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Article Look but Don't Lick! Find out How These Brightly Colored Frogs
The Power of Poison Look But Don’t Lick! GRADES K-2 NOTES FOR EDUCATORS Common Core State Standards: W.K-2.2, W.K-2.8 Have students read the article “Look but Don’t Lick!” Have them write notes RI.K-2.1, RI.K-2.2, RI.K-2.4, RI.K-2.7, RI.K-2.10 in the large right-hand margin. For example, they could underline key passages, paraphrase important information, or write down questions that New York State Science Core Curriculum: they have. LE 3.1a Next Generation Science Standards: If it is not possible to create color handouts, use a computer projector to PE 1-LS1-2 display the reading so that students can see the colorful frog photos. You DCI LS1.A: Structure and Function may also have them color their black and white copies to match the actual All organisms have external parts. Different colors. animals use their body parts in different ways to see, hear, grasp objects, protect Ask: themselves, move from place to place, and • What does it mean for an animal to be poisonous? (A: An animal is seek, find, and take in food, water and air. poisonous if its body contains a substance that is harmful or fatal to other Plants also have different parts (roots, animals.) stems, leaves, flowers, fruits) that help • How does being poisonous help the frogs in this article survive? (A: them survive and grow. Predators will not eat an animal that is poisonous to them. The frogs signal that they are poisonous by their bright colors, which warn predators not to eat them. -
Manganese and Its Compounds: Environmental Aspects
This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organization, or the World Health Organization. Concise International Chemical Assessment Document 63 MANGANESE AND ITS COMPOUNDS: ENVIRONMENTAL ASPECTS First draft prepared by Mr P.D. Howe, Mr H.M. Malcolm, and Dr S. Dobson, Centre for Ecology & Hydrology, Monks Wood, United Kingdom The layout and pagination of this pdf file are not identical to the document in print Corrigenda published by 12 April 2005 have been incorporated in this file Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals. World Health Organization Geneva, 2004 The International Programme on Chemical Safety (IPCS), established in 1980, is a joint venture of the United Nations Environment Programme (UNEP), the International Labour Organization (ILO), and the World Health Organization (WHO). The overall objectives of the IPCS are to establish the scientific basis for assessment of the risk to human health and the environment from expos ure to chemicals, through international peer review processes, as a prerequisite for the promotion of chemical safety, and to provide technical assistance in strengthening national capacities for the sound management -
HISTORY of LEAD POISONING in the WORLD Dr. Herbert L. Needleman Introduction the Center for Disease Control Classified the Cause
HISTORY OF LEAD POISONING IN THE WORLD Dr. Herbert L. Needleman Introduction The Center for Disease Control classified the causes of disease and death as follows: 50 % due to unhealthy life styles 25 % due to environment 25% due to innate biology and 25% due to inadequate health care. Lead poisoning is an environmental disease, but it is also a disease of life style. Lead is one of the best-studied toxic substances, and as a result we know more about the adverse health effects of lead than virtually any other chemical. The health problems caused by lead have been well documented over a wide range of exposures on every continent. The advancements in technology have made it possible to research lead exposure down to very low levels approaching the limits of detection. We clearly know how it gets into the body and the harm it causes once it is ingested, and most importantly, how to prevent it! Using advanced technology, we can trace the evolution of lead into our environment and discover the health damage resulting from its exposure. Early History Lead is a normal constituent of the earth’s crust, with trace amounts found naturally in soil, plants, and water. If left undisturbed, lead is practically immobile. However, once mined and transformed into man-made products, which are dispersed throughout the environment, lead becomes highly toxic. Solely as a result of man’s actions, lead has become the most widely scattered toxic metal in the world. Unfortunately for people, lead has a long environmental persistence and never looses its toxic potential, if ingested. -
Letter from the Desk of David Challinor December 1992 We Often
