Poisons and Poisoning [382]
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Murder by Poison in Scotland During the Nineteenth and Early Twentieth Centuries
Merry, Karen Jane (2010) Murder by poison in Scotland during the nineteenth and early twentieth centuries. PhD thesis. http://theses.gla.ac.uk/2225/ Copyright and moral rights for this thesis are retained by the author A copy can be downloaded for personal non-commercial research or study, without prior permission or charge This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the Author The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the Author When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given Glasgow Theses Service http://theses.gla.ac.uk/ [email protected] Murder by Poison in Scotland During the Nineteenth and Early Twentieth Centuries Karen Jane Merry Submitted for the Degree of Doctor of Philosophy School of Law Department of Forensic Medicine Faculty of Law, Business and Social Science Faculty of Medicine © Karen Jane Merry July 2010 ABSTRACT This thesis examines the history of murder by poison in Scotland during the nineteenth and early twentieth centuries, in the context of the development of the law in relation to the sale and regulation of poisons, and the growth of medical jurisprudence and chemical testing for poisons. The enquiry focuses on six commonly used poisons. Each chapter is followed by a table of cases and appendices on the relative scientific tests and post-mortem appearances. The various difficulties in testing for these poisons in murder and attempted murder cases during the period are discussed and the verdicts reached by juries in poisoning trials considered. -
Signs and Symptoms of Pesticide Poisoning
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Historical Materials from University of Nebraska-Lincoln Extension Extension 1997 EC97-2505 Signs and Symptoms of Pesticide Poisoning Larry D. Schulze University of Nebraska - Lincoln, [email protected] Clyde Ogg University of Nebraska - Lincoln, [email protected] Edward F. Vitzthum University of Nebraska - Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/extensionhist Part of the Agriculture Commons, and the Curriculum and Instruction Commons Schulze, Larry D.; Ogg, Clyde; and Vitzthum, Edward F., "EC97-2505 Signs and Symptoms of Pesticide Poisoning" (1997). Historical Materials from University of Nebraska-Lincoln Extension. 1225. https://digitalcommons.unl.edu/extensionhist/1225 This Article is brought to you for free and open access by the Extension at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Historical Materials from University of Nebraska-Lincoln Extension by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. University of Nebraska Cooperative Extension EC97-2505-A Signs and Symptoms of Pesticide Poisoning Larry D. Schulze, Extension Pesticide Coordinator Clyde L. Ogg, Extension Assistant, Pesticide Training Edward F. Vitzthum, Coordinator, Environmental Programs z Manage Your Risk z Signal Words z Read the pesticide Label z Routes of Exposure z Pesticide Toxicity z Recognizing Signs and Symptoms of Poisoning z Recognizing Common pesticide Poisonings { Organophosphate and Carbamate Insecticides { Organochlorine Insecticides { Synthetic Pyrethroid Insecticides { Plant-derived Insecticides { Inorganic Insecticides { Microbial Insecticides { DEET Repellent { Bipyridyl Herbicides { Chlorophenoxy Herbicides { Arsenical Herbicides { Wood Preservatives { Fumigants { Rodenticides { Fungicides z What To Do When Pesticide Poisoning Occurs z References z Pesticide Safety Telephone Numbers Accidental exposure or overexposure to pesticides can have serious implications. -
Strychnine Poisoning
