ...... 20

Propylene glycol ...... 34 St. John's wort ...... 39 Prothrombin complex concentrate ...... 20 Substance abuse ...... 29 Proton Pump Inhibitors...... 28 Suicide ...... 18 Psychiatric aspects ...... 17 Superwarfarin ...... 37 Psychotropic Drugs ...... 28 Synthetic Cannabinoids ...... 25 Pterois russelli ...... 39 Synthetic Cathinones ...... 25 Pyrethroid insecticides, general ...... 37 Tebuconazole ...... 37 Quaternary ammonium...... 34 Thallium...... 36 Radiation ...... 34 Theophylline ...... 29 Reprotoxicity ...... 17 Titanium ...... 36 Ricin...... 38 Toluene ...... 34 Risk assessment...... 17 Toxicology, general ...... 8 Risperidone ...... 23 Tranexamic Acid ...... 29 Rodenticides ...... 37 Tricyclic Antidepressants ...... 29 Salicylates ...... 29 True vipers...... 40 Sarin ...... 38 Tryptamines ...... 29 Scorpions ...... 39 Twostriped walkingstick ...... 39 Silica ...... 34 Vincristine ...... 23 Silicon ...... 36 Viperinae ...... 40 Simeprevir ...... 23 Vitamins...... 29 Snake bites ...... 39 VX ...... 38 Sodium hydroxide ...... 34 Warfarin ...... 22 Sodium oxybate ...... 20 Water pollution ...... 30 Sodium polystyrene sulfonate ...... 20 Wood dusts ...... 34 Solvents ...... 34 Wood smoke ...... 34

The NPIS is commissioned by Public Health England