Letter from the Desk of David Challinor December 1992 We often identify poisonous animals as snakes even though no more than a quarter of these reptiles are considered venomous. Snakes have a particular problem that is ameliorated by venom. With nothing to hold its food while eating, a snake can only grab its prey with its open mouth and swallow it whole. Their jaws can unhinge which allows snakes to swallow prey larger in diameter than their own body. Clearly the inside of a snake's mouth and the tract to its stomach must be slippery enough for the prey animal to slide down whole, and saliva provides this lubricant. When food first enters our mouths and we begin to chew, saliva and the enzymes it contains immediately start to break down the material for ease of swallowing. We are seldom aware of our saliva unless our mouths become dry, which triggers us to drink. When confronted with a chocolate sundae or other favorite dessert, humans salivate. The very image of such "mouth watering" food and the anticipation of tasting it causes a reaction in our mouths which prepares us for a delightful experience. Humans are not the only animals that salivate to prepare for eating, and this fluid has achieved some remarkable adaptations in other creatures. scientists believe that snake venom evolved from saliva. Why it became toxic in certain snake species and not in others is unknown, but the ability to produce venom helps snakes capture their prey. A mere glancing bite from a poisonous snake is often adequate to immobilize its quarry. -
Acute Poisoning: Understanding 90% of Cases in a Nutshell S L Greene, P I Dargan, a L Jones
204 REVIEW Postgrad Med J: first published as 10.1136/pgmj.2004.027813 on 5 April 2005. Downloaded from Acute poisoning: understanding 90% of cases in a nutshell S L Greene, P I Dargan, A L Jones ............................................................................................................................... Postgrad Med J 2005;81:204–216. doi: 10.1136/pgmj.2004.024794 The acutely poisoned patient remains a common problem Paracetamol remains the most common drug taken in overdose in the UK (50% of intentional facing doctors working in acute medicine in the United self poisoning presentations).19 Non-steroidal Kingdom and worldwide. This review examines the initial anti-inflammatory drugs (NSAIDs), benzodiaze- management of the acutely poisoned patient. Aspects of pines/zopiclone, aspirin, compound analgesics, drugs of misuse including opioids, tricyclic general management are reviewed including immediate antidepressants (TCAs), and selective serotonin interventions, investigations, gastrointestinal reuptake inhibitors (SSRIs) comprise most of the decontamination techniques, use of antidotes, methods to remaining 50% (box 1). Reductions in the price of drugs of misuse have led to increased cocaine, increase poison elimination, and psychological MDMA (ecstasy), and c-hydroxybutyrate (GHB) assessment. More common and serious poisonings caused toxicity related ED attendances.10 Clinicians by paracetamol, salicylates, opioids, tricyclic should also be aware that severe toxicity can result from exposure to non-licensed pharmaco- -
Toxicity Forecaster (Toxcasttm)
science in ACTION www.epa.gov/research INNOVATIVE RESEARCH FOR A SUSTAINABLE FUTURE Toxicity Forecaster (ToxCastTM) ADVANCING THE NEXT GENERATION OF CHEMICAL SAFETY EVALUATION Tens of thousands of chemicals are currently in commerce, and hundreds more are introduced every year. Because current chemical testing is expensive and time consuming, only a small fraction of chemicals have been fully evaluated for potential human health effects. Through its computational toxicology research (CompTox), the U.S. Environmental Protection Agency (EPA) is working to figure out how to change the current approach used to evaluate the safety of chemicals. CompTox research integrates advances in biology, biotechnology, chemistry, and computer science to identify important biological processes that may be disrupted by the chemicals and tracing those biological the potential to limit the number of of sources; including industrial and disruptions to a related dose and required laboratory animal-based consumer products, food additives, human exposure. The combined toxicity tests while quickly and and potentially “green” chemicals information helps prioritize efficiently screening large numbers that could be safer alternatives to chemicals based on potential human of chemicals. existing chemicals. These 2,000 health risks. Using CompTox, chemicals were evaluated in over thousands of chemicals can be The first phase of ToxCast, 700 high-throughput assays that evaluated for potential risk at a small appropriately called “Proof of cover a range of high-level cell cost in a very short amount of time. Concept”, was completed in responses and approximately 2009 and it evaluated over 300 300 signaling pathways. ToxCast A major part of EPA’s CompTox well studied chemicals (primarily research is the Toxicity Forecaster research is ongoing to determine pesticides) in over 500 high- which assays under what conditions (ToxCast™). -
TOXICOLOGY and EXPOSURE GUIDELINES ______(For Assistance, Please Contact EHS at (402) 472-4925, Or Visit Our Web Site At