0++- Poison HOTLINE Partnership between UnityPoint Health and University of Iowa Hospitals and Clinics November 2013 Strychnine Poisoning Strychnine is a chemical naturally found in the seeds of the tree Strychnos nux- vomica. It is mainly used as a pesticide to control rats, moles, gophers, and coyotes. Commercial baits are pelleted and often dyed red or green. Strychnine has on rare occasions been found to be mixed with street drugs such as LSD, heroin, and cocaine. Strychnine is a white, odorless, bitter tasting crystalline powder that can be taken by mouth, inhaled or given intravenously. Strychnine is highly toxic and Did you know …… only a small amount is needed to produce severe health effects in people. As little as 30 mg may cause death in an adult. Vaporizing alcohol and “smoking” the vapors (inhaling Strychnine blocks the action of the neurotransmitter glycine which controls how is a more accurate term) is a nerve signals are sent to muscles. Glycine is an inhibitory neurotransmitter and new method for alcohol works like an “off switch” for muscles. When this “off switch” is not working consumption. The alcohol is because it is being blocked by strychnine, muscles throughout the body have poured into a vaporizing severe, painful spasms. While these spasms may look like the patient is having machine or over dry ice and a seizure, it is not a true seizure and there is no post-ictal phase. Repetitive inhaled. The alcohol enters muscle spasms caused by strychnine will lead to fever, muscle break down the lungs where it is rapidly (rhabdomyolysis), severe metabolic acidosis and respiratory failure. -
Dermal Exposure to Strychnine
Journal of Analytical Toxicology, Vol. 25, July/August 2001 [CaseReport Dermal Exposureto Strychnine Richard Greene 1 and Robert MeatheralP,* 1Emergency Department, Grace General Hospital and 2Laboratory Medicine, St. Boniface General Hospital, Winnipeg, Manitoba, Canada Downloaded from https://academic.oup.com/jat/article/25/5/344/778260 by guest on 24 September 2021 t Abstract ] tents into the toilet. She accidently spilled about 1 cupful on the floor, which she wiped up with a cloth soaked in a diluted Javex A non-fatal case of strychnine poisoning through dermal exposure is solution (sodium hypochlorite). Her dermal exposure was limited described. About 24 b after cleaning up a strychnine spill, a 50-year- to her left palm; she washed her hands about 30 rain after old woman presented to the emergency department with classical cleaning up the spill. During the prodromal time period, she signs of strychnine poisoning, consisting of marked pain in the experienced no irritation or dermatitis to the left hand. Except for muscles of her lower limbs, dermal sensitivity, and stiffness in her a tingling sensation in her left hand, she was asymptomatic until jaw. Her treatment was intravenous fluid replacement and about 22:00 h when her arms and legs began to shake, pro- alkalinization in anticipation of potential renal failure due to gressing to spasms. Over the course of the night, the frequency rhabdomyolysis. Her plasma creatine kinase was elevated to 677 and duration of these muscle contractions increased. By U/L with no rise in the heart specific MB fraction. Serum myoglobin morning, the pain was more severe in the muscles of her lower level obtained retrospectively was 195 pg/L. -
Adverse Health Effects of Heavy Metals in Children
TRAINING FOR HEALTH CARE PROVIDERS [Date …Place …Event …Sponsor …Organizer] ADVERSE HEALTH EFFECTS OF HEAVY METALS IN CHILDREN Children's Health and the Environment WHO Training Package for the Health Sector World Health Organization www.who.int/ceh October 2011 1 <<NOTE TO USER: Please add details of the date, time, place and sponsorship of the meeting for which you are using this presentation in the space indicated.>> <<NOTE TO USER: This is a large set of slides from which the presenter should select the most relevant ones to use in a specific presentation. These slides cover many facets of the problem. Present only those slides that apply most directly to the local situation in the region. Please replace the examples, data, pictures and case studies with ones that are relevant to your situation.>> <<NOTE TO USER: This slide set discusses routes of exposure, adverse health effects and case studies from environmental exposure to heavy metals, other than lead and mercury, please go to the modules on lead and mercury for more information on those. Please refer to other modules (e.g. water, neurodevelopment, biomonitoring, environmental and developmental origins of disease) for complementary information>> Children and heavy metals LEARNING OBJECTIVES To define the spectrum of heavy metals (others than lead and mercury) with adverse effects on human health To describe the epidemiology of adverse effects of heavy metals (Arsenic, Cadmium, Copper and Thallium) in children To describe sources and routes of exposure of children to those heavy metals To understand the mechanism and illustrate the clinical effects of heavy metals’ toxicity To discuss the strategy of prevention of heavy metals’ adverse effects 2 The scope of this module is to provide an overview of the public health impact, adverse health effects, epidemiology, mechanism of action and prevention of heavy metals (other than lead and mercury) toxicity in children. -
