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XXXV International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 26–29 May 2015, St Julian's, Malta

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XXXV International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 26–29 May 2015, St Julian's, Malta Clinical Toxicology ISSN: 1556-3650 (Print) 1556-9519 (Online) Journal homepage: http://www.tandfonline.com/loi/ictx20 XXXV International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 26–29 May 2015, St Julian's, Malta To cite this article: (2015) XXXV International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 26–29 May 2015, St Julian's, Malta, Clinical Toxicology, 53:4, 233-403, DOI: 10.3109/15563650.2015.1024953 To link to this article: http://dx.doi.org/10.3109/15563650.2015.1024953 Published online: 26 Mar 2015. Submit your article to this journal Article views: 3422 View related articles View Crossmark data Citing articles: 2 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ictx20 Download by: [UPSTATE Medical University Health Sciences Library] Date: 28 December 2016, At: 10:31 Clinical Toxicology (2015), 53, 233–403 Copyright © 2015 Informa Healthcare USA, Inc. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.3109/15563650.2015.1024953 ABSTRACTS XXXV International Congress of the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) 26–29 May 2015, St Julian ’ s, Malta 1. Modelling dose-concentration-response Introduction: The American Association of Poison Control Cen- ters (AAPCC) published its fi rst annual report in 1983. Call data Ursula Gundert-Remy from sixteen US poison centers was chronicled in that report. Seven submitted data for the entire year. By July 2000, 63 centers Institute for Clinical Pharmacology and Toxicology, Charit é were part of the national poison center system, but only 59 submit- Medical School, Berlin, Germany ted data for the full year. Currently the US poison center system is comprised of 55 regional poison centers serving all 50 states, Introduction: It is the aim of modeling to quantitatively describe Puerto Rico, US Virgin Islands, and three Pacifi c jurisdictions. The the relationship between dose, concentration and response and its centers continuously upload data to the AAPCC ’ s National Poison time course. Data System (NPDS). From 2000 forward, poison center call data Methods and results: Pharmaco-/toxicokinetic (PTK) data is infor- including fatality data is available from NPDS online. Since incep- mation about the entrance and fate within the body of a substance, tion of the PC database, exposure-related death analysis has been including its metabolites. The data needed to describe these phe- a priority. Over the years, death report evaluation methodology nomena can be obtained by in vivo experiments. With this approach, has evolved. A poison center death is defi ned as a poison center modeling means that the concentration-time profi le is driven by data call resulting in the medical outcome of Death associated with the and that key data (clearance, half-life) are derived from it (top down reported exposure. If no inquiry was made to the poison center, approach). Physiologically based PTK (PBPTK) modeling uses results a death is defi ned as Death, Indirect Report. The singular ques- from in silico, in vitro and in vivo studies in a bottom up approach. tion that must be answered in reviewing and categorizing deaths This PBPTK modeling approach is helpful in estimating target organ is: Did the exposure cause the death? In 2000, only poison center doses that can be expected from human external exposure. The fact deaths (Death and Death, Indirect Report) judged to be probably or that PBPTK models are mechanism-based allows them to be “ generic ” undoubtedly related to the exposure were identifi ed in the annual to a certain extent enabling simulations and predictions of the kinetics report as poison-related fatalities. under special circumstances, e.g. the implementation of age- and dis- Methods: Beginning in 2006, a new system of evaluating and ease-dependent physiological changes and also the kinetics in organs classifying deaths was implemented. Each death (Direct or Death, which are experimentally diffi cult to access, e.g. the liver. The need Indirect Report) was evaluated by a medical and a clinical toxi- for high-quality in vitro and in silico data on absorption, distribution, cologist, reviewed by a medical toxicologist fatality manager and metabolism as well as excretion (ADME) as input for PBPTK models computer scored based on the review results. Deaths and Death, is necessary to predict human concentration-time profi le. Pharmaco-/ Indirect Reports were assigned to one of six Relative Contribution toxicokinetic-pharmaco-/toxicodynamic (PTK/PTD) modeling means to Fatality (RCF) categories. RCFs were designated separately by to develop a model for the concentration/AUC-effect relationship which the regional PC and the AAPCC review team with difference reso- is coupled to the PTK model. Empirical models are non-mechanistic lution part of the review process. The RCFs denote the