(Revised 1/03) TOXICOLOGY AND EXPOSURE GUIDELINES ______________________________________________________________________ (For assistance, please contact EHS at (402) 472-4925, or visit our web site at http://ehs.unl.edu/) "All substances are poisons; there is none which is not a poison. The right dose differentiates a poison and a remedy." This early observation concerning the toxicity of chemicals was made by Paracelsus (1493- 1541). The classic connotation of toxicology was "the science of poisons." Since that time, the science has expanded to encompass several disciplines. Toxicology is the study of the interaction between chemical agents and biological systems. While the subject of toxicology is quite complex, it is necessary to understand the basic concepts in order to make logical decisions concerning the protection of personnel from toxic injuries. Toxicity can be defined as the relative ability of a substance to cause adverse effects in living organisms. This "relative ability is dependent upon several conditions. As Paracelsus suggests, the quantity or the dose of the substance determines whether the effects of the chemical are toxic, nontoxic or beneficial. In addition to dose, other factors may also influence the toxicity of the compound such as the route of entry, duration and frequency of exposure, variations between different species (interspecies) and variations among members of the same species (intraspecies). To apply these principles to hazardous materials response, the routes by which chemicals enter the human body will be considered first. Knowledge of these routes will support the selection of personal protective equipment and the development of safety plans. The second section deals with dose-response relationships. -
Role of the Inflammasome in Defense Against Venoms
Role of the inflammasome in defense against venoms Noah W. Palm and Ruslan Medzhitov1 Department of Immunobiology, and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520 Contributed by Ruslan Medzhitov, December 11, 2012 (sent for review November 14, 2012) Venoms consist of a complex mixture of toxic components that are Large, multiprotein complexes responsible for the activation used by a variety of animal species for defense and predation. of caspase-1, termed inflammasomes, are activated in response Envenomation of mammalian species leads to an acute inflamma- to various infectious and noninfectious stimuli (14). The activa- tory response and can lead to the development of IgE-dependent tion of inflammasomes culminates in the autocatalytic cleavage venom allergy. However, the mechanisms by which the innate and activation of the proenzyme caspase-1 and the subsequent – immune system detects envenomation and initiates inflammatory caspase-1 dependent cleavage and noncanonical (endoplasmic- – fl and allergic responses to venoms remain largely unknown. Here reticulum and Golgi-independent) secretion of the proin am- matory cytokines IL-1β and IL-18, which lack leader sequences. we show that bee venom is detected by the NOD-like receptor fl family, pyrin domain-containing 3 inflammasome and can trigger In addition, activation of caspase-1 leads to a proin ammatory cell death termed pyroptosis. The NLRP3 inflammasome con- activation of caspase-1 and the subsequent processing and uncon- “ ” ventional secretion of the leaderless proinflammatory cytokine sists of the sensor protein NLRP3, the adaptor apoptosis-as- sociated speck-like protein (ASC) and caspase-1. Damage to IL-1β in macrophages. -
Ethylene Glycol Ingestion Reviewer: Adam Pomerlau, MD Authors: Jeff Holmes, MD / Tammi Schaeffer, DO
Pediatric Ethylene Glycol Ingestion Reviewer: Adam Pomerlau, MD Authors: Jeff Holmes, MD / Tammi Schaeffer, DO Target Audience: Emergency Medicine Residents, Medical Students Primary Learning Objectives: 1. Recognize signs and symptoms of ethylene glycol toxicity 2. Order appropriate laboratory and radiology studies in ethylene glycol toxicity 3. Recognize and interpret blood gas, anion gap, and osmolal gap in setting of TA ingestion 4. Differentiate the symptoms and signs of ethylene glycol toxicity from those associated with other toxic alcohols e.g. ethanol, methanol, and isopropyl alcohol Secondary Learning Objectives: detailed technical/behavioral goals, didactic points 1. Perform a mental status evaluation of the altered patient 2. Formulate independent differential diagnosis in setting of leading information from RN 3. Describe the role of bicarbonate for severe acidosis Critical actions checklist: 1. Obtain appropriate diagnostics 2. Protect the patient’s airway 3. Start intravenous fluid resuscitation 4. Initiate serum alkalinization 5. Initiate alcohol dehydrogenase blockade 6. Consult Poison Center/Toxicology 7. Get Nephrology Consultation for hemodialysis Environment: 1. Room Set Up – ED acute care area a. Manikin Set Up – Mid or high fidelity simulator, simulated sweat if available b. Airway equipment, Sodium Bicarbonate, Nasogastric tube, Activated charcoal, IV fluid, norepinephrine, Simulated naloxone, Simulate RSI medications (etomidate, succinylcholine) 2. Distractors – ED noise For Examiner Only CASE SUMMARY SYNOPSIS OF HISTORY/ Scenario Background The setting is an urban emergency department. This is the case of a 2.5-year-old male toddler who presents to the ED with an accidental ingestion of ethylene glycol. The child was home as the father was watching him. The father was changing the oil on his car. -
Venom Week 2012 4Th International Scientific Symposium on All Things Venomous