The Deactivation of Industrial SCR Catalysts—A Short Review
energies Review The Deactivation of Industrial SCR Catalysts—A Short Review Agnieszka Szymaszek *, Bogdan Samojeden * and Monika Motak * Faculty of Energy and Fuels, AGH University of Science and Technology, Al. Mickiewicza 30, 30-059 Kraków, Poland * Correspondence: [email protected] (A.S.); [email protected] (B.S.); [email protected] (M.M.) Received: 2 July 2020; Accepted: 24 July 2020; Published: 29 July 2020 Abstract: One of the most harmful compounds are nitrogen oxides. Currently, the common industrial method of nitrogen oxides emission control is selective catalytic reduction with ammonia (NH3-SCR). Among all of the recognized measures, NH3-SCR is the most effective and reaches even up to 90% of NOx conversion. The presence of the catalyst provides the surface for the reaction to proceed and lowers the activation energy. The optimum temperature of the process is in the range of 150–450 ◦C and the majority of the commercial installations utilize vanadium oxide (V2O5) supported on titanium oxide (TiO2) in a form of anatase, wash coated on a honeycomb monolith or deposited on a plate-like structures. In order to improve the mechanical stability and chemical resistance, the system is usually promoted with tungsten oxide (WO3) or molybdenum oxide (MoO3). The efficiency of the commercial V2O5-WO3-TiO2 catalyst of NH3-SCR, can be gradually decreased with time of its utilization. Apart from the physical deactivation, such as high temperature sintering, attrition and loss of the active elements by volatilization, the system can suffer from chemical poisoning. All of the presented deactivating agents pass for the most severe poisons of V2O5-WO3-TiO2. -
Detection,Prevention and Management of Arsenicosis in India
Detection,Prevention and Management of Arsenicosis in India A Field Guide Directorate General of Health Services Ministry of Health and Family Welfare Government of India 1 FOREWORD Arsenicosis has been known to be a health problem in some parts of our country. It occurs mainly by drinking Arsenic contaminated ground water and also through contaminated food chain or Industrial pollution for prolonged period. It results in skin manifestations such as Kerotosis, Melanosis and may also affect lungs, liver or lead to various types of cancers. The condition is preventable if measures are taken to provide safe drinking water to the community, promotion of nutrition and also if diagnosed early. With a view to formulate Guidelines for prevention, control and management of Arsenicosis, an Expert Group was constituted under my Chairmanship. After detailed round of discussions and subsequent exchange of communications, these Guidelines have now been finalized. I am sure that these Guidelines shall be very useful for sensitizing the Health Programme Managers and for training of Medical & Paramedical personnel in the field. I compliment the officials of the Nutrition & IDD Cell of the Dte. General of Health Services for facilitating in preparation and finalization of these Guidelines. It is hoped that these Guidelines shall be helpful in prevention and control of Arsenicosis in the affected areas of the country. Dr. Jagdish Prasad Director General of Health Services, Ministry of Health & Family Welfare, Government of India. 2 CONTENTS 1. Preamble 2. Health Impacts of exposure 3. Detection and Management of Arsenicosis Goal and Objectives Components Linkages & Coordination mechanism Recording and Reporting Review and Evaluation 4. -
Question of the Day Archives: Monday, December 5, 2016 Question: Calcium Oxalate Is a Widespread Toxin Found in Many Species of Plants