probability and the parameters may be adequate for describing the longitudinal of the exposure substance(s) being responsible for the death: 1) data at hand (e.g. the time course of an effect), but that may not be Undoubtedly responsible (Proximate Cause of Death) - beyond a biologically relevant. A semi-mechanistic model is a compromise. reasonable doubt, 2) Probably responsible - some reasonable doubt Discussion and conclusion: The goal of modelling is to describe remains, 3) Contributory - the substance(s) alone did not cause the the time course of xenobiotic actions that are most represented in death, but combined with other factors, were partially responsible, the (PKPD) measurements or the responses (the “ data ” ), with sim- 4) Probably not responsible - establishes to a reasonable probabil- ple but adequate complexity. Physiologically-based modeling of ity, but not conclusively, that the death was not poison related, 5) pharmaco-/toxicodynamics requires an a priori knowledge on the Clearly not responsible (and Not Contributory) - establishes beyond underlying mechanisms causing toxicity or causing the disease. a reasonable doubt that the substance(s) did not cause the death, and 6) Unknown - insuffi cient evidence to establish a causative rela- 2. Epidemiology of fatal poisonings: National Poison tionship between the substance(s) and the death. The fi rst iteration Data System (NPDS) data 2000–2014 of this revised process was published in Table 21 of the 2006 NPDS Annual report and included fatalities with RCFs 1-4. Although all 1,2 Alvin C Bronstein deaths received by the poison centers were reported, only those 1 Department of Emergency Medicine, University of Colorado with an RCF of 1-4 were listed in Table 21. This changed with School of Medicine, Denver, USA; 2 Rocky Mountain Poison the 2007 report when only deaths with an RCF of 1, 2, or 3 were Center, Denver Health, Denver, USA listed. The reporting process changed again in the 2010 Annual 233 234 XXXV International Congress of the EAPCCT Report with Death, Indirect Report only being assigned a RCF by Objective: To review homicidal poisonings in the UK and else- the regional center. Thus this scoring process attempts to quantify where since 2000. exposure relatedness to the cause of death. Only deaths with an Methods: A systematic search of the newspaper database Nexis, RCF of 1, 2, or 3 are designated true poison related fatalities. together with online indexes of several relevant journals, for the Results: In 2000, 920 deaths (Direct and Death, Indirect Report) terms “ murder ” and “ poison ” . Languages were limited to English, were recorded. This number increased to 1728 deaths (Direct and Dutch, and French. Death, Indirect, includes all RCFs) by 15 December 2014. Although Results: Sixty-one separate cases in which murder or attempted NPDS human exposures peaked in 2008, the proportion of deaths murder was alleged or proven were identifi ed in 19 different coun- has remained relatively constant from 2000-2014 (15 December). tries. In one case a man became psychotic after taking 3-methoxy- The median number of all deaths was 1544 [range: 920, 2937] or phencyclidine, and methylenedioxypyrovalerone, and repeatedly 0.06% [0.04, 0.13] (median [min, max]) of all human exposures. stabbed his father; and in another a man was found hanged by his Subtle differences are observed in exposure route and substance turban after having been poisoned with parathion. Otherwise, all count between all human exposures and deaths. Over the 15 year deaths or intended deaths were directly caused by poisoning. The period the top 3 routes for all human exposures were: Ingestion largest number killed was 42, poisoned with tetramine by a restau- (81.9%), Dermal (7.6%), and Inhalation/nasal (6.0%) compared to rateur after a row with a neighbouring restaurant in Nanjing, China. all reported deaths: Ingestion (79.4%), Inhalation/nasal (8.8%), and Arsenic, cyanide, and opioids were among the traditional poisons Parenteral (5.3%). Routes for fatalities with RCF 1, 2, or 3 were: used; and ricin and aconite among the plant poisons employed. Ingestion (83.8%), Inhalation/nasal (9.1%), and Parenteral (4.3%). A number of cases of poisoning by healthcare workers involved Although most human exposures were single substance exposures ajmaline, insulin, pethidine, potassium and suxamethonium. (90.7%), only 42.8% of all fatalities with RCF 1, 2, or 3 were due to Conclusion: Reports of murder by poisoning remain rare, but the one substance. In 2000, the top 5 substance categories associated with wide range of agents used, the potential diffi culties of diagnosis, human poisoning-related deaths were: Analgesics, Antidepressants, and the lack of systematic reporting make the true incidence of Sedative/Hypnotics/Antipsychotics, Stimulants and Street Drugs, homicidal poisoning diffi cult to ascertain. and Cardiovascular Drugs. By late 2014, this ranking had changed to Sedative/Hypnotics/Antipsychotics, Cardiovascular Drugs, Opioids, Stimulants and Street Drugs, and Alcohols, refl ecting changing use, 4.
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