17th World Congress of the International Society on Toxinology Animal, Plant and Microbial Toxins & Venom Week 2012 4th International Scientific Symposium on All Things Venomous Honolulu, Hawaii, USA, July 8 – 13, 2012 1 Table of Contents Section Page Introduction 01 Scientific Organizing Committee 02 Local Organizing Committee / Sponsors / Co-Chairs 02 Welcome Messages 04 Governor’s Proclamation 08 Meeting Program 10 Sunday 13 Monday 15 Tuesday 20 Wednesday 26 Thursday 30 Friday 36 Poster Session I 41 Poster Session II 47 Supplemental program material 54 Additional Abstracts (#298 – #344) 61 International Society on Thrombosis & Haemostasis 99 2 Introduction Welcome to the 17th World Congress of the International Society on Toxinology (IST), held jointly with Venom Week 2012, 4th International Scientific Symposium on All Things Venomous, in Honolulu, Hawaii, USA, July 8 – 13, 2012. This is a supplement to the special issue of Toxicon. It contains the abstracts that were submitted too late for inclusion there, as well as a complete program agenda of the meeting, as well as other materials. At the time of this printing, we had 344 scientific abstracts scheduled for presentation and over 300 attendees from all over the planet. The World Congress of IST is held every three years, most recently in Recife, Brazil in March 2009. The IST World Congress is the primary international meeting bringing together scientists and physicians from around the world to discuss the most recent advances in the structure and function of natural toxins occurring in venomous animals, plants, or microorganisms, in medical, public health, and policy approaches to prevent or treat envenomations, and in the development of new toxin-derived drugs. -
Poison Hemlock G
Pasture Weed Fact Sheet W 325 Poison Hemlock G. Neil Rhodes, Jr., Professor and Extension Weed Management Specialist Trevor D. Israel, Extension Assistant Department of Plant Sciences Poison Hemlock Conium maculatum L. Classification and Description Poison hemlock, also called deadly hemlock, poison parsley, spotted hemlock, and California fern, is a highly poisonous bien- nial weed that is a member of the family Apiaceae, which is also referred to as the carrot family. It was originally introduced as a garden plant because of its attractive flowers. Other members of this family include wild carrot (Daucus carota L.), wild chervil (Anthriscus syvlestris (L.) Hoffm.), and a close relative to poison hemlock, water hemlock (Cicuta maculata L.). This native of Eurasia is found throughout Tennessee where it usually occurs in patches in cool-season grass pastures, roadsides, drainage ditches and stream banks. The cotyledons or seed leaves of seedlings are Fig. 1. Poison hemlock flowers in compound umbels. oblong-lanceolate, and the first true leaf is pinnately compound and glabrous. Flowers are small and white in large, compound umbels 1.5 to 2.4 inches wide (Fig. 1). The hollow stems of this plant are ridged, glabrous, and purple-spotted (Fig. 2). Leaves form a basal rosette; they are alternate upward, petioled, approxi- mately 8 to 16 inches long, broadly triangular-ovate, and com- pound. Leaflets are lanceolate to ovate-oblong, finely cut, less than 0.5 inch long. Crushed leaves have a mouse-like odor. Ma- ture plants can be 3 to 4 feet tall (Fig. 3) with fibrous roots branching from a turnip-like taproot (Fig. -
Mercury Spill Fact Sheet
This fact sheet is intended to be a quick reference tool for people who are involved in a mercury spill and cleanup event. MERCURY Mercury mercury MERCURY MERCURY MERCURY Elemental mercury, also called “quicksilver,” is a heavy, silvery, form of the metal mercury that is liquid at room temperature. It can slowly change from a liquid into a gas that is invisible to the naked eye. The gas or “vapors” that are released will start to fill a room if mercury is spilled indoors. MERCURY EXPOSURE Mercury is a very toxic or poisonous substance that people can be exposed to in several ways. If it is swallowed, like from a broken thermometer, it mostly passes through your body and very little is absorbed. If you touch it, a small amount may pass through your skin, but not usually enough to harm you. Mercury is most harmful when you breathe in the vapors that are released when a container is open or a spill occurs. HEALTH EFFECTS Pregnant women, infants and young children are particularly sensitive to the harmful effects of mercury. The health effects that can result from mercury exposure depend on how much mercury you are exposed to and how long you are exposed. Some of the acute effects, ones that may come soon after exposure to high concentrations of mercury are: • Headaches, chills, fever • chest tightness, coughs • hand tremors • nausea, vomiting, abdominal cramps, diarrhea Some effects that may result from chronic, or longer term exposure to mercury vapor can be: • Personality changes • Decreased vision or hearing • Peripheral nerve damage • Elevated blood pressure Children are especially sensitive to mercury and at risk of developing a condition known as acrodynia or “Pinks Disease” by breathing vapors or other exposure circumstances.