Question Of the Day Archives: Monday, December 5, 2016 Question: Calcium oxalate is a widespread toxin found in many species of plants. What is the needle shaped crystal containing calcium oxalate called and what is the compilation of these structures known as? Answer: The needle shaped plant-based crystals containing calcium oxalate are known as raphides. A compilation of raphides forms the structure known as an idioblast. (Lim CS et al. Atlas of select poisonous plants and mushrooms. 2016 Disease-a-Month 62(3):37-66) Friday, December 2, 2016 Question: Which oral chelating agent has been reported to cause transient increases in plasma ALT activity in some patients as well as rare instances of mucocutaneous skin reactions? Answer: Orally administered dimercaptosuccinic acid (DMSA) has been reported to cause transient increases in ALT activity as well as rare instances of mucocutaneous skin reactions. (Bradberry S et al. Use of oral dimercaptosuccinic acid (succimer) in adult patients with inorganic lead poisoning. 2009 Q J Med 102:721-732) Thursday, December 1, 2016 Question: What is Clioquinol and why was it withdrawn from the market during the 1970s? Answer: According to the cited reference, “Between the 1950s and 1970s Clioquinol was used to treat and prevent intestinal parasitic disease [intestinal amebiasis].” “In the early 1970s Clioquinol was withdrawn from the market as an oral agent due to an association with sub-acute myelo-optic neuropathy (SMON) in Japanese patients. SMON is a syndrome that involves sensory and motor disturbances in the lower limbs as well as visual changes that are due to symmetrical demyelination of the lateral and posterior funiculi of the spinal cord, optic nerve, and peripheral nerves. -
Survival After Deliberate Strychnine Self-Poisoning, with Toxicokinetic Data
University of Wollongong Research Online Faculty of Science, Medicine and Health - Papers: part A Faculty of Science, Medicine and Health 2002 Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data David Michael Wood Guy’s and St. Thomas’ Hospital Emma Webster Royal Oldham Hospital Daniel Martinez Guy’s and St. Thomas’ Hospital Paul Ivor Dargan Guy’s and St. Thomas’ Hospital Alison L. Jones University of Wollongong, [email protected] Follow this and additional works at: https://ro.uow.edu.au/smhpapers Part of the Medicine and Health Sciences Commons, and the Social and Behavioral Sciences Commons Recommended Citation Wood, David Michael; Webster, Emma; Martinez, Daniel; Dargan, Paul Ivor; and Jones, Alison L., "Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data" (2002). Faculty of Science, Medicine and Health - Papers: part A. 1903. https://ro.uow.edu.au/smhpapers/1903 Research Online is the open access institutional repository for the University of Wollongong. For further information contact the UOW Library: [email protected] Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data Abstract Introduction Strychnine poisoning is uncommon, and in most severe cases, the patient dies before reaching hospital. The management of strychnine poisoning is well documented, although there are few data on the kinetics of elimination of strychnine after overdose. Case report A 42-year-old man presented shortly after ingestion of an unknown quantity of strychnine powder. After a respiratory arrest, with intensive supportive management requiring admission to an intensive care unit, he survived. Eight serum samples were taken over the first 5 days and analysed subsequently for strychnine concentrations. -
Ingested Lethal Ageni's Strychnine
REVIEW OF CURRENT VERTEBRATE PESTICIDES D. Glen Crabtree Bureau of Sport Fisheries and Wildlife, Wildlife Research Center, B1dg. 45, Denver Federal Center, Denver 25, Colorado. For the purpose of this brief review, EmG>hasis will be placed on development, physical properties, physiological action, experience and limitations of vertebrate pesticides primarily of current opera- tional 1.m;portance in the control of field rodents and predatory animals. INGESTED LETHAL AGENI'S STRYCHNINE (C21H~202) 'Dlis al.kaloid was discovered by Pelletier and Cavento,}/in 1817 as a constituent in the seeds of Strychnos Nux-vomica or Strychnos !gnatii, which were used :for killing dogs, cats and birds in Europe at least as early as J.6ljo • Strychnine (probably the sulfate) appears to have been introduced as a pesticide in the United States about 1847 and became the g/ principal tool of the professional "wolfer" during the years 1800-1885. PHYSICAL PROPERTIES: ~e alkaJ.oid of commerce is a white or greyish white powder prepared from seeds grown in Southern Asia. It is quite stable, almost insoluble in water, but soluble in many organic solvents and to varying degrees in dilute acids With which it forms salts having limited solubility in water. Strychnine and its salts have an exceedingly bitter taste and are not absorbed through the normal intact skin. 327 Both the alkaloid and strychnine sul.fate are widely used today as vertebrate pesticides. In the case of the latter, allowance must be made in preparing l.ethal baits since it contains onl.y 78.04~ strychnine. PHYSIOLOGICAL ACTION: Ingested strychnine is proJJG>tly absorbed, mainly, from the intestinal tract. -
N-Acetylcysteine in the Treatment of Human Arsenic Poisoning
J Am Board Fam Pract: first published as 10.3122/jabfm.3.4.293 on 1 October 1990. Downloaded from N-Acetylcysteine In The Treatment Of Human Arsenic Poisoning Debra S. Martin, M.D., Stephen E. Willis, M.D., and David M. Cline, M.D. Abstract: A 32-year-old man was brought to the emergency department 5 1/2 hours after ingesting a potentiaIly lethal dose (900 mg) of sodium arsenate ant poison in a suicide attempt. The patient deteriorated progressively for 27 hours. After intramuscular dimercaprol and supportive measures failed to improve his condition, he was given N-acetylcysteine intravenously. The patient showed remarkable clinical improvement during the following 24 hours and was discharged from the hospital several days later. (J Am Board Fam Pract 1990; 3:293-6.) Arsenic has been used since medieval times, known use of intravenous NAC in a patient with both as medicine and poison. Although its me arsenic poisoning. dicinal use has declined, arsenic can still be found as an ingredient in certain homeopathic Case Report formulas, I which are available in some health A 32-year-old man was brought to the emer food stores. Arsenic also is present in high con gency department by ambulance 5 hours after centrations in many easily obtainable ant kill he ingested approximately 900 mg of sodium ers, and this source is responsible for most toxic arsenate - five times the lethal doseJ,6 - in a human ingestions. 2 Other sources include in suicide attempt. He was lethargic but arousable secticides, herbicides, and rodenticides. Com by voice and answered questions appropriately. -
CHAPTER E49 Heavy Metal Poisoning
discussion with respect to the four most hazardous toxicants (arsenic, CHAPTER e49 cadmium, lead, and mercury). Arsenic, even at moderate levels of exposure, has been clearly linked with increased risks for cancer at a number of different tissue Heavy Metal Poisoning sites. These risks appear to be modified by smoking, folate and selenium status, and other factors. Evidence is also emerging that low-level arsenic may cause neurodevelopmental delays in children Howard Hu and possibly diabetes, but the evidence (particularly for diabetes) remains uneven. Metals pose a significant threat to health through low-level environ- Serious cadmium poisoning from the contamination of food mental as well as occupational exposures. One indication of their and water by mining effluents in Japan contributed to the 1946 CHAPTER e49 importance relative to other potential hazards is their ranking by outbreak of “itai-itai” (“ouch-ouch”) disease, so named because the U.S. Agency for Toxic Substances and Disease Registry, which of cadmium-induced bone toxicity that led to painful bone frac- maintains an updated list of all hazards present in toxic waste sites tures. Modest exposures from environmental contamination have according to their prevalence and the severity of their toxicity. The recently been associated in some studies with a lower bone density, first, second, third, and seventh hazards on the list are heavy metals: a higher incidence of fractures, and a faster decline in height in lead, mercury, arsenic, and cadmium, respectively (http://www. both men and women, effects that may be related to cadmium’s atsdr.cdc.gov/cercla/07list.html) . Specific information pertaining calciuric effect on the